Download Lecture No. 7

FOOD TOXINS 1
Lecture No. 7
Copyright © Mgr. Zuzana Široká, PhD.
Toxic agents in food of plant origin
Glucosides
• This is the largest group of secondary metabolites.
• Substances consisting of sugar part and non-sugar part,
so called aglycone. These two parts are connected by a
bond of ether character – by glucosidic bond.
• Generally speaking, we can say that these substances
usually affect blood and circulatory system.
• These agents are not toxic themselves, but are easily
hydrolysed in acid environment and release cyanic acid
Cyanogenic glucosides:
• Very common in plants, found in more than
one thousand species in more than one
hundred families.
• They are bitter and primarily act as repellents.
• We know more than fifty cyanogenic
glucosides.
• In table there are some most known ones:
Glucoside
Plants
HCN (mg/kg) content
in fresh flesh
Linamarin
Manioc, white clover, cultivated flax
Manioc-bitter type
-peel of bulbs 840
-pulp of bulbs 330
Faseolunatin
Sugar bean
Lotaustralin
Bird´s-food trefoil, white clover, manioc
Linustatin
Neolinustatin
Cultivated flax
Prunasin
Plum tree
Sambunigrin
Elder – Sambucus nigra
Amygdalin
Plum tree, kernels of stone-fruits: bitter
almonds, apricot, peach
Vicianin
Bob, vetch
Taxifyllin
Common yew, bamboo
Dhurrin
Sorghum
100-4000
-seeds 200-380
Kernels of these plants
approximately 3 %
• Aglycones (non-sugar parts) are formed by αhydroxynitriles, which are stabilised by
glucosyl bound to hydroxyl group of a sugar.
Aglycone:
R1
OH
C
R2
C N
α-hydroxynitrile
O- β-glycosyl
R1
C
R2
C N
cyanogenic glucoside
Manioc (kasawa, cassava):
• Originally south-american species from
Euphorbiaceae family
• It is widespread in all tropic areas
• Root bulbs contain starch and
hydrocyanic acid, which can be removed
by cooking or baking
• Bulbs are used as potatoes, they are dried
and flour is made of them
• We distinguish bitter and sweet types of
manioc, bitter can contain up to 500
mg/kg of HCN
Sorghum:
• From Poaceae family
• Has been known since ancient Egypt times
• It is an annual plant, about 3 m high with
minute grains containing a lot of starch
• Dhurrin is mainly in germs, seeds usually
don’t contain cyanic acid
Almond, apricot, peach:
• Contain glucoside called amygdalin
• HCN is very poisonous, but in plants occurs in
quite low concentrations
• Additionally, releasing process is slow so there is
not sufficient amount cumulated in one time
• Lower concentration of amygdalin is found in
plums, blackthorns, cherries, sour cherries and
apples.
Mechanism of action:
• The carrier of toxicity is HCN, released from glucoside
• In blood it binds to haemoglobin and methaemoglobin
and forms cyanhaemoglobin and cyanmethaemoglobin
respectively
• Its affinity to methaemoglobin (which is higher than to
haemoglobin) is used for treatment
• Cyanides and cyanic acid act as neurotoxins and they also
bind to several proteins damaging enzyme systems.
• They decrease tissue breathing, block cytochromoxidase
(HCN binds to Fe and Cu), cause tissue asphyxia
(suffocation), because oxygen is not passed on to tissues,
blood is oversaturated by oxygen and is of bright brick
red colour
• In acute poisoning we can see increased respiration due
to chemoreceptors´ and respiration centre damage
• Then the decrease of blood pressure, seizures, coma and
exitus due to respiratory centre collapse follows
• In chronic intoxications is typical tremor, conjunctivitis,
inappetence, neuropathies, headaches
• In manioc it is called tropic ataxic neuropathy
Biotransformation:
• Dissociation of cyanogenic glucosides goes on in two
steps
• First, β-D-glucopyranose is dissociated due to action of
enzyme called β-D-glucosidase and α-hydroxynitrile is
formed
• This substance is dissociated to HCN and aldehyde or
ketone due to enzyme hydroxynitrillyase
Dissociation of cyanogenic glucosides:
O- β-glucopyranose
R1
R1
C
R2
OH
C
C=
N
+ H2O
R2
+ glucose
C = N
α-hydroxynitrile
cyanogenic glucoside
β –glucosidase
R1
OH
R1
C
R2
C=O
C= N
+ H2O
+
HCN
R2
Aldehyde and ketone
α-hydroxynitrile
α-hydroxynitrillyase
• In normal plant tissues free HCN doesn’t occur
• Described dissociation takes place in mechanically
damaged tissues, where glucosides and enzyme,
normally stored separately, come into touch and start to
react together
• It can be during cutting of plants, crushing of seeds, if
the plant is frozen, in extreme drought
• Efficient β –glucosidase is also a part of bacterial
microflora in GIT of mammals
• Released HCN must be detoxified in plant or in animal
somehow - product of detoxification is thiocyanate SCN• This change is possible thanks to one of two enzymes sulphurtransferases. Cyanide-sulphurtransferase, also
called rhodanase, which is a part of mitochondria and 3 merkaptopyruvatesulphurtransferase (also in
mitochondria)
Detoxification of cyanides:
S2O3
thiosulphate
+
CNnitrile rhodanase
CH2 - C - COOH + CN-
SO32sulphite
+
SCNthiocyanate
CH3- C -COOH
+
SCN-
3-merkaptopyruvatesulphur
transferase
SH
O
Mercaptopyruvate
O
Pyruvate
thiocyanate
• Similar mechanism is found in animals
• It takes place in liver and thiocyanates are excreted by urine or
faeces
• Detoxification is dependent on sufficient amount of sulphur
substances in an organism
Treatment:
• Administration of nitrites – formation of methaemoglobin, which
binds cyanides – formation of cyanmethaemoglobin –
administration of thiosulphates – cyanides released from
methaemoglobin react with them and form thiocyanates
• Now a new antidote is tested – hydroxocobalamin – with cyanides
in blood forms cyanocobalamin (vitamin B12)
• Lethal doses:
- In fruit containing amygdalin they are 5-25 pieces of seed for
children.
- Lethal dose for humans is 0,5 – 3,5 mg/kg HCN
Glycoalkaloids of potatoes
(Solanum tuberosum, Solanaceae)
• Potatoes are fourth most important crop-plant in the world
• Toxic glycoalkaloids are found in the whole plant of potato
Solanum tuberosum, and also in majority of other species from
family Solanaceae, e.g. tomato or aubergine - Solanum melongena
• These alkaloids are so called steroid glycoalkaloids (SGA), or
pseudoalkaloids, because their precursors are not aminoacids like
in genuine alkaloids
• They can be also classified as glucosides – they contain glucosidic
bond in their molecule
• Glycoalkaloids are formed of:
- polar, in water soluble saccharide part – mono-tetrasaccharide
- non-polar steroid (aglycone)
Potatoe:
• The whole overground part of the plant is poisonous
• In green parts, germs and berries there is solanin and
less potent solanidin, in tubers, there are solanin and
chaconin
• In general we call all these alkaloids Solanin
• The concentration of alkaloids varies according to
many conditions (warm, dryness, humidity). Also
quality of soil, fertilizers added, stress factors (e.g.
insect attacks, mechanical damage or light)
influence the concentration
• These stress factors and increased amount of
magnesium in soil increase the concentration of
alkaloids, on the other hand, molybdenum in soil
decreases their concentration
• In starch parenchyma of tubers, there is only about 1 %
of solanin
• Glycoalkaloids are termostable, so you cannot destroy
them by cooking, frying or drying. They bear
temperatures higher than 300°C. But during cooking
potatoes in water majority of alkaloids pass to water
• Solanin – in fresh unpeeled tubers there can be
concentration of solanin more than 100 mg/kg. The
limit for potatoes determined to eat is 200 mg/kg. But at
about 150 mg/kg, the taste starts to be bitter and in
higher concentration this taste disallows to eat them.
• In tubers for consumption , the vast majority of
glycoalkaloids is in 1.5 mm thick part of cortex, of peel
• By peeling we remove 60-95 % of solanin
• It is recommended not to expose them to light. Tuber
reacts with rapid synthesis of alkaloids as a defence
against stress
• Once formed, these alkaloids cannot be removed during
storage in dark
• Another danger is mechanical damage which also leads
to alkaloid synthesis
• Data on temperature and humidity differs among
sources, low temperatures lengthen high quality of
tubers, but cold can cause increased synthesis of
alkaloids
• For decreasing of alkaloid formation we use chemical
retardants or vacuum package, because lack of oxygen
and decreased respiration block metabolism in tubers
Toxic effects of glycoalkaloids:
• They posses two mechanisms of action:
- First: they disturb cell membranes containing steroid substances (an effect
similar to those in saponines)
- Second: they inhibit serum cholinesterase too (similar to organophosphates)
• Glycoalkaloids cause gut mucosa and liver damage
• Early signs of intoxication are colic, diarrhoea with blood in excrements,
apathy, halucinations. Then follow seizures, coma and respiration paralysis
• We suppose, that many of slight intoxications are considered as common gut
problems and we dont attribute them to potatoes
• For humans, toxic dose is 2-5 mg/kg of body weight and lethal dose between
3-6 mg/kg body weight
• Other group of glycoalkaloids in potatoes are leptins. They are natural
pesticides and genetics try to put the gene for leptins to other plants to protect
them
• Tubers also contain so called protease inhibitors, which dissociate trypsine,
chymotrypsine, kathepsine D and karboxypeptidases. These inhibitors can be
removed and destroyed by exposure to heat
• BEWARE - Inhibitors are also in:
- peanuts, wheat, red beet, onion, soya beans
Organ, tissue
Content (mg/kg)
Germs
2000-4000
Roots
180-400
Stalk
20-30
Leaves
400-1000
Flowers
3000-5000
Berry
4200
Whole tuber (bulb)
75
Peel
300-500