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황산동의 성장촉진효과 (Copper Medication)
[Home]
요약
NRC, ARC 추천 권장사용량(돼지의 경우 6~9 ppm 수준)보다 훨씬 과량의 황산동을
사료내에 투입함으로써 (Cu 로서 250 ppm = CuSO4.H2O 로서 750 ppm)
돼지의 성장촉진효과 5 ~ 10 %
사료효율 증대 3 ~ 8%
항생물질과의 상승효과 및 대체효과
듁질의 개선
배설물의 색깔 및 냄새 개선
축산농가에서의 동의 영양학적 역할 (한글 및 영문)
Larry L. Berger, Ph. D.
Prof. animal Sciences
University of Illinois
동(Copper)
- BC 400 년경부터 동을 의약품으로 사용하였으나 동물의 필수 원소로 알려진 것은 겨우
1920 년대
- 동의 결핍현상 : 빈혈,설사,이상골육,갓난새끼의 활동부진, 모발의 변색/변화, 불임,
혈관이상,당
지질대사 이상, 명역시스템 저하
- 생리적 역할 : 직접/간접적으로 결핍현상에 관여하는 효소의 주요 구성원
축종별 효과
- 동은 축종별 효과 및 중독성의 수준에 있어서으 격차가 매우 심하다. NRC 권장량을
기준하면 소
10 ppm, 가금류 8 ppm, 돼지 10 ppm (성장촉진감안 250 ppm)이나 양의 경우 10 ppm
수준에서도
간에 축적되는 정도가 매우 심하다.
동의 공급원
- 곡물보다 초지사료가 동의 함유를 많이 하고 있으며 NRC 권장량 이상이나 사료과정에서
대부분이
불활성화 된다 (Phytate, Lignin)
- 산화동과 황산동이 주 공급원인데 간에서의 함유수준 분석에서 매우 유의할 만한 결과가
나왔다.
- 초산동을 100 % 기준으로 산화동 - 5%, 황산동 107 %, 탄산동 60 %의 생체이용결과
(양계용사료)
- 125 ~250 ppm 수준의 동(황산동으로부터 얻어진)을 젖먹이에게 투여하여 성장 촉진효과을
가겨왔
으나 산화동의 경우 효과가 없었다(Cromwell, et.al 1989)
- 젖소에 15 ppm 수준의 동을 투여한 결과 황산동의 이용성의 좋았으나 산화동을 이용성이
현저하게
떨어졌다.(축우용사료, Clark st al. 1993)
미량광물질 상효 작용(생략)
스트레스와 동
- IBR 바이러스에 감염된 소, 면역기능이 저하된 소, 스트레스를 받은 소는 NRC 권장량
수준을 상회
하여 동의 섭취를 필요로 한다. (Orr et al., Xin et al.,Waterman st al.)
Effective Copper Nutrition for Farm Animals
by Larry L. Berger, Ph.D.
Professor, Animal Sciences
University of Illinois
Why Copper?
With copper more than any other nutrient, factors such as specie, source,
mineral interactions and stress can affect farm animal's copper requirements.
Recent research has shown that these factors can interact to increase the
complexity of the copper nutrition story. This article examines each of these
factors so that nutritionists, veterinarians and livestock producers can evaluate
more accurately their copper supplementation program.
While copper compounds were used for medicinal purposes as
early as 400 BC, it was not until the 1920's that copper was first
recognized as an essential nutrient for animals. Today, copper
deficiency is known to cause anemia, diarrhea, bone disorders,
neonatal ataxia, changes in hair and wool pigmentation, infertility,
cardiovascular disorders, impaired glucose and lipid metabolism
and a depressed immune system (Davis and Mertz, 1987). Copper
is a key component of many enzyme systems which when impaired
can directly or indirectly cause many of the symptoms of copper
deficiency.
Because many of the copper deficiency symptoms are general in
nature, a clear diagnostic tool that accurately reflects the copper
status of the animal is needed. Although serum and plasma copper
concentrations are often measured, blood levels may not show the
deficiency until severe symptoms develop (Hemken et al. 1993).
Liver copper concentration is probably the most sensitive indicator
of changes in copper status and its determination is recommended
when liver biopsies can be obtained. Ceruloplasmin concentrations
and superoxide dismutase activity in the blood or red blood cells
can be useful indicators of copper status.
Specie Effects
Dietary copper requirements vary greatly among species. The recommended
levels for one specie may cause toxicity in another. For example, 10 ppm is the
NRC recommended level for dairy cattle but under certain conditions 10 ppm
can cause toxicity in sheep (Church and Pond 1988). By comparison, growing
pigs are often fed 100 to 250 ppm of copper in the diet to improve growth.
According to the National Reserch Council, poultry require approximately 8 ppm
copper.
Sheep are unique in that they accumulate copper in the liver more
readily than other farm animals. Over a period of time, 1,000 3,000 ppm copper on a dry basis may be achieved. Usually there
are no clinical signs until there is a sudden release of copper into
the blood. Plasma copper levels then increase 10 to 20 fold. These
elevated blood copper concentrations (500-2000 mg/dl) usually
precede clinical signs by 24 to 48 hours (Kimberling 1988). The
most common symptoms are anorexia, excessive thirst and
depression. Most sheep will die within 2 to 4 days after blood
concentrations sky rocket.
Because of the variation in recommended copper concentrations, it
is difficult to have one copper level in a trace mineralized salt for
all species. One alternative is to have a low-copper product for
sheep and a high-copper product for the other species. This would
insure that all species would receive an appropriate amount of
copper without the risk of copper toxicity in sheep. Those swine
producers feeding copper as a growth promotant will continue to
supplement copper in addition to that in the trace mineralized salt.
Copper Source
Knowing the copper concentration in a diet without knowing the source of
supplemental copper is of little nutritional value. Absorption of copper can vary
from zero to as high as 75% (Linder, 1991) depending on a number of factors.
Copper availability in most feedstuffs fed to farm animals is between 1% and
15% (Hemken et al. 1993). Grains are lower in copper than are forages. Most
forages will contain copper at levels equal to or above the NRC requirement for
ruminants. However, as plants mature and the phytate and lignin content
increases, bioavailability of the copper decreases rapidly.
Copper oxide and copper sulfate have been the two predominant
sources of supplemental copper used in animal feeds. In the last
ten years there has been considerable research comparing the
bioavailability of these and other copper sources in the different
species. In 1987 Ledoux et al. compared the biological availability
of reagent grade copper acetate, and feed grade copper oxide,
copper carbonate and copper sulfate by feeding each copper
source at 0, 150, 300, and 450 ppm to broiler chicks in a corn-soy
diet. Liver copper levels were used as the indicator of absorption.
Using the slope-ratio technique with acetate set at 100%, the
relative biological availability values were -5, 107, and 60% for the
oxide, sulfate and carbonate forms, respectively.
Cromwell et al. (1989) conducted a study to determine the effects
of feeding weanling pigs 0, 125, 250, and 500 ppm supplemental
copper from copper oxide or copper sulfate on rate and efficiency
of gain and liver copper stores. Feeding 125 or 250 ppm copper
from copper sulfate increased (P<0.01) rate and efficiency of gain
and liver copper levels. All dietary levels of copper oxide failed to
influence performance or liver copper levels.
One criticism of the previous studies has been that feeding very
high levels of copper may give a lower biological availability for
copper oxide than if it were fed closer to the dietary requirement.
To answer this question Clark et al. (1993b) compared adding 15
ppm copper from copper oxide or copper sulfate on the copper
status of yearling Holstein cattle. Copper availability was
compared by determining the liver and blood copper levels after 30,
60 and 90 days on the two copper sources. Liver copper
concentrations for cattle fed copper sulfate were higher (P<0.01)
than for cattle fed copper oxide or unsupplemented cattle at day
60 (196, 87, and 93 ppm) and at day 90 (268, 142 and 90 ppm,
respectively). Blood copper levels were found to be a poor
indicator of copper status. Copper oxide was shown to have low
bioavailability and to be better than no copper supplementation
only after 90 days on the deficient diet. These data are interpreted
to show that the bioavailability of copper oxide is much below
copper sulfate, even when fed at levels near the NRC requirement.
Several other recent studies have shown copper sulfate to be
superior to copper oxide because of differences in bioavailability.
Baker et al. (1991) compared cuprous oxide (Cu2O) to copper
sulfate and found them to have similar bioavailabilities. Copper
carbonate is considered to have intermediate availability. Copper
metal is totally unavailable.
Mineral Interactions
If copper nutrition was as simple as determining the copper in the basal diet and
adding a highly available copper source, copper deficiency would not be a
problem. However, because copper absorption and metabolism can be affected
by molybdenum, sulfur, calcium, zinc, iron, manganese, cobalt, lead, cadmium,
and selenium, deciding how much supplemental copper is required is not always
straightforward.
For example, in sheep, dietary molybdenum levels can be the
primary factor affecting copper requirements. If molybdenum
levels are low (<1 ppm), sheep are more susceptible to copper
toxicity. However, if molybdenum intakes exceed 10 ppm, copper
deficiency may occur on diets that would normally be adequate.
This has been a significant problem in sheep grazing pastures low
in copper but high in molybdenum and sulfur. Newborn lambs from
ewes on these pastures often exhibit neonatal ataxia and have a
low survival rate.
The formation of totally unavailable thiomolybdates from the
complexing of molybdenum, copper and sulfur is the reason that
copper status is easily affected by molybdenum and sulfur levels.
Thiomolybdate is formed in the rumen because sulfate is converted
to sulfide, which is a key intermediate in forming thiomolybdate.
Sulfates are stable in the monogastric stomach and so this does not
occur in monogastric animals. High sulfur in combination with
normal or low molybdenum concentrations can still reduce copper
bioavailability by the formation of copper sulfide in the rumen.
Copper sulfide is also poorly absorbed. If high sulfur is a problem,
adding copper carbonate may be recommended over copper sulfate
to avoid adding more sulfur to the diet.
Recent research suggests that organic-sulfur compounds may also
affect copper absorption. Linder (1991) reported that feeding the
sulfur amino acids methionine and homocysteine inhibited copper
absorption in the rat. With the increasing use of synthetic amino
acids in the swine and poultry diets copper absorption could be
depressed.
In monogastrics, high levels of zinc, calcium, and iron can reduce
copper absorption. Zinc has been shown to inhibit copper
absorption by displacing copper from a copper-binding protein in
the intestinal mucosa of the chick (Church and Pond, 1988). High
calcium reduces copper absorption by increasing the pH of the
intestinal contents. Iron in the form of ferrous sulfide reduces
copper absorption by forming insoluble copper sulfide.
Animal Stress
Typically nutrient requirements are determined in environments where disease
and other stressors are minimized. As animal production intensifies, the
requirement for nutrients involved in combating stress may also increase. For
example, Orr et al. (1990) showed that blood copper levels decreased and
urinary copper excretion increased as morbidity increased in calves infected
with the infectious bovine rhinotracheitis (IBR) virus. With chronic disease, liver
copper stores may become depleted resulting in increased susceptibility to
secondary infections.
Xin et al. (1991) showed that immune function in cattle was
impaired even though there was no evidence of anemia or
depression in growth. Cattle that were marginally deficient in
copper had reduced superoxide dismutase activity and decreased
neutrophil bacteriocidal capability. These animals were less
efficient at killing Staphylococcus aureus, an organism which often
causes mastitis in cattle. This could explain the observation that
dairy herds which are marginal in their copper status often seem to
have a higher incidence of mastitis.
The stress associated with fetal development and calving may also
increase the copper requirement. Recent Kentucky research
showed that dairy cows had significantly lower liver copper stores
at calving than at later stages of lactation (Waterman et al. 1991).
Hemken et al. (1993) reported that at least 15 ppm copper in the
diet is required to replenish the mothers' liver stores because the
fetal liver was taking up the copper more rapidly than the mother.
These data suggest that the 10 ppm copper requirement
prescribed by NRC may not be adequate during late gestation when
there is rapid fetal development.
Summary and Conclusions
Although there is an abundance of scientific data to show that specie, copper
source, mineral interactions and stress can affect copper nutrition, do these
factors actually affect production efficiency under practical conditions? The
answer is "yes" as illustrated by the following scenario.
Clark et al. (1993a) reported on a field study with beef cattle that
demonstrated a copper deficiency while the cattle were being
supplemented with copper oxide. The deficiency symptoms
observed the previous year included low fertility, diarrhea and
some loss of hair pigment. Blood samples were taken and copper
deficiency confirmed by the fact that plasma copper levels were
0.3-0.5 ppm. The herd was then divide into three groups of 40 to
60 cows each and supplemented with copper oxide, copper sulfate
or copper proteinate. All three supplements contained 0.04%
copper. After 28 days, liver copper levels were 34.3, 56.8 and 79.3
ppm for cows fed the copper oxide, copper sulfate and copper
proteinate supplements respectively. Conception rates were
increased to 85% for cows on copper oxide and to 94% and 90%,
respectively for cows fed copper sulfate and copper proteinate.
The 9 percent unit increase in conception rate (85% vs 94%) could
easily result in a 100-fold return on the increased cost of
supplementing with copper sulfate compared to copper oxide.
Feeding the appropriate level of a trace mineralized salt containing
a highly available copper source is one of the best nutritional
investments a producer can make.
Literature Cited
Baker, D.H., J. Odle, M. A. Frank, and T.M. Wieland. 1991. Bioavailability of
copper in cupric oxide, cuprous oxide and in a copper-lysine complex. Poultry
Sci. 70:177.
Church, D.C. and W.G. Pond. 1988. Basic Animal Nutrition and
Feeding.3rd Edition. Published by John Wiley and Sons, New York,
NY. pp. 196-199.
Clark, T.W., Z. Xin, Z. Du, and R.W. Hemken. 1993a. A field trial
comparing copper sulfate, copper proteinate and copper oxide as
copper sources for beef cattle. J. Dairy Sci. 76.(Suppl. 1):334.
(Abstr.).
Clark, T.W., Z. Xin, R.W. Hemken and R.J. Harmon. 1993b. A
comparison of copper sulfate and copper oxide as copper sources
for the mature ruminant. J. Dairy Sci. 76:(Supple.1):318 (Abstr.)
Cromwell, G.L., T.S. Stahly and H.J. Monegue. 1989. Effects of
sources and level of copper on performance and liver copper
stores in weanling pigs. J. Anim. Sci. 67:2996.
Davis, G.K. and W. Mertz. 1987. Copper. In: W. Mertz (Ed.) Trace
Elements in Human and Animal Nutrition. pp 301-364. Academic
Press, Inc., San Diego, CA.
Hemken, R.W., T.W. Clark and Z. Du. 1993. Copper: Its Role in
Animal Nutrition. In: T. Lyons (Ed.) Biotechnology in the Feed
Industry. pp 35-39. Altech Technical Publications, Nicholasville,
KY.
Kimberling, C.V. 1988. Jensen and Swifts Diseases of Sheep. 3rd
Edition. Lea and Febiger, Philadelphia, PA.
Ledoux, D.R., C. B. Ammerman and R.D. Miles. 1987. Biological
availability of copper sources for broiler chicks. Poultry Sci.
66(Supple. 1):24. (Abstr.)
Linder, M.C. 1991. Biochemistry of Copper. Plenum Press. New
York, NY.
Orr, C.L., D.P. Hutcheson, R.B. Grainger, J.M. Cummins and R.E.
Mock. 1990. Serum copper, zinc, calcium and phosphorus
concentrations of calves stressed by bovine respiratory disease
and infectious bovine rhinotracheitis. J. Anim. Sci. 68:2893.
Waterman, D.F., Z. Xin, R.J. Harmon and R. W. Hemken. 1991.
Relationship of trace mineral status between stages of production
in dairy cattle. J. Dairy Sci. 74:(Supple. 1)297. (Abstr.).
Xin. Z., D.F. Waterman, R.W. Hemken and R.J. Harmon. 1991.
Effects of copper status on neutrophil function, superoxide
dismutase and copper distribution in steers, J. Dairy Sci. 74:3078.