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Biomedical subjects

O R Koch

Publications and source records attributed to O R Koch.

17 recordsLinked to original sources
PubMed1991

Alcohol-induced oxidative stress in rat liver.

1. Livers from rats treated acutely with ethanol showed increased chemiluminescence, malondialdehyde production, and diene formation. Previous administration of (+)-cyanidanol-3 completely abolished acute ethanol-induced chemiluminescence. 2. Rats fed alcohol liquid diets for 3 weeks showed significant increases in microsomal and mitochondrial malondialdehyde formation, and in microsomal H2O2 and O2-. generation. 3. Rats fed a solid basal diet plus ethanol solution for 12 weeks also showed increased microsomal production of O2-. and increased content of microsomal cytochrome P-450. Hydroperoxide-induced chemiluminescence was higher in homogenates, mitochondria and microsomes from ethanol-treated rats than from controls. Vitamins E and A were more effective inhibitors of hydroperoxide-stimulated chemiluminescence in liver homogenates from ethanol-treated rats than from control animals. 4. Results are consistent with peroxidative stress leading to increased lipid peroxidation in liver of rats fed ethanol both acutely and after long-term dosing.

Animals↗
PubMed1988

Liver and heart mitochondria in rats submitted to chronic hypobaric hypoxia.

Mitochondrial mass was determined in the heart and liver of rats submitted to 4,400 m (simulated altitude) for 9 mo and their controls at sea level. This was done 1) by evaluation of isolated mitochondrial protein per gram of tissue, 2) by evaluation of the ratio between cytochrome oxidase activity in tissue homogenate and in isolated mitochondria, and 3) by evaluation of mitochondrial numerical and volume density in fixed tissues analyzed by electron microscopy. An increase in mitochondrial mass and a more homogeneous distribution of mitochondria were found in liver. In cardiac tissue an increase in numerical density of mitochondria accompanied by a slight decrease in their mean volume was observed. Maximal physiological rate of mitochondrial respiration (state 3, active respiration), resting respiration, ADP/O, and acceptor control ratio were determined in the isolated mitochondria. No differences were found in the intrinsic properties of mitochondria. The results suggest that chronic mild hypoxia promotes tissue adaptation by increasing the mitochondrial mass or number in liver and heart, respectively, and improves intracellular O2 diffusion by adopting a more homogeneous intracellular distribution of mitochondria in the liver.

Animals↗
PubMed1988

Lindane-induced oxidative stress. I. Time course of changes in hepatic microsomal parameters, antioxidant enzymes, lipid peroxidative indices and morphological characteristics.

1. Lindane (60 mg/kg) administered orally to rats increased liver cytochrome P-450 content and superoxide radical (O2-.) generation 24 h after treatment, while formation of thiobarbituric acid reactants and NADPH/ADP-supported microsomal chemiluminescence were significantly increased 4 h after treatment. 2. Hepatic superoxide dismutase (SOD) and catalase decreased 6 h after lindane treatment and SOD/O2-. ratio progressively decreased during 4 to 24 h after lindane treatment. 3. Morphological evidence of hepatic cell injury after lindane treatment was seen at all times studied, and appeared to increase with time. 4. Lindane administration results in time-dependent oxidative stress in liver which involves an early component (4-6 h) related to the reductive metabolism of lindane, and a late component (24 h) associated with the induction of cytochrome P-450; the biochemical changes correlated with the observed morphological lesions.

Animals↗
PubMed1987

Effect of vitamin E- and selenium-deficiency on rat liver chemiluminescence.

The role of vitamin E and selenium as protective agents against oxidative stress was evaluated by measuring liver chemiluminescence in situ. Weanling rats fed a vitamin E- and selenium-deficient diet showed liver chemiluminescence that was increased 60 and 100% over control values at 16 and 18 days respectively after weaning. At day 21, the double deficiency led to hepatic necrosis, as observed by optical and electron microscopy, and increased serum levels of lactate dehydrogenase and alanine aminotransferase. Single deficiencies, in either vitamin E or selenium, did not produce liver necrosis but increased liver chemiluminescence. Vitamin E deficiency led to a 23 and 50% increase in liver emission at days 18 and 20 respectively; selenium deficiency produced a 64% increase at day 16. The activity of liver selenium-glutathione peroxidase diminished to 13% of the control value in the rats fed doubly deficient and selenium-deficient diets. Activities of superoxide dismutase, catalase and non-selenium-glutathione peroxidase were not modified by the different diets. These results suggest that oxy-radical generation may play a major role in hepatic necrosis in vitamin E- and selenium-deficiency.

Animals↗
PubMed1979

[Hepatic function in vivo and in the isolated liver of rats poisoned with parathion].

Enzyme determinations and hepatic histological studies were carried out in normal rats and in rats intoxicated with the organophosphorus pesticide parathion. No significative evidence of hepatocellular damage was seen in parathion -- intoxicated rats as responsible of the impaired bile flow and sulfobromophthalein biliary excretion that were previously reported. On the contrary, the isolated perfused rat liver from normal and intoxicated rats showed a similar behavior when the perfusate flow through the liver was maintained at a similar rate. We conclude that altered hepatic blood flow may be a factor determinant of an impairment of bile flow and of biliary excretion of several organic anions like sulphobromopthalein that were observed in parathion -- intoxicated rats.

Alanine Transaminase↗
PubMed1978

Effects of quinestrol on hepatic function in the rat.

Hepatic function in female rats given 200 microgram of quinestrol every 15 days for up to 210 days was studied. Prolonged treatment with quinestrol affected liver weight, serum cholestrol levels, biliar flux, and bromosulphthalein test, but these parameters tended toward control levels after 30 days of treatment. Quinestrol failed to affect alkaline phosphatase, oxalacetic and pyruvic transaminases and the concentration of bilirubin in serum and bile. The effects of quinestrol on hepatic function are similar to the effects of other estrogen derivatives.

Alkaline Phosphatase↗
PubMed1978

Ultrastructural and biochemical aspects of liver mitochondria during recovery from ethanol-induced alterations. Experimental evidence of mitochondrial division.

To study the morphologic and biochemical changes occuring in liver mitochondria during recovery from ethanol-induced injury, rats fed a 6-month high-alcohol regimen plus a nutritionally adequate diet which did not induce fatty liver were compared with isocalorically fed controls. After this period the alcohol-fed animals displayed striking ultrastructural changes of liver mitochondria and a decreased respiratory activity with succinate or malate-glutamate as substrate. On the contrary, the respiratory rate with I-glycerophosphate was 50% increased. Regression changes were studied after alcohol was withdrawn from the diet. Enlarged mitochondria rapidly disappeared (in 24 hours), although a few megamitochondria were still present after 8 days of abstinence. A similar recovery was observed for the functional alterations. At the end of the experimental period, only a slight decrease of the maximal respiratory rate using malate-glutamate as a substrate was noted. The ultrastructural findings and the morphometric data suggest that the way in which mitochondrial normalization takes place is based on partition of these organelles.

Animals↗