Difference between revisions of "Copper"
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*Copper – cofactor for enzymes (lysyl oxidase), electron transport proteins (cytochrome c oxidase) and antioxidant molecules (superoxide dismutase). | *Copper – cofactor for enzymes (lysyl oxidase), electron transport proteins (cytochrome c oxidase) and antioxidant molecules (superoxide dismutase). | ||
| − | *Primarily absorbed through the [[Small Intestine - Anatomy & Physiology|small intestine]] and [[ | + | *Primarily absorbed through the [[Small Intestine Overview - Anatomy & Physiology|small intestine]] and [[Monogastric Stomach - Anatomy & Physiology|stomach]] (upper small intestine in the dog). |
*Enterocyte regulation of absorption – metallothionein and a copper transport protein – ATPase7A. | *Enterocyte regulation of absorption – metallothionein and a copper transport protein – ATPase7A. | ||
*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. | *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. | ||
*ATPase7A – transmembrane copper transporter in a number of cell types. | *ATPase7A – transmembrane copper transporter in a number of cell types. | ||
| − | *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. | + | *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|copper deficiency]]. |
| − | *Chronic diet | + | *[[Copper Toxicity|Chronic diet excess of copper]] leads to accumulation in the [[Liver - Anatomy & Physiology|liver]] . |
*Serum copper – in 2 pools | *Serum copper – in 2 pools | ||
**Exchangeable pool – loosely bound to carrier molecules; 80% of it bound to transcuperin, the rest bound to albumin. | **Exchangeable pool – loosely bound to carrier molecules; 80% of it bound to transcuperin, the rest bound to albumin. | ||
**Other pool – tightly bound to carrier molecules. | **Other pool – tightly bound to carrier molecules. | ||
| − | + | [[Category:Minerals]] | |
| − | [[Category: | ||
Latest revision as of 12:56, 15 February 2011
- Copper – cofactor for enzymes (lysyl oxidase), electron transport proteins (cytochrome c oxidase) and antioxidant molecules (superoxide dismutase).
- Primarily absorbed through the small intestine and stomach (upper small intestine in the dog).
- Enterocyte regulation of absorption – metallothionein and a copper transport protein – ATPase7A.
- 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.
- ATPase7A – transmembrane copper transporter in a number of cell types.
- 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 and brain that have little of the transporter experience copper deficiency.
- Chronic diet excess of copper leads to accumulation in the liver .
- Serum copper – in 2 pools
- Exchangeable pool – loosely bound to carrier molecules; 80% of it bound to transcuperin, the rest bound to albumin.
- Other pool – tightly bound to carrier molecules.