Mitochondria were isolated from regenerating rat liver 12, 24 and 48 h after partial hepatectomy. The "State 3" and "State 4" respiration were measured in the presence of succinate. The P/O quotient and respiratory control index (RCI) were calculated. The experimental data showed that the partial uncoupling of oxidative phosphorylation in regenerating liver mitochondria occurring in the early period of regeneration is partly due to free fatty acids.
Sensitivity of various mitochondrial enzymes to oxidative damage was tested on isolated rat liver hepatocytes
permeabilized by digitonin. In permeabilized hepatocytes
normal respiratory control
values were obtained and
mitochondrial membranes remained intact. Respiratory rate
s of NADH-dependent (glutamate+malate, palmitylcarnitine
+ malate) and flavoprotein-dependent (succinate) substrates were determined in hepatocytes exposed for 5 min to
0.5-3 mM
tert
-butyl hydroperoxide before addition of digitonin.
Our data showed that oxidation of NADH-dependent
substrates is much more sensitive to oxidative stress than ox
idation of flavoprotein-dependent ones, evidently due to the
modification of iron-sulfur clusters or SH groups in the NADH dehydrogenase enzyme complex (Complex I).
Glycerol-3-phosphate oxidation in brown adipose tissue mitochondria of cold-adapted hamster is strongly inhibited by phospholipase A2 (PLA2)- Our data show that the glycerol-3-phosphate branch of the respiratory chain is sensitive to PLA2 action more than the succinate branch and that the transfer of reducing equivalents from the glycerol-3-phosphate dehydrogenase to arteficial electron acceptor is especially sensitive to the PLA2 action.
The recovery of total DNA content and recovery of total cytochrome c oxidase activity in the rat liver after partial hepatectomy is accelerated by triiodothyronine applied in three doses, two before and one immediately after liver resection. Triiodothyronine-treated animals already have higher cytochrome c oxidase activity before resection. The recovery of the tissue oxidative capacity after partial hepatectomy is more rapid in triiodothyronine-treated animals. These data indicate that hormonal activation of the liver regeneration process is involved.
Aging is a process drawing attention of many researchers, and at present many theories exists, which try to explain this chain of inevitable events leading to death of organism. In this article we focused our attention on a theory explaining the degenerative changes occurring during aging by the effect of oxygen free radicals. These highly reactive radicals are produced during oxidative phosphorylation in mitochondria. All cellular components appear to be sensitive to oxygen-radical damage. Lipids, proteins and nucleic acids are probably the most susceptible to this injury. Lipoperoxidation of lipids together with cross-linking of proteins with phospholipids and nucleic acids caused changes in membrane fluidity. Mitochondrial DNA coding several subunits of respiratory chain enzymes can be also damaged by these radicals. All these changes together have negative impact on mitochondrial metabolism resulting progressive decrease of the efficiency of oxidative phosphorylation and thus of the whole organism.