PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Mitochondrial function”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 973 records · Page 54Linked to original sources
PubMed1982

Role of zinc as an activator of mitochondrial function in rat liver.

The effects of zinc on the enzymes of hepatic mitochondria were investigated in rats that had been given zinc sulfate (10 mg Zn2+/100 g body wt) p.o. Administration of zinc caused a marked elevation of succinate dehydrogenase, glutamate dehydrogenase, cytochrome c oxidase and ATPase activities, whereas it did not cause significant changes in pyruvate carboxylase, malate dehydrogenase and isocitrate dehydrogenase activities. The effect of zinc as a function of time was greatest on succinate dehydrogenase. Zinc also produced a marked elevation of ATP concentration in the hepatic cytosol and a corresponding increase in ATPase activity in the hepatic mitochondria. Zinc content of the inner membrane of mitochondria was raised significantly by administration of zinc. The removal of zinc by washing in 10 mM EDTA caused a significant decrease of the increased succinate dehydrogenase activity caused by administration of zinc, while it did not lower ATPase activity. The addition of zinc in amounts of 10-10(3) ng Zn2+ per mg protein produced a significant increase in succinate dehydrogenase activity in the inner membrane of mitochondria, whereas ATPase activity was elevated significantly at 10(3)-10(4) ng Zn2+ per mg protein, indicating that zinc activated succinate dehydrogenase more sensitively than ATPase. The present investigation suggests that zinc taken up by hepatic mitochondria stimulates the electron transport system and oxidative phosphorylation and, as a result, increases the ATP concentration in the hepatic cytosol.

2,4-Dinitrophenol↗
PubMed1994

Effect of methyl methacrylate on mitochondrial function and structure.

1. Treatment of isolated rat liver mitochondria with methyl methacrylate (MM) produced membrane disruption as evidenced by the release of citrate synthase, and changes in the ultrastructure of mitochondria. 2. At concentration 0.1%, MM uncoupled oxidative phosphorylation as evidenced by stimulation of state 4 respiration supported either by pyruvate plus malate or succinate (+rotenone) and ATP-ase activity in intact mitochondria. 3. At concentration 1% MM stimulated ATP-ase activity in intact mitochondria and succinate (+ rotenone) oxidation at state 4 and was without effect on this substrate oxidation at state 3. 4. MM inhibited pyruvate plus malate oxidation either at state 3 or in the presence of uncoupling agents. 5. MM inhibited the NADH oxidase of electron transport particles at a concentration which failed to inhibit either succinic oxidase or the NADH-ferricyanide reductase activity. 6. The data presented suggest that in the isolated mitochondria MM inhibits NADH oxidation in the vicinity of the rotenone sensitive site of complex I. 7. The general conclusion is that MM may block an electron transport and to uncouple oxidative phosphorylation in rat liver mitochondria. The overall in vitro effect would be to prevent ATP synthesis which could result in cell death under in vivo conditions.

Adenosine Triphosphatases↗