Poisons affecting oxygen uptake to the tissue

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    Transition group metal with high

    electrical and thermal conductivity.

    Abbreviation Cu comes from the Latin

    word cuprum which refers to the islandsof Cyprus.

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    Whole grain cereals

    Sprayed foliage

    Salt licks Supplements

    Ponds treated from copper

    Poultry ( Manure)

    Organ meats

    Leafy green vegetables

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    It is Caustic in nature.

    Cu exists in the +2(cupric, divalent)

    & +1(cuprous) oxidation states.

    In sheep toxic dose is 20mg/kg

    In cattle toxic dose is 200mg/kg

    In chicks toxic dose is 325mg/kg

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    Age

    Species

    Decrease in nutrition plane

    Fasting

    Physical Activity

    Stress

    Molybdenum Deficiency

    Ingestion of hepatoxins

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    Cu absorbed from intestine & enters a carrier statein blood (RBCs & Serum).

    Liver removes from blood most of it but soft tissuesstore some also.

    Cu bound to active site in nucleus, mitochondria &lysosomes.

    Lysosomes increases in number, volume & density

    to accumulate Cu.

    This leads to peroxidative damage to lysosomalmembrane & leakage of hydrolytic enzymes.

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    Cu also bound to other high affinity siteslike sulfhydryl groups of cytoplasmic(chelatin) & metal binding(metallothionein).

    Cu can induce the synthesis of theseproteins.

    Cu is not stored to same degree by liver

    in all species, it excretes in bile butresorption from intestine also there.

    Cu crosses the placenta also & stored infetal liver.

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    In ruminants liver & other tissues cannot storean infinite amount.

    So inhibition of vital enzymes & increase inhydrolytic enzymes from lysosomes lead tomalfunction & initiate liver necrosis.

    Result in increased in serum glutamicoxaloacetic transaminase, plasma arginase &plasma bilirubin.

    Ultrastructural changes in mitochondria, ER,Golgi apparatus & sinusoidal borders alsohistochemical distribution of acid phosphataseis disturbed.

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    Vascular system is damaged resulting inloss of fluid & increased blood colloidalosmotic pressure.

    Blood Cu enters in erythrocytes & cannotbe released leads to oncominghemolytic crisis.

    Hemolysis occurs with a series ofreactions like conversion of ferrous

    hemoglobin to methemoglobin,glutathione, peroxidation, protein &cell concentration.

    Erythrocyte autoimmune mechanismalso involved.

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    Kidney failure due to renal tubule &glomerular necrosis brought by excessiveCu.

    Plasma creatinine phophokinaseconcentration indicate skeletal muscledamage thought to be due anoxia.

    Brain lesions due to blood urea,

    ammonia concentration & alteration inglial transport mechanism by inhibition ofATP caused by metabolic changes in theglia.

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    Weakness, trembling, anorexia,hemoglobinurea, jaundice & bloody

    nasal discharge. Signs of respiratory insufficiency

    (dyspnea, panting) & shock (tachycardia, weak pulse, cold

    extremities). Death occur in 1-4 days after onset of

    clinical signs.

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    Icterus, hemolysis, methemoglobinemia,&congestion of abomasum & intestine.

    Liver enlarge, yellow or friable.

    Gall bladder is distended & filled with thick greenish

    bile.

    Kidneys are large, hemorrhagic & friable.

    Spleen is enlarged & dark brown to black.

    Hemorrhagic heart & edematous lungs.

    Excessive fluid in body cavities.

    Muscular necrosis.

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    Microscopically, lesions are consist

    with gross findings.

    Liver cell vacuolated & necrotic. Kidney manifest tubular & glomerular

    necrosis & hemoglobin clogging in

    tubules.

    Brain manifest spongy degeneration &

    astrocyte damage

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    History Clinical examination Serum & whole blood copper

    examination Urine examination for hemoblobinurea Blood Cu levels 10-20x normal(50-

    200g/dl) K

    idney Cu levels postmortem (>100ppm) Liver Cu levels postmortem (>350pp)

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    Decreasing absorption

    1) Water, Milk or Activated charcoal

    Supportive measures Ammonium molybdate(50-500mg) + sodium

    sulfite(0.3-1g) orally for 3weeks.

    Chelating therapy

    D-Penicillamine, Dimercaprol / BAL,Calcium disodium ethylenediaminetetraacetate.

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    Nicholas H.Booth, Lieslie E. McDonald

    (6th edition) Veterinary Pharmacologyand Therapeutics. 1023-1027.

    Ramesh C.Gupta, Veterinary Toxicology.

    427-429 www.google.com

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