Cytochrome oxidase repair during treatment of copper deficiency: relation to mitochondrial turnover

[Karmeleon]

Cytochrome oxidase repair during treatment of copper deficiency: relation to mitochondrial turnover - PubMed

The repair of cytochrome oxidase depletion during the treatment of copper deficiency was studied in the rat. The purpose of this study was to distinguish the role of new cell production from the possibly more specific role of mitochondrial turnover in determining the rate of this repair. In rats...

pubmed.ncbi.nlm.nih.gov

Cytochrome oxidase repair during treatment of copper deficiency: relation to mitochondrial turnover​

The repair of cytochrome oxidase depletion during the treatment of copper deficiency was studied in the rat. The purpose of this study was to distinguish the role of new cell production from the possibly more specific role of mitochondrial turnover in determining the rate of this repair. In rats on a copper-deficient regimen until 2.5-3 months of age, activities of cytochrome oxidase expressed as per cent of control were as follows: skeletal muscle (quadratus lumborum), 18%; heart, 27%; liver, 34%; and intestinal mucosa, 34%. After 2-3 days of dietary supplementation with cupric acetate, repair of decreased cytochrome oxidase activity in intestinal mucosa is complete. Histochemical studies indicated that this repair starts in the newly differentiating cells at the base of the villus and then progresses toward the tip of the villus at a rate approximating the normal rate of migration of the mucosal cells. In liver and skeletal muscle, cytochrome oxidase activity returned to control values after 10-15 days of treatment with cupric acetate. In heart muscle, control values were approached more slowly as indicated both by activity of the enzyme and by mitochondrial difference spectra which reflect enzyme concentration. Although cytochrome oxidase repair in the intestine appeared to be limited by the rate of production of new mucosal cells, the rate of repair in liver and skeletal muscle was several times too rapid to be accounted for by known rates of new cell production. Incorporation of tritiated thymidine into DNA in these tissues in both the deficiency state and during repair indicated no major differences in new cell production compared to that of control animals. However, the time required for cytochrome oxidase repair in liver was similar to the turnover reported for other mitochondrial constituents in this tissue. The rate of cytochrome oxidase repair may therefore be more directly determined by the rate of synthesis of new mitochondrial material than by the rate of production of new cells.

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Interesting, i also experienced an enormous boost in digestive capacity after supplementing 3mg copper chelate after 3-4 days. Point is i thought i would ingest enough copper rich foods, namely seafood clams goatmilk and liver. Seems not to be the case if digestion is damaged. I also found a study about lead intoxication, which toxic effects are mediated by copper displacement and copper was partially protective. Supermarket liver could be very high in lead or maybe lead stored already in bone?

 

[Karmeleon]

Protective value of dietary copper and iron against some toxic effects of lead in rats​

D S Klauder et al. Environ Health Perspect. 1975 Dec.

Both dietary iron and copper were inversely related to lead absorption as indicated by erythrocyte and kidney lead levels, dietary iron having the greatest effect. Kidney copper values were depressed when dietary iron was low, a condition which was worsened by lead. Lead tended to lower heart cytochrome c oxidase especially when dietary copper was low, but also when dietary copper and zinc were high. Lead interfered with hematopoiesis when dietary copper and/or iron were low, the effect being expecially severe when both essential nutrients were low. These results show the importance of copper and iron nutriture and metabolism as factors which reduce lead toxicity, and emphasize the necessity of considering nutritional status in evaluating lead toxicity.

 

[Karmeleon]

Lead tended to lower heart cytochrome c oxidase especially when dietary copper was low, but also when dietary copper and zinc were high.

I hope this isn't true for humans too, that would mean zinc supplementation could make lead toxicity way worse. A point to keep zinc supps on the low end and better food sourced.