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Category:Liver - Toxic Pathology (view source)

Revision as of 22:39, 7 June 2010

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== Copper and liver disease ==
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*Copper – cofactor for enzymes (lysyl oxidase), electron transport proteins (cytochrome c oxidase) and antioxidant molecules (superoxide dismutase).
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*Primarily absorbed through the [[Small Intestine - Anatomy & Physiology|small intestine]] and [[Forestomach - Anatomy & Physiology|stomach]] (upper small intestine in the dog).
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*Enterocyte regulation of absorption – metallothionein and a copper transport protein – ATPase7A.
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*Metallothionein is a low molecular wt cytoplasmic protein, in all tissues; expression in response to heavy metals, various hormones and stress. metallothionein in cytoplasm of enterocytes leads to absorption of copper.
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*ATPase7A – transmembrane copper transporter in a number of cell types.
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*Defective in people with Menke’s disease – the animal model is the mottled mouse – results in faulty transport of copper out of the cell –leads to copper accumulation in enterocytes. [[Liver - Anatomy & Physiology|Liver]] and brain that have little of the transporter experience copper deficiency.
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*Chronic diet XS of copper leads to accumulation in the [[Liver - Anatomy & Physiology|liver]] .
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*Serum copper – in 2 pools
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**Exchangeable pool – loosely bound to carrier molecules; 80% of it bound to transcuperin, the rest bound to albumin.
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**Other pool – tightly bound to carrier molecules.
   
[[Category:Liver_-_Pathology]]
 
[[Category:Liver_-_Pathology]]
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