Mercury and Other Heavy Metal Toxicity and Mitocheondral Dysfunction. Part of a Coordinated Programme of Isotopic Tracer-Aided Studies of the Biological Side-Effects of Foreign Chemical Residues in Food and Agriculture. Final Repo

摘要

Mercury and other heavy metal toxicity and mitochondrial dysfunction: kidney mitochondria isolated from Hg-poisoned rats (4mgHg exp ++ /kgb.wt.,i.v.) exhibited a considerable loss of capacity for oxidative phosphorylation, apparently related to Mg exp ++ depletion and inhibition of ATP synthesis. Liver mitochondria remained unaffected. It is maintained that acute Hg poisoning is related to kidney failure. Selenium was found to provide protection as ascertained by partial restoration of the kidney mitochondrial oxidative phosphorylation and prolongation of time of death of the poisoned animals. In contrast to Hg, acute Cd-poisoning in rats (4mgCd exp ++ /kg,b.wt.,i.v.) is probably related to liver failure, where hepatic mitochondria loses its capacity for oxidative phosphorylation, through the same mechanism postulated for kiney mitochondria isolated from Hg-poisoned rats. Again, selenium provided a similar protective effect. That Hg and Cd have two different target organs may be ascribed to the relative distribution of both elements in the animal body. Preliminary data in the rabbit showed that Cd caused an increase of heart beat as well as an increased difference between systolic and diastolic pressures. Studies on Pb-poisoned rats, using 2,4-Dinitrophenol as uncoupling agent in mitochondria, suggested inhibition of the electron transport chain. (Atomindex citation 09:414586)