Peculiarities of the free radical processes in rat liver mitochondria under toxic hepatitis on the background of alimentary protein deficiency

The activity of free radical processes in liver mitochondria was investigated in rats kept on high-sucrose and low protein/high-sucrose diets. Excess of dietary sucrose caused intensification of free radical processes in liver mitochondria as evidenced by increased hydroxyl radical generation, accumulation of primary (conjugated dienes, ketodienes) and secondary products (TBA-reactive products) of lipid peroxidation, increased cholesterol/phospholipids ratio and also accumulation of oxidative modification products of proteins (carbonyl derivatives). Additional nutritional protein deficiency (low protein/high-sucrose diet) enhanced destructive changes in liver mitochondria. This suggests a critical role of nutrient protein supplementation for maintaining the functional activity of mitochondria. The established changes can be considered as one of possible mechanisms of functional liver activity violation in conditions of nutrient imbalance.

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Effect of chalone and antichalone on free radical processes in rat liver

Bulletin of Experimental Biology and Medicine ◽

10.1007/bf02496858 ◽

1998 ◽

Vol 125 (2) ◽

pp. 197-199 ◽

Cited By ~ 1

Author(s):

A. N. Pashkov ◽

A. Yu. Maslov

Keyword(s):

Free Radical ◽

Rat Liver ◽

Free Radical Processes ◽

Radical Processes

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Expression of Glutathione Peroxidase and Glutathione Reductase and Level of Free Radical Processes under Toxic Hepatitis in Rats

Journal of Toxicology ◽

10.1155/2013/870628 ◽

2013 ◽

Vol 2013 ◽

pp. 1-9 ◽

Cited By ~ 16

Author(s):

Igor Y. Iskusnykh ◽

Tatyana N. Popova ◽

Aleksander A. Agarkov ◽

Miguel Â. A. Pinheiro de Carvalho ◽

Stanislav G. Rjevskiy

Keyword(s):

Free Radical ◽

Glutathione Peroxidase ◽

Glutathione Reductase ◽

Toxic Hepatitis ◽

Free Radical Oxidation ◽

Inflammatory Cells ◽

Maximum Increase ◽

Radical Oxidation ◽

Free Radical Processes ◽

Radical Processes

Correlation between intensity of free radical processes estimated by biochemiluminesce parameters, content of lipoperoxidation products, and changes of glutathione peroxidase (GP, EC 1.11.1.9) and glutathione reductase (GR, EC 1.6.4.2) activities at rats liver injury, after 12, 36, 70, 96, 110, and 125 hours & tetrachloromethane administration have been investigated. The histological examination of the liver sections of rats showed that prominent hepatocytes with marked vacuolisation and inflammatory cells which were arranged around the necrotic tissue are more at 96 h after exposure to CCl4. Moreover maximum increase in GR and GP activities, 2.1 and 2.5 times, respectively, was observed at 96 h after exposure to CCl4, what coincided with the maximum of free radical oxidation processes. Using a combination of reverse transcription and real-time polymerase chain reaction, expression of the glutathione peroxidase and glutathione reductase genes (Gpx1 and Gsr) was analyzed by the determination of their respective mRNAs in the rat liver tissue under toxic hepatitis conditions. The analyses of Gpx1 and Gsr expression revealed that the transcript levels increased in 2.5- and 3.0-folds, respectively. Western blot analysis revealed that the amounts of hepatic Gpx1 and Gsr proteins increased considerably after CCl4administration. It can be proposed that the overexpression of these enzymes could be a mechanism of enhancement of hepatocytes tolerance to oxidative stress.

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THE RATIO OF UBIQUINON REDOX FORMS IN THE RAT LIVER MITOCHONDRIA UNDER CONDITIONS OF DIFFERENT NUTRIENT SUPPLY

Fiziolohichnyĭ zhurnal ◽

10.15407/fz66.06.082 ◽

2020 ◽

Vol 66 (6) ◽

pp. 82-87

Author(s):

O.M. Voloshchuk ◽

◽

G. P. Kopylchuk ◽

М.S. Ursatyу ◽

◽

...

Keyword(s):

Free Radical ◽

Rat Liver ◽

Liver Mitochondria ◽

Oxidative Modification ◽

Mitochondrial Proteins ◽

Rat Liver Mitochondria ◽

Carbonyl Derivatives ◽

High Sucrose Diet ◽

Redox Forms ◽

High Sucrose

The relationship between the quantitative ratio of redox forms of ubiquinone and the degree of free radical damage to mitochondrial proteins in rat liver against the background of nutritional imbalance was investigated. The animals were divided into the following experimental groups: I – animals receiving full-value semi-synthetic ration (control group); II – animals receiving high-sucrose diet; III – animals receiving low-protein high-sucrose diet. The content of total and oxidized ubiquinone was determined spectrophotometrically at 275 nm, the content of reduced ubiquinone was determined by the difference between the content of total and oxidized ubiquinone. The intensity of the oxidative modification of proteins was assessed by the accumulation of carbonyl derivatives in the reaction with 2,4-dinitrophenylhydrazine (2,4-DNPH), the content of free SH-groups was assessed by using the Elman reagent. It was found that the most pronounced decrease in the content of total ubiquinone (almost twice) and the redistribution of its redox forms (reduction of the content of reduced ubiquinone by 7.2 times against the background of an increase in the level of oxidized ubiquinone by 2 times) in rat liver mitochondria is observed in animals that received a diet high in sucrose against the background of alimentary protein deprivation. In addition, the animals of this group showed the most pronounced free radical oxidation of mitochondrial proteins, as evidenced by a 3.5-fold increase in the content of carbonyl derivatives and a 2.6-fold decrease in the content of free protein SH- groups. It was shown that nutritional protein deficiency is a critical factor affecting the intensity of free radical processes in mitochondria. The established changes in the ratio of the redox forms of ubiquinone and the degree of oxidative modification of mitochondrial proteins in rat liver could be considered as prerequisites for deepening the energy imbalance and violation of the functional activity of mitochondria under conditions of nutritional imbalance.

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Free-radical metabolism of carbon tetrachloride in rat liver mitochondria. A study of the mechanism of activation

Biochemical Journal ◽

10.1042/bj2460313 ◽

1987 ◽

Vol 246 (2) ◽

pp. 313-317 ◽

Cited By ~ 60

Author(s):

A Tomasi ◽

E Albano ◽

S Banni ◽

B Botti ◽

F Corongiu ◽

...

Keyword(s):

Free Radical ◽

Carbon Tetrachloride ◽

Rat Liver ◽

Liver Microsomes ◽

Liver Mitochondria ◽

Rat Liver Mitochondria ◽

Radical Species ◽

Hypoxic Conditions ◽

Free Radical Species ◽

Transport Chain

Alterations in liver mitochondria as consequence of rat poisoning with carbon tetrachloride (CCl4) have been reported over many years, but the mechanisms responsible for causing such damage are still largely unknown. Isolated rat liver mitochondria incubated under hypoxic conditions with succinate and ADP were found able to activate CCl4 to a free-radical species identified as trichloromethyl free radical (CCl3) by e.s.r. spectroscopy coupled with the spin-trapping technique. The incubation of mitochondria in air decreased free-radical production, indicating that a reductive reaction was involved in the activation of CCl4. However, in contrast with liver microsomes (microsomal fractions), mitochondria did not require the presence of NADPH, and the process was not significantly influenced by inhibitors of cytochrome P-450. The addition of inhibitors of the respiratory chain such as antimycin A and KCN decreased free-radical formation by only 30%, whereas rotenone displayed a greater effect (approx. 84% inhibition), but only when preincubated for 15 min with mitochondria not supplemented with succinate. These findings suggest that the mitochondrial electron-transport chain is responsible for the activation of CCl4. A conjugated-diene band was observed in the lipids extracted from mitochondria incubated with CCl4 under anaerobic conditions, indicating that stimulation of lipid peroxidation was occurring as a result of the formation of free-radical species.

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