Download C: CHON F: C: energy Store,Supply,Structure P: Structural




Components & Functions
Biological Molecules:
Carbohydrates, Proteins, Lipids,
Vitamins, Nucleic Acids, Water






Define Risk Factor & Metabolism
Monomers & Polymers:
Carbohydrates, Proteins, Nucleic
Acids
Condensation VS Hydrolysis
Reactions
C: CHON
F:
C: energy Store,Supply,Structure
P: Structural components, Antibodies, Membrane carrier &
pores, Enzymes, Hormones, Growth & Repair
L: Hormones, thermal Insulation, Membrane
V: act Coenzymes, form Larger molecules (anabolic reactions)
NA: Store & Carrier info
H2O: Support plants, Solvent, Transport
RF: increasing chance of developing a particular disease
M: sum total biochemical reactions in cells of organismsanabolic (build small into large-muscle growth, protein
synthesis)/catabolic (break down large into small-respiration,
digestion)

C,P,NA: All anabolic, form similar, smaller
molecules
Monomer
Polymer
Carbohydrate Monosaccharide Polysaccharide
Amino acids
Polypeptide
Proteins
Nucleotide
DNA & RNA
Nucleic Acids
Bonds
Glycosidic
Peptide
H
(between
bases)

Con: anabolic, H2O released, bond forms,

catalysed by enzymes, monomerpolymer
H: catabolic, H2O added, bond broken, cbe,
polymermonomer
Carbohydrates





Function: see 1st card^^ St (starch), Su (glucose during
respiration),Str (cellulose (plant cell wall), chitin(exoskeleton
insects), peptidoglycan(bacteria cell wall))
CHO
Sweet, Soluble, Small, form Crystals
5 carbon monosaccharide-pentose sugar, furranose, 5
membered ring structure e.g. Fructose, Ribose, Deoxyribose
6 carbon monosaccharide-hexose sugar, pyrranose, 6
membered ring structure e.g. Glucose, Galactose
Same molecular formula, different structural formula
Structural Isomer: Define & α & β Glucose
Glucose Monosaccharides bond to form…
α
H
β
hydroxyl (OH) group of carbon 1 is
below the plane of the ring
--above—
Break down for respiration (Glucose+
O2Co2+H2O+ATP)
Animals & Plants cannot break
down different arrangement, can’t
used respiration
Rotated 180˚
Long, straight chains
No rotation
Coiled (Amylose), Branched
(Amylopectin)
Starch, Glycogen
Page 1 of 24
Cellulose, Micro&Macrofibrils
How Glycosidic bond
forms
Starch VS Glycogen α
1,4 Glycosidic bond form maltose… amylose (coil, spring
shape=compact, trap iodine in coils(test turn blue-black)
/amylopectin (branched, 1,6 Glycosidic bond)…starch
Starch




Cellulose β, Micro &
Macrofibrils &
Structure:Function
Glycogen
Mix long, straight Amylose

Only 1,4 Glycosidic
bonds shorter, more
(1,4, coil, compact, iodine) &
branches
branched Amylopectin 1,4
&1,6 (branches)

More compact
Stored chloroplasts & cells

Forms Glycogen
granules, found muscle
of storage organs- lots
starch grains
& liver cells
Plants

Animals
α Glucose, energy stores, insoluble, stored don’t affect ψ,
chains easily hydrolysed for respiration
β glucose

Glucose has a no. of OH groups, so H bonds can
form. 60-70 βG=Micro fibrils crosslinked H bonds,
lots microf=macrof- form cell wall,

S:F---S:cell walls made macrof crosslinked with
H bonds, F: adds strength & support

S:Cellulose plant cell walls when H2O moves in
stops bursting becomes turgid, F: support

Arrangement of macrof determines how cell
grows/changes shape, F:e.g. Guard cells,
stomata, inner edge, help open for photosynthesis/
inadvertently transpiration


CHON S (cytosteine in R Group)
Function: see 1st card^^ S,A,M,E,H, G&R
Proteins
Acid group



Amphoteric (both basic & acidic properties)
R group determines characteristics
o P need nitrates (DNA) from soil to manufacture aa
o Animals need essential aa can’t build from materials
taken in, found in meat, vegetarians have soya (Plants
have fewer essential aa)
o A can’t store aa, toxic, removed deamination in liver,
converted to urea & removed in urine
aadipeptidepolypeptide(condensation reaction)protein
Page 2 of 24




Primary sequence: 2D, aa, aa specific sequence
as code for a specific protein & determined by
DNA
Condensation/hydrolysis reactions are catalysed
by enzymes-Hydrolysis of peptide bondsProtease enzymes. E.g. ageing (lose elasticity,
older build less collagen (protein))/hormone
regulation (need to break down so effects not
permanent, any cell targeted by hormones needs
enzymes to hydrolyse hormone)
Secondary: β pleated sheets & α helix- held H
bonds,
Tertiary: 3D, globular/fibrous, specific shape, has
disulphide bridges (cysteine), ionic bonds(attraction
between opposite charges), hydrophobic interactions, H
bonds (uneven distribution of e-)
Quaternary: more than 1 polypeptide chain, 2 identical/
a no. of different subunits

Globular: globe shape, hydrophobic turn in, hydrophilic turn out,
make proteins H2O-soluble H2O easily clusters-metabolic role,
enzymes, have tertiary & quaternary structure as well
Fibrous: regular, repetitive sequence of aa, insoluble, structural
role-keratin/collagen, generally only primary & secondary structure

Heat protein temp beyond optimum, KE increase,
molecules vibrate, break weak bonds, hold tertiary
structure, unravel & protein not function, even if cooled
will not reform- denatured
Haemoglobin

Haemoglobin VS Collagen
S:F
Lipids: Function,
Made up of, Fatty
Acids
Triglyceride VS
Phospholipid VS
Cholesterol













Wide range aa in
primary sequence,
wound α helix
4 polypeptide chains:
2 α, 2 β
Globular-H2O-soluble
4 Haem group (nonprotein, no aa) contain
ferrous ions, carries 4
O2 molecules,
associates at lungs,
disassociates at tissues
Collagen


35% primary- glycine
CHON

3 polypeptide chains:
coil, compact
Fibrous-insoluble
H bonds between, add
strength e.g. artery
walls stop blood
bursting walls at high
pressure e.g. tendons
allow bone to move


Function see 1st card: H, I, M, So (more e than carbohydrates), St e
Dissolve in alcohol not H2O
Not polymer, not made up of identical subunits & can’t add more
CHO
Fat- control fluidity, Unsaturated (HDL, healthy, e.g. Oleic acid, c=c,
fewer H bonds, changes shape pushes molecules apart, greater fluidity,
lots in plants )
o Saturated (LDL, unhealthy, stearic acid, c-c, lots in animals)
Triglyceride
1 glycerol &
3 fatty acids
(carboxylic acid &
hydrocarbon chain)
Energy store
Insoluble doesn’t affect
ψ
Stored fat, protection,
insulation
joined ester bonds
Page 3 of 24


Phospholipid
1 glycerol, 2 fatty acids
(hydrophobic tail)&
phosphate group
(hydrophilic head)
Phosphatecarbohydrate,
carbohydrate attached
to protein= glycolipid,
involved cell signalling



Cholesterol
4 Carbon based
ring structures
joined
Strengthen,
support bilayer
Used form
steroid hormones



H bonding, Role of H2O






Chemical Tests
Biuret (proteins), Starch
(carbohydrates), Ethanol
Emulsion & Grease Spot (lipids),
Reducing & Non-Reducing
Sugars

Uneven distribution of e- creates electrostatic
attraction
H bonds continuously making & breaking, allow
movement
High specific heat capacity great amount of
energy to raise temp 1kg of H2O by 1˚c, lots of
energy for H bonds to break, difficult turn (Lg)
evaporating uses lots energy, heat to 100˚c before
boils. reason why temp lakes stable even when
dramatic changes in temp. takes lots energy for a
small variations temp, doesn’t heat up/cool quicklyacts thermal buffer
(s-ice) temp falls, H2O less movement, less KE,
less vibrations, H bonds form don’t break as easily,
forms semi-crystalline shape, less dense than
(L), free to move, spread out whereas (s) H2O
pushed apart by H bonds. Cools density
increases until 4˚c then density lowers
ice forms on surface, insulates below, organism
survive winter, don’t freeze, allows H2O to
circulate
cohesive-sticks to each other creates high
surface tension
charged will dissolve, - & + charges interact with
H2O, H2O clusters around charged part,
dissolves
See sheet
Quantitative: quantities/amounts have changed
e.g. carry out Benedict’s test on each conc, filter
liquid from precipitate, more reducing sugar, more
precipitate, place liquid in curvette, measure
absorbance of liquid using colorimeter (measures
how much light can pass through), more cu
sulphate used up, more precipitate form, less light
transmitted, after each reading, zero colorimeter
reset with water, 100% transmission, make
calibration curve plot conc (x axis) against
absorbance (y)
Qualitative: observation, e.g. colour
IV
Independent &
Dependent Variable,
Control, Reliability,
Precise









DV
Reaction rate (y)
Lines are DV
IV (x axis)
Variable/Limiting Factor, measure no. time intervals
IV: Factor investigated, know values, set up by
investigator, must be accurate & precise so DV are valid
C
DV: Factor measured each change of IV, don’t know
values
1 Variable measured, rest kept constant
Control: test to show observed results due to IV no other
factor
Reliability: confidence data obtained again repeated.
E.g. repeat x3, identify anomalous results, take a mean
Valid: data is reliable & answers original question e.g.
control conc substrate, pH, temp
Accuracy: value close to true value, e.g. more
intermediate values, narrower range
Page 4 of 24





DNA
All DNA acts as
info store

RNA
3 forms: messenger RNA
(template coding strand, moves
out nuclear pore, attaches to
ribosome, contains genetic
information-protein synthesis),
transfer RNA (brings aa to
ribosome in correct order to form
polypeptides, interprets code
genetic info on mRNA into aa,
specific sequence peptide bonds
form giving rise to primary &
thus… secondary, tertiary,
quaternary structure can form,
clover shape), ribosomal RNA
(forms structure of ribosome, 2
subunits, assembly site
aaproteins)
Pentose ribose sugar
Replicates in Interphase

Pentose
deoxyribose
sugar
 Adenine=Uracil, Guanine (3
Nitrogenous
organic bases:
hydrogen bonds) Cytosine
Adenine=Thymin  RNA bases can be
e, Guanine (3
complementary to DNA bases
hydrogen bonds)
Cytosine
Double stranded,
 Single stranded
antiparallel5’Prime end to
3’Prime end on
left & 3-5’ on right
Hold coded info to build organism, sugar-phosphate
backbone
1.
2.
3.
4.
5.
Semiconservative Replication
DNA Structure: Function
Enzymes Key Terms
DNA helicase unwinds & unravels
double helix, breaking H bonds
between complementary base
pairs.
Each strand of parent DNA acts as
a template.
Free nucleotides attracted & align
with exposed bases, bind to
complementary base pairs, H
bonds form A=T, C (3 H bonds) G.
DNA Polymerase forms bonds
between nucleotides to complete
sugar-phosphate backbone
Produces 2 DNA molecules
genetically identical, 1 strand from
each from original, parent DNA & 1
strand from each from new,
daughter DNA.





Info store-protein synthesis, info to build organism
Long- so lots of info stored
Bases complementary- info can be replicated
Double helix- stability
Weak H bonds- easy unzip



Globular-H2O Soluble (see pg3)
Complementary & Specific shape
Reaction catalysed enzymes: need 1 specific enzymeGlycosidic, ester, peptide. More than 1 enzymerespiration, photosynthesis
Acts as a Catalyst- speeds up a reaction by lowering
the activation energy (amount energy required for
reaction to proceed), not used up, unchanged after
reaction
3D/Tertiary shape
Activity can be effected by: temp, pH, (anything that
affects no. of collisions which form ES complexes &
shape of active site)
E.g. lactase breaks down lactoseα Glucose +
Galactose




Page 5 of 24


Define Heterotroph

bread, amylase. Branching hyphae penetrate bread, secrete
digestive enzymes & absorb soluble products,
o Enzymes digest carbohydrates (Amylase breaks down
starchmaltose. maltase (disaccharide) breaks down
maltoseα Glucose & α Glucose---- lactase. Lactose
αGlucose & Galactose, sucrose, break down sucrose
αGlucose & Fructose)
o Proteins (protease. Break down paa)
o Lipids (lipase. Break down to glycerol & hydrocarbon
fatty acid chain)
Intracellular & Extracellular
Enzyme Action

Lock & Key
Heterotrophs-organisms obtain nutrients by consuming
others
Intrac: enzymes catalyse inside cell. E.g. defence in
phagocytosis/ DNA replication DNA polymerase
Extrac: enzymes catalyse outside cell e.g. mould digests

Induced Fit
LK: enzymes, proteins specific tertiary shape due to sequence
of aa in primary structure, specific active site, only bind to one
type of specific, complementary shaped substrate,
IF: enzyme changes shape, due to flexibility/ charges on R
groups of aa in active site, opposite charges attract, active
site fit closely/widens slightly to allow larger substrate (e.g.
competitive inhibitors)
form E-S complex, change in enzyme shape add strain to
substrate, reaction occurs more easily
E-P complex forms, product different shape to active site
moves away, enzyme returns to original shape & catalyses
another reaction
Limiting Factors affect
enzyme activity: Temp, pH,
Enzyme & Substrate conc



Only models: simple representation of the process or

showing people how it works
IF more likely, supported by more evidence, more evidence
fits more closely (than lock & key)
1 Variable measured, rest kept constant
T: (use a water bath with controlled thermostat to control) higher,
more KE, bonds vibrate more & greater strain, molecules move faster,
enzyme & substrate moving faster a greater no. & more successful
collisions with enzyme active site, more E-S complexes form, more EP complexes form, more products, higher rate of reaction, optimum,
max rate of reaction (40-50˚c)Temp goes beyond optimum, too high
weak bonds break, hold tertiary structure, unravel & protein not
function, even if cooled will not reform, can’t be restored- denatured.

pH: (Maintain use buffer solutions, e.g. optimum= pH 7) Higher conc
H+, more acidic, lower pH. Significant increase/decrease pH away from
the optimum, alter tertiary structure & thus active site, held in place by
no. of bonds (H+, ionic) rely on charges to form. Lower pH, more H+,
attract – charges on α helix, replace H bonds, change structure, active
site changes shape, specific & complementary substrate can no longer
fit, new bonds interfere binding substrate, few E-S & E-P complexes,
rate reaction slows/reduced. Only denatures if extreme pH changes.
E.g. pepsin, in stomach optimum pH2, trypsin, small intestine pH7.
Temp&pH

Enzyme conc: (accurately measured volume, in living tissue
measure mass, must ensure all tissue has same no. of enzyme
molecules) if EC variable (thing that changes) then fixed SC. More
enzymes, greater no. available active sites, more ES & EP complexes,
more products, higher rate of reaction. Further increase in EC, not
enough substrates, limits rate, flattens (at max rate)

Substrate & Enzyme conc
Substrate conc: (accurately measure volume/mass, have to
ensure same no. of substrates) if SC variable (thing that changes (in
excess)) then fixed EC. More substrates, more freq collisions….
Further increase, meet max rate reaction, all available enzyme active
sites will be full, rate flatten can’t increase further, limits rate
Page 6 of 24

A
B




Initial Rate
Competitive &
Non-Competitive Inhibitors
Inhibitor-slows the rate by affecting the enzyme

Comp: similar, complementary, tertiary structure to active
site, form E-I complexes, no product forms, inhibitor doesn’t
break up, prevents substrate enters directly competes for
active site, E-S & E-P complexes reduced, rate slows. Amount
inhibition depends on conc substrate & inhibitor, Higher
substrates, inhibitor less effect, substrate more likely to
collide with active site e.g. Penicillin- permanent, (bind
effectively denatured) Statins- reversible (when remove
inhibitor, enzyme unaffected)

Non c: don’t compete, inhibitor binds away from active site,
distorts tertiary structure, changes specific shape of active
site, substrate not complementary, doesn’t fit, less E-S &E-P
complexes form, rate decreases. High conc of inhibitor,
reaction slows, rate reduced, substrate can’t collide different
shape e.g. Potassium Cyanide- Permanent

Cofactor -some enzymes only catalyse if certain non-
Cofactors (+ Inorganic ion
cofactors)

& Coenzymes (Prosthetic
group)
Metabolic Poisons
Initial Rate- max possible rate it’s when enzyme &
substrate first mixed together. Reaction proceeds,
products formed, substrate broken down & used
up, less available, less freq & less successful
(product gets in way) collisions, rate slows,
flattens
Always be a limiting factor (reason why
plateaus)- could be temp, pH, enzyme/substrate conc
When describing the graph, describe each region
Rate of Reaction=1/time
Compare DV compare initial rates, take several
reading & plot on graph IV (x axis), DV (lines/y
axis), take tangent at steepest portion=initial rate
protein groups present (not involved in reaction, just
have to be present), only bind for short time either same
time/just before substrate binds
o Inorganic ion cofactors- e.g. amylase breaks
down starchmaltose only if Cl- present
Coenzyme- involved in reaction & change as a result,
recycled, link metabolic pathways that need to take
place in sequence (1st enzyme product becomes 2nd
enzyme’s substrate…final enzyme’s product is 1st
enzyme’s substrate/non comp inhibitor so end product
doesn’t build up)
o Prosthetic group- co e, permanent part of
enzyme

Inhibit/Over activate enzymes

Potassium Cyanide-non comp, permanent
inhibitor-inhibits cell respiration in enzyme,
cytochrome oxidase in mitochondria,
decreases respiration so less O2 & ATP
produced organism only anaerobic respiration
so build up lactic acid in blood. Untreated,
unconsciouscomadeath 2hrs
Page 7 of 24

Biosensor

Drugs work inhibiting
enzyme activity (Viruses,
(Penicillin) Bacteria,
Antibiotics, Cystic Fibrosis



BS: Uses enzyme reactions to detect presence of
substances, if present enzyme reactions take place to
break down, reduce amount
Virus- treatment use protease inhibitors, prevent virus
replicating, stops virus build new virus coats- comp
inhibitor
Bacteria- treat Penicillin, competes substrate used in
cell walls & inhibits enzyme forms crosslinks, add
strength, penicillin binds instead, walls weak & fall apart,
bacteria can’t replicate
Antibiotics- inhibit growth of microorganisms cause
bacterial infections
Cystic Fibrosis- digestive enzymes in pancreas blocked,
can’t digest, treat: enzyme, acid resistant coat not
denatured in stomach
1. Natural Selection
2. Genetic Variation/ Random mutations
3. Resistant/ Survival of fittestmust be a selection
pressure e.g. antibiotics, climate, enviro
4. Those best adapted (selective advantage) survive,
passing on alleles (selective advantage) to
offspring
5. Allele only confers resistance/survival to that
particular selection pressure in that specific
conc/temp/pH etc.
6. Happens for many generations, selective
advantage passed on, helping o to survive
Resistance
Define Balance Diet

BD: all nutrients required for health in appropriate
proportions
C:St,Su,Str e.g. bread, sugar–P:Str,A,M,E,H,G&R e.g.
eggs, meat--V: C, L, H20/Fat soluble--H2O: Su, So,T
60% body (See pg1, card 1) Mi: Inorganic, Essential—
Fibres: Indigestible, Essential—F/L: M, Energy e.g.
Nutrients: Function & e.g.
(Carbohydrates, Proteins,
Vitamins, H2O, Minerals,
Fibre, Fats/Lipids)


57% carbohydrates, 30% fats, 13% proteins
Level of Activity



More active, need more ^^ nutrients
If increase in weight, eating too many energy
containing foods (carbohydrates, fats, proteins)
vice versa for decrease in weight. Energy
Intake=Outake, no weight put on or lost
O: 20%+ heavier than recommended weight for
height, BMI 30+, important dietary factor lead to
Cancer, CVD, Type 2 Diabetes
Malnutrition- unbalanced diet-obesity/defiency

BMI=
dairy, oil
Define Obesity

Define Malnutrition
BMI
Page 8 of 24
𝑀𝑎𝑠𝑠 𝑖𝑛 𝑘𝑔
(ℎ𝑒𝑖𝑔ℎ𝑡 𝑖𝑛 𝑚)2

Coronary Heart Disease
Hypertension




Fats/Lipids, Cholesterol &
Lipoproteins





Humans depend on plats
for food

Make food production
efficient


Result fatty deposits by atherosclerosis,
increase friction (no longer smooth
endothelium), energy lost going over deposits,
encourage more deposition, narrows lumen,
restricts blood flow, if lumen becomes blocked
starve cells of O2 & nutrients required to survive,
cells die. Blocks coronary artery, starve heart O2.
E.g. excess salt, decrease ψ of blood, more H2O
moves into blood plasma, (increase blood
pressure= hypertension)
Fats: Sat (c-c, unhealthy),Unsat (see page 3)
Cholesterol: Sa f, in cell/skin membrane, insoluble in H2O
Lipoproteins transport fats & cholesterol around body, made
up of lipids, cholesterol, proteins. Don’t eat but diet effects
conc of them. In Blood, taken up cells correct receptors (on
plasma membrane)
HDL
LDL
Healthy

Unhealthy
Carry cholesterol from tissues

Carry c liver to
back to liver
tissues
Produced by uns fats

Sa f
At Liver used to make bile
Decreases cholesterol (Sa f,

Increases cholesterol
LDL) levels in blood, reduces
in blood, less able to
amount deposited in artery walls
removed, more to be
by atherosclerosis
deposited
Basis of food chain, Omnivores- directly eat
plants/indirectly eat herbivorous animals
P: Use pesticides/insecticides-reduce loss plants
by pests/disease-----Use fertilisers-increase
fertility of crops & thus size of yield
A: Increase productivity, rate of growth &
resistance to disease (selective
breeding/artificial selection)
1.
2.
Selective
Breeding/Artificial
Selection
Genetic Variation/ Random mutations
Resistant/ Survival of fittestmust be a selection pressure
e.g. climate, enviro
3. Those best adapted (selective advantage) survive.
4. Isolation: Humans select offspring showing the specific
characteristics/ selective advantage to breed
5. Inbreeding: When they breed, they pass on alleles (selective
advantage) to offspring
6. Allele only confers resistance/survival to that particular
selection pressure in that specific conc/temp/pH etc.
7. Happens for many generations, selective advantage passed
on, helping organisms to survive & increase growth rate/yield/
productivity.
(don’t use words already in question, no marks)
Animals
In Viro
Fertilisation,
surrogate mother
place (fertilised
egg) embryo into
uterus
Artificial
insemination
Plants
Prevent cross pollination, reduce gene pool,
reduce genetic diversity, maintains carefully
selective bred traits, by cutting off stamens
Test if plant has desirable characteristics e.g.
want it to be salt tolerant, test in soil with high
salt conc. E.g. low pH etc.
Marker Assisted Selection: section DNA used as marker to
identify desirable characteristic, selection begin young age when
Page 9 of
24
DNA checked

Microorganisms-Penicillin on bread, extracellular
enzyme action, enzymes catalyse outside cell, mould
digests bread, amylase. Branching hyphae penetrate
bread, secrete digestive enzymes & absorb soluble
products/nutrients, Salmonella,
Food Spoilage & Methods
to prevent

Prevent FS
o Pickling- low pH, high acidity, denature
enzymes prevent it from breaking down food
o Dry, Salting & Coat in Sugar- dehydrates,
H2O leaves by osmosis
o Cook- high temp denature enzymes prevent it



Example of how
Microorganisms can make
food
+
+
+
+



Define Health, Disease,
Parasite, Pathogen
Cause Disease

o
o
o
o
from breaking down food
Prevent further contamination- canning (heated &
sealed, denatured & can’t enter), vacuum wrapping
(no air, microbes can’t respire aerobically)
E.g. Alcohol & Bread- yeast, anaerobic,
release CO2 causes rise
Quorn: microorganism, single cell protein,
made from edible fungus, meat substitute
+
No
- Conditions grow in
fats/cholesterol
are also ideal for
pathogens- take care
No animal welfare
prevent infection of
to consider
wrong organism
Production can
- Different taste other
increase/decrease
proteins
with demand
Grows on waste,
- People don’t want to
econ viable
eat things grown on
waste
H: state mental, physical & social wellbeing
D: departure from good health caused by malfunction of
mind/body
Par: organism lives on (external p- head louse)/in
(internal p- tapeworm) another living thing, causes harm
to host which lead secondary infections allow other o to
invade
Pat: organism causes disease
Protoctista (Kingdom) enter host & feed contents as
grows, e.g. Causive Agent: Malaria, Plasmodium feeds
on RBC contents
Prokaryote (Kingdom) Bacteria reproduce rapidly, cause
damage to cells. E.g. CA: Mycobacterium Tuberculosis/
M. Bovis
Fungi (Kingdom) e.g. Ringworm lives in skin sends out
reproductive hyphae grow surface of skin release
spores
Virus- invade cells takes over organelles, nucleus,
cause cells manufacture more virus, host cell
bursts releases virus
Page 10 of 24
Cause & Transmission &
Global Impact of
TB
Cause

Transmission

Mycobacterium
Bovis/ Tuberculosis
Droplet Infection
from infected- coughing, sneezing
etc.
Infected when inhale droplets
Contract milk/meat of cattle
Effects
Lungs



More likely if…
Close contact over
prolonged period
Poor ventilation,
diet, health
Homeless

Worldwide




Many inactive/controlled immune
system
Global Impact
Cause & Transmission &
Global Impact of
Malaria
Cause
Parasite:
Transmission

Spread Vector female anopheles
Plasmodium
mosquito
falciparum/
1. If host already has malaria, suck parasite
vivax
gametes into stomach
2. Gametes fuse, Zygote develops in stomach
3. Infective stages formed (spread disease),
move to mosquito’s salivary glands
4. Mosquito bites another, injects saliva as
anticoagulant, reduce blood clotting
5. Salivary glands contain infective stages
6. In host, salivary glands enter liver, where
they multiply before passing into blood
again
7. In blood enter RBCs, gametes are produced

Malarial parasites live RBC of host feed
Haemoglobin
Global Impact

Limited where vector female anopheles mosquito can
survive
Cause

1.
HIV (human
Cause & Transmission &
Global Impact of
immunodeficiency virus)
infective agent: causes
AIDS (Acquired Immune
Deficiency Syndrome)
opportunistic infections
3.
4.

HIV / AIDS
2.
Takes control when
entered T cells: viral
DNA, inserted in host
DNA, viral RNA
produced & codes for
viral proteins




Transmission
Physical Contact
Virus enters, remains inactive
(HIV Positive)
Active-attacks & destroys T
helper cells (WBCs help to
prevent infection, ability to resist
infection is reduced, unable to
defend) vulnerable
Contract range of opportunistic
infections
Effect of these diseases that kills
T: Use unsterilized surgical
equipment
Exchange body fluids(blood-toblood contact)
Sharing hypodermic needles
From Mother to Baby during
breastfeeding
Global Impact

Worldwide
Page 11 of 24


Key terms
They determine:
o
o
o
o
Incidence (no. new cases in pop per year)
Prevalence (no. people with the disease at a given time)
Mortality (no. who die from disease each yr)
Morbidity (no. people with disease as a proportion of
pop)
o Identify countries at greatest risk, age range at risk
With info ^^ health organisations can: target research find
cures major diseases, target advertisement raise awareness
 LEDCs tend poorer health- poverty, poor hygiene &
nutrition, less educated

Immune Response:
Primary>>>


Immune Response:
Secondary
Pandemic (worldwide epidemic), Endemic (always
present in pop), Epidemic (spreading rapidly large no.
over large area)
Epidermiology- study of distribution of disease in pop,
calculate average risk of a person in a certain pop
developing a disease & factors influence spread

Pathogens: transmitted, when reach host need
pass through primary defences (attempt prevent
pathogens entering & causing harm to host), inside
pass through secondary defences/immune
response
Primary (non-specific)
Skin- act as a physical barrier, prevent entry of
microorganisms
Mucous Membrane- certain substances need to
enter/ exit, leaves body exposed to infection. e.g.
gut, ears, nose--epithelial layer of goblet cells,
secrete mucus & trap pathogens & cilia, removes
pathogens, moves synchronised pattern wafts
mucus up trachea, swallowed down oesophagus to
stomach, high acidity, low pH, kills pathogens
Other- eyes protected antibodies in tear fluid, kills
bacteria
Phagocytes
Neutrophils
Macrophages
 Multi-lobed nucleus
 Larger
 Manufacture bone marrow
 Manufacture bone marrow
 Travel in blood move out into TF
 Travel in blood as monocytes, settle organs &
 Short lived
develop into macrophages
 Involved specific response
1. Phagocytes engulf & destroy. Pathogen enters,  Infected cells release histamine, attracts
recognised as ‘foreign’ by antigens on outer
neutrophils
plasma membrane, (own cells have antigens
 Histamine makes capillaries more leaky, more
recognised as ‘self’ & don’t produce a response)
fluid leaves capillaries into TF into lymphatic
2. Phagocytes have receptors on plasma
system leads pathogens towards fixed
membrane attach to antibodies bind antigens on
macrophages in lymph nodes
pathogen.
3. Once phagocyte bound pathogen, envelop
pathogen by infolding membrane, form a
phagosome (vacuole). Lysosomes fuse
phagosome, release hydrolytic enzymes, digest
pathogen. End products, harmless, absorbed
into cytoplasm.
 Immune Response- activation of lymphocytes in blood& production of antibodies to fight disease
Page 12 of 24


Antigen: stimulate immune response
Antibody/Immunoglobulin: proteins identify &
neutralise antigens
Define Antigen & Antibody
Complementary shape to
particular antigen, immune system
manufacture 1 antibody for
every antigen
Structure of Antibody
Agglutination &
Neutralisation
2 light + 2 heavy chains= 4
polypeptide chains held
by disulphide bridges
Constant Regionsame on all, so
antibodies can attach
to receptors on
plasma membrane of
phagocytes in
phagocytosis
Hinge Region-flexibility,
allows branches move further
apart & bind more than 1
antigen

A: large antibody binds many antigens, too
large to enter host, many specific variable
regions

N: attach antigen, cover pathogen binding
site, prevent binding & entering to host cell

P: Infecting agent (pathogen) enters, stimulates
immune response, immune system produces
antibodies, few days find correct lymphocyte
(clonal selection) & divide& replicate (clonal
expansion) to sufficient levels to combat infection
successfully
S: Antibodies don’t stay in blood. If same pathogen
invades again, memory cells recognise it, response
starts earlier, greater quantity & more rapid
production of antibodies, rises to sufficient level
faster

Immune Response:
Primary & Secondary
Variable Region- specific aa
sequence, complementary &
specific shape so only
specific antigens can bind
Page 13 of 24

Communication between cells to coordinate a
response, involves glycolipids & glycoproteins,
release cytokines (signal), target cell detects
signal, signal+ receptor bind, complementary
shape. B+T lymphocytes receptors on plasma
membrane complementary to specific foreign
antigens, antigen detected, lymphocytes
activated, e.g. stimulate production
antibodies/phagocytosis etc.

Identification: pathogen has foreign antigens on its
plasma membrane, act as markers, signal
pathogen is foreign
T & B cells have antibodies attached to plasma
membrane, complementary to only one type of
antigen.
o Clonal selection- select specific T/B cell by
antigen presenting cells (macrophages
fixed in lymph node, act as phagocytes
engulf & digest, separate antigens &
incorporate in plasma membrane of
macrophage=antigen presenting cell,
function: find lymphocytes neutralise
particular antigen)/T helper cells (role:
release cytokines (signals) & interleukins,
stimulate B cells to divide & stimulate
phagocytosis and plasma cells which
produce antibodies).
o Clonal expansion- T & B cells divide by
mitosis, increasing no. of lymphocytes, all
with identical receptors/variable regions in
their antibodies attached.
Cell Signalling
Structure & Mode of action
of T & B Lymphocytes
o
Communication using
Cytokines (signals)
o
e.g. macrophages release monokines: attract
neutrophils by chemotaxis &--- stimulate B cells to
differentiate & release antibodies
o
T, B cells & macrophages release interleukins, stimulate
proliferation & differentiation of B & T cells (B cells
differentiate & grow in Bone Marrow, T cells grow in Bone
Marrow & differentiate in Thymus Gland)

T cells- cell mediated immunity, grow bone
marrow & matures thymus gland
B cells-humoral immunity, grow & matures bone
marrow

T Cells
B Cells
T cells differentiate:
B cells differentiate:
 Form plasma cells
 T helper cells
produce antibodies
 T killer cells-recognise
complementary to
& destroy infected cells
antigen
by apoptosis, can’t
spread the infection.
 T & B memory cells-remain in ., ready to respond
in future if the same pathogen with same antigens,
provides immunological memory.


Invades again-memory cells recognise antigen, produce
clone, form B plasma cells (produce antibodies against
antigen), destroy before symptoms appear, form T
helper/killer/more memory cells
Instructions: cytokines (signals) released act as
instructions to target cells, bind to receptor on plasma
membrane, triggers response, release 2nd messenger
inside cell triggers further response.
 When cells send distress signals: pathogens enter &
infect cells, causes damage to pathogen (lysosomes in
cell attempt break down) & body cells (pathogen remain
on plasma membrane of body cell- act distress signal &
marker show cell is infected
See sheet
Page 14of 24

Vaccination: Define,
Natural, Artificial,
Passive, Active, Ring,
Herd
Passive
(produced not
manufactured??,
immunity without
activation of
lymphocytes,
short-lived)
Active (activate
immune system,
lymphocytes
produced, longlasting)




New sources of
medicine & HIV
Deliberate exposure to antigenic material, actives immune system to
make immune response& provide immunity

Artificial (deliberate
exposure to
antigen/antibody)

Immunity provided by
injection of antibodies
made by another
individual (tetanus
injection )

Immunity provided by
antibodies made in
immune system as
result of vaccination.
Deliberate exposure
to antigenic material
that is harmless
(dead/attenuate
weakened, harmless
version) activates
immune system treats
as real disease,
produces antibodies &
memory cells (TB &
Influenza)

Ring V: new case reported, vaccination all in immediate vicinity-e.g.
used control livestock disease
Herd V: provide immunity all pop at risk- e.g. vaccination programmes
New strains form by mutations, existing vaccinations have little/no
effect, especially viruses (Influenza-strain changes/mutates every
year, different antigens, antibody produced needs match antigen)
New drugs needed: antibiotics less effective as
microorganisms evolve, random mutations, new drugs act
as selection pressure & new diseases are emerging
HIV- if receptors on plasma membrane blocked,
pathogen can’t enter & cause harm to host. Isolate & look
at aa sequence, use modelling determine shape of
receptor, produce drug identical shape, no major side
effects

Smoking Short & Long
Term Effects
Natural (gained
immunity through
exposure during
normal life)
 Antibodies
provided via
placenta,
baby immune
to disease
Mother’s
immune to
 Immunity
provided by
antibodies
made in
immune
system as
result of
infection
 Suffer once
then immune
(chicken pox)
Short:
o Tar settles lining airways, increases diffusion
pathway, narrows bronchioles, reduces
elasticity, causes allergic reaction-smooth
muscle contracts, narrows lumen, constricts
airways

Long:
o Lead COPD (Chronic Obstructive Pulmonary
Disease)
o Damage lining airways by constant cough,
o
Page 15 of 24
replaced scar tissue, reflex to remove scar
tissue, damage thicker (increases diffusion
pathway, narrows lumen, airways restricted)
Elasticity reduced alveoli &bronchioles, exhale
don’t recoil, bronchioles collapse, decreases
SA, traps air, pressure increases, alveoli burst

Lung Cancer: Symptoms
S: Continual coughing, chest pain, shortness of
breath
Entrance to bronchi, smoke hits fork in airway,
deposits tar contains carcinogen compounds in
smoke. Tar destroys cilia can’t remove, longer time in
contact with epithelial cells, enter nucleus of
epithelial cells in lung tissue, effect DNA controls cell
division, causes mutation-uncontrollable cell
division, forms tumour

&…

Emphysema (COPD):
Symptoms & …

Chronic Bronchitis
(COPD): Symptoms & …





Smoke contains:



Atherosclerosis

Thrombosis
CHD



Stroke
& Symptoms



S: tired, breathing shallow & rapid, harder exhale, loss
elastin
Phagocytes invade secrete enzyme ,elastin destroyed, alveoli
fail to recoil ; constriction of bronchioles, forced
expiration, causes alveoli to burst , reduces SA
S: Cough mucus, Lung irritation
Inflammation airways, Tar destroys cilia, mucus not removed
& over-active goblet cells, build-up of mucus leads to
bronchitis
Tar (see page 15)
CO (enters RBCs, combines haemoglobin, more readily
than O2 form carboxyhaemoglobin, reduces O2 carrying
capacity, less O2 associate, less disassociates at
respiring tissues, less O2 for respiration, less ATP
produced &energy released, strain on heart, has to
increase heart rate to pump sufficient O2 to tissues,
damage artery lining)
Nicotine (addictive--makes platelets sticky, increase
chance blood clots/thrombosis,--mimics transmitter
substances at synapses between nerves, makes
nervous system more sensitive, smoker more alert)
Deposition under endothelium, in artery wall
CO & high blood pressure damages endo, repaired by
(WBCs) phagocytes, encourages growth smooth muscle
& deposition fatty substances (e.g. LDLs, unhealthy,(see
page 9) & cholesterol (LDLs transport)).
Deposits/Atheromas. Atheromas build up under endo-,
breaks through endo- forms plaque (sticks out in
lumen), less flexible& rougher, narrows lumen,
reduces blood flow.
Increase chance blood clot (thrombus) caused by: plaque
increases friction, blood slows & deposits further when flowing
over plaque &---nicotine makes platelets stickier.
Blood clot/thrombus block artery. Clot can break free, travel until
blocks artery, stops blood flow.
S:hard to exercise, shortness of breath
Coronary artery supplies Cardiac muscle with O2, high pressure,
lumen narrowed plaques, reduces blood flow, less O2 for
respiration, (increase heart rate, pump faster get sufficient O2) lead
CHD: Angina (chest pain), Myocardial Infarction (S: severe pain
chest & arms, death of part of heart muscle, caused thrombus),
Heart Failure (can’t sustain pumping action- blockage coronary
artery).
S: numbness, trouble walking & seeing
Multifactorial- No single factor causes it
Death part of brain tissue- loss blood flow to part of brain. Cause:
blood clot (thrombus), haemorrhage (artery bursts)
Page 16 of 24
CVD Problem
Risk Factors
increase/decrease CVD
& Less of a Problem in
LEDCs
Types of Risk
& Define Correlation,
Cause




•
•
•
•


Key Terms





Importance Biodiversity
Discrepancies in
Biodiversity Estimates
•
•
•
•
•
•
Expensive treat, long term drugs/surgery
Multifactorial- links unclear
Increase risk: Age (older, more time build-up fatty
deposits-atherosclerosis), Gender (Men more likely
under 50yrs)
Less problem LEDCs: different lifestyle, lower life
expectancy, higher chance developing other
diseases
Perceived- different due to factors:
– Personal experiences
– Media representation
– Lack of info
Actual- supported by scientific research
Correlation is link/relationship between two
patterns.
Cause: The reason why something happens.
Species Diversity-measure of biodiversity of a
particular area.
Species- group of organisms-share common
morphological, physiological and behavioural
characteristics, can interbreed to produce fertile
offspring.
Habitat- range of physical, biological and environmental
factors within which a species can survive.
Variety of life- the range of living organisms in an area
Ecosystem: All the living and non-living components in
a specific area and their interactions.
Biodiversity- measure how varied an ecosystem is. It
can be measured in terms of genes, species or habitats.
Catalogue of Life-catalogue of all known species
Many species not yet discovered could be
potential life-saving drugs or miracle foods
Intrinsic value
Ensures ability of organisms to adapt to
environmental change
Many species becoming endangered or are
becoming extinct
Large areas not yet explored
Continuing evolution and speciation
Page 17 of 24


Random Sampling



How Random Samples
Taken
Study small part of habitat & assume
representative of whole habitat, should count all
individuals-not practical e.g. single celled organism
impossible
Random no. generator table/computer plot
coordinates
Need to give accurate measure of no. species &
relative abundance
Small plants too numerous measure % ground
cover
Sample- study how human activities effect enviro
so reduce impact
Plants
Animals
•
Quadrat, Transect
• Sweep Netting
(Interrupted/Continuous • Trees-white sheet
Belt Transect)
SR: no. species present in habitat. Doesn’t take into
account no. individuals in each species. No. different types
species not individuals, qualitative
SE: measure abundance (%) of individuals in each
species, quantitative
𝑛 2
(𝑆𝑖𝑚𝑝𝑠𝑜𝑛𝑠 𝐼𝑛𝑑𝑒𝑥 𝑜𝑓 𝐷𝑖𝑣𝑒𝑟𝑠𝑖𝑡𝑦)𝐷 = 1 − [𝛴 × [ ] ]
𝑁
n= total no. individuals
N=total no. all individuals of all species
Σ=Sum of…
Species Richness &
Evenness
Simpsons Index of
Diversity
Define: Classification, Phylogeny
& Taxonomy
•
•
Difference between Taxonomy &
Classification
•
•
Relationship Phylogeny &
Classification
Difference between
Phylogenetic System &
Hierarchy
Recent Common Ancestor
C- process of sorting living things into groups.
Study similarities between species. Classify based
on phylogeny, taxonomy,
T- study principles of classification & differences
between species e.g. physical.
P- study of evolutionary relationships between
organisms. (e.g. Human&Gorillas-shared common
ancestor) How closely related.
P studies evolutionary relationship, C groups
organisms based on common ancestors, based
on evolutionary relationship/phylogeny


P: evolutionary relationships, arranged in groups
H: based on shared characteristics (Hierarchylarge groups spilt into smaller groups)

Recent common ancestor, more closely related,
short evolutionary distance, closer on
evolutionary tree-basis for natural classification
Page 18 of 24
Outline characteristics of 5 kingdoms
Prokaryotes
Kingdom: Prokaryota/
Monera

e.g. salmonella,
e.coli

circular DNA (naked,
not associated
histone protein)

no mbo

smaller ribosomes
(70S, 18nm)



Free Living
Autotrophic &
Heterotrophic
nutrition
Cell WallPeptidoglycan
Protoctista
K: Protoctista

e.g. Amoeba,
Euglena

Single celled+
multicellular

Both plant/ animal
features
Fungi
Plants
K:Fungi

E.g. Rhucor

Multinucleate

Cause decay of
organic matter
Animals
K: Plantae

E.g. Moss, Roses

Multicellular
K:Animalia

E.g. Mammals, Fish

Multicellular

Eukaryote- MBO, larger ribosomes (80S, 22nm), linear chromosomes associated histone proteins

Autotrophic &
Heterotrophic
nutrition
Cell WallSometimes


Heterotrophic
nutrition

Autotrophic
nutrition

Heterotrophic
nutrition

Cell Wall: Chitin

Cell Wall:
Cellulose

No
Autotrophic- Gain nutrients from photosynthesis
Heterotrophic- Gain nutrients by digesting and absorbing organic matter
Domain
Kingdom
Phylum
Class
Order
Family
Genus
Species
Taxonomic Hierarchy
Compare & Contrast
Domain
3 D- Bacteria (Eub-), Archaea
(Archaeab), Eukaryote
5 K- Prok, Protoctista, Fungi, Plants,
Animals
Down- more
diverse, fewer
similarities
Different
Same
Structural
o Bacteria has: different cell
membrane structuresometimes-flagella,
o Different internal
structure-different
enzymes
o No histone proteins
bound to DNA
o Different mechanism DNA
replication (Binary
Fission)
Archae share Euk:
o Similar enzymes building
RNA
o Similar mechanisms for
DNA replication
(mitosis)
Reason for Classification




Define Binomial system of
nomenclature & Dichotomous
Key

Common name doesn’t work
Dear
King
Philip
Came
Ordered
Fat
Greasy
Sausages




Page 19 of 24
see relationships
easier to identify
convenience
BSN: 2 names identify each species. Latin. GENUS
(CAPITAL) species (lower case). printed text italics,
written underlined
DK: series questions 2 alternative answers help
identify specimen
Same common name used different species in
other parts world
Different common name, different countries
Translation languages give different name
Latin-universal lang


CC is protein needed for respiration.
All living respire, few exceptions, therefore all
organisms have cc, not identical all species.
CC is protein made aa, compare from 2 different
species: greater similarity, closer related.
Not identical due to (variation) mutations (random
changes in the nucleotide bases). The aa for
proteins are initially coded for from genes on DNA,
then transfers info to mRNA in the nucleus etc...
Therefore DNA bases & genes must be very similar
to then code for similar aa & similar protein, cc.
Genes are made up of a sequence of nucleotide
bases.
D: more similar nucleotide bases, more closely
related

Classify organisms

Compare: Cytochrome C/
DNA Sequence


Define variation


Differences between individuals caused by
DNA/Environment
Variation within species- skin colour, eye colour
Variation between species- used to separate
members of 1 species from another- wings,
backbone
Continuous

Difference between
continuous& discontinuous
variation





Causes of Variation

Page 20 of 24
Range of intermediate
values between 2
extremes
Quantitative
Most individuals close
to mean
No. individuals at
extremes is low
e.g. length of stalk,
height humans
Discontinuous





2+ distinct categories
Qualitative
No intermediate values
Members species
evenly distributed
between different
forms/ more 1 type
than other
e.g. Human blood
groups: A or B or AB or
O, Gender-F/M/H,
Genetic: genes inherited, define characteristics,
combination alleles unique (unless identical twin).
Share similarities other species never exactly
same.
Environmental: diet:overfed=obese, sunlightskin=tan, enviro affects direction + amount of
growth, stunted, malnourished


Define Adaptation

Behavioural, Physiological,
Anatomical, Xerophytic
Adaptations of Organisms
Speciation


Adaptation- enhances survival and long term
reproductive success.
B: behaviour enhances survival- earthworm touches&
withdraws
P: correct functioning of cell processes-yeast respire
sugars an&aerobically to release energy, depending
how much O2 in enviro
A: structure enhances survival- bacteria- flagella for
movement
X:
+ B: roll leaves reduces water loss traps moist air
less steep water vapour potential gradient, less
SA exposed,
+ P: mechanism plant opens/closes stomata,
photosynthesis
+ A: long roots reach H2O deep underground
Speciation/Evolution
1. Through Natural Selection
2. Genetic Variation/ Random mutations
3. Resistant/ Survival of fittestmust be a selection
pressure e.g. climate, enviro (diseases, availability of
food)
4. Those best adapted (selective advantage) survive,
passing on alleles (selective advantage) to offspring
5. Allele only confers resistance/survival to that particular
selection pressure in that specific conc/temp/pH etc.
6. Happens for many generations, selective advantage
passed on, helping organisms to survive. Over time
small variations arise, if aid survival, change.
Eventually 1 group of organisms belonging to 1 species
could give rise to another species-speciation. New
species, must have reproductive barrier so different
can’t interbreed with original species evolved from to
produce fertile offspring,

Reproductive Barrier
causes Speciation



Evidence Supports
Evolution
Gaps in Fossil Record



Geographical separation. Different groups same
species on different islands unlikely interbreed.
Speciation-Allopatric speciation
Biochemical change prevents fertilisation due to
behavioural changes- courtship dance not
recognised/gamete incompatibility:sexual organs
not compatible can’t mate. Sympatric s
Biological molecules-certain molecules found in most.
1 species gives rise to another, both likely to have same
biological molecules. Evidence for all species coming
from 1 original ancestor.
CC & DNA sequence(see pg 19)
2 closely related species, recently evolved as separate
species, similar biological molecules.-speciation
Gaps in records: only hardest part survives, many
living things don’t have hard parts-no fossil. Only form
certain conditions. Damaged/destroyed by
movements rock.
Page 21 of 24


Selection Pressure
Conc pesticides in food chain. Insect resistant
survives then Predator eats lots of insecticide,
large conc, predator eaten, conc increases up
food chain reaches humans.
Antibiotics strong selection pressure, kills most of
bacteria. Small no. resistant, rarely completely
unaffected, more resistant than most. Most b killed,
feel better, stop antibiotic course, resistant survive
and reproduce more resistant. Overuse+
incorrect use- strains b resistant nearly all
antibiotics in use. Prescribe multiple antibodies
reduce chances of bacteria surviving.

Reasons for Conservation
of animal and plant
species: Economical,
Ecological, Ethical &
Aesthetic Reasons






Climate Change Impacts
on Biodiversity,
Agricultural & Diseases



Important conserve
Biodiversity
Human activities cause harm indirectly/ directly other
species thus loss biodiversity & extinction e.g. loss bd:
monoculture,(reduces variation, diversity, lead
extinction) habitat destruction: deforestation, (reduces
pop, decreases variation, decreases ability to evolve)
Econ: regulation atmos (photosynthesis)
+climate, (without O2 unable breath)
Ecol: answers technical problems (best
aerodynamic shape in H2O)
Eth: loss habitat+biodiversity prevents things living
where they should
Aes: patients recover quicker stress+injury exposed
natural enviro
C: Species already lost genetic variation won’t be able to
adapt & evolve to changing temp etc. Forced move,
whole ecosystems forced migrate- problem for national
parks, protected species move as climate unsuitable,
more vulnerable to extinction-hunting etc.
A: Climate change increase CO2 effect photosynthesis,
temp increase growing rates, increase evaporation rates
more precip.
Domesticated plants & animals at risk, selectively bred
to provide best yield in specific conditions, as conditions
change unable adapt & evolve
D: crops grown new areas, encounter new diseases &
pests, not be resistant. Higher temp, longer growing
season, longer for pests to increase.

Page 22 of 24
Wild plants & animals hold answers to climate
change, thousands of years to evolve & adapt
to enviro problems

In Situ- Define, Advantage
& Disadvantages


Ex Situ- Define,
Advantage &
Disadvantages
Conserving species in normal enviro, minimise
human impact & protect natural enviro e.g.
conservation parks
+ Conserved natural enviro
+ Permanently protects biodiversity &
representative examples of ecosystem
+ Facilitates scientific research
- People continue to hunt protected animals for
food
- Tourists feed/leave litter
- Illegal harvesting timber etc.
Repopulation-increase biodiversity e.g. recreating
wildlife habitats
Conserving endangered species by activities taking
place outside natural enviro e.g. zoos, botanical
gardens, seed banks (level moisture affects storage)
+
+
+
-

Protected predators
Health maintained
Sufficient food
Space limited, limit no. individuals, limits
genetic diversity, reduces variation, gene
pool restricted, may be less able to adapt
to changing conditions, affect if breed
successfully
- Reproduction successful, still have to
survive reintroduction- find food, survive
predators
Modern techniques- preserve genetic material- e.g.
artificial insemination, sperm freezing, carry out
research on domestic species similar to target
species effective & save rare, endangered
individuals from experimental work
Conservation Plants +&-
-
+
+
+
Plants- bred asexually,
only need 1
In life cycle have dormant
stage-seed, produce large
no. (large supply for
research) & can be
collected in wild without
much disturbance
-
-
Bred asexually will be
genetically identical,
reduce genetic
variation
Seeds of same species
from different areas will
be genetically different,
may not succeed.
 C I T E S (Convention on International Trade in Endangered
Species of Wild Fauna and Flora)

CITES & CBD



Aims: Regulates & monitors international trade in
selected species plants & animals
o Less endangered may be traded subject to
permit
o Ensure trade of wild plants for commercial
purposes prohibited
Difficult-where demand, attempts to smuggle
C B D Convention on Biological Diversity
Aims: conserve biodiversity
o Appropriate shared access to genetic resources
& sharing scientific knowledge & tech
+ Import genetic material, save time,
cheaper, less distress to rare animals
Page 23 of 24


EIA


Environmental Impact Assessment-assess
enviro impact of development, can lead to
improvements in planning & design
International Level: avoid/minimise adverse
effects on biodiversity of area & ensure potential
enviro consequences taken into account
Local Level consider- size of development, enviro
sensitivity, types of impact expected
3 stages: developer complies enviro statement,
publicised, authority takes into account when
making planning decision
Page 24 of 24