Respiration Rate Of Liver Mitochondria Research Articles

Inconsistent responses of liver mitochondria metabolism and standard metabolism in Silurus meridionalis when exposed to waterborne cadmium

We investigated the standard metabolic rate and liver mitochondria metabolism of the southern catfish when exposed to waterborne cadmium. Juvenile southern catfish were exposed to waterborne cadmium concentrations (0, 62.5, 125, 250 and 500 μg/L, respectively) for 8 weeks, and the final body mass, the standard metabolic rate, the state III respiration rate, the activity of cytochrome C oxidase (CCO) of liver mitochondria, and the hepatosomatic index (HSI) were determined. The results showed that the 62.5 μg/L, 125 μg/L, and 250 μg/L experiment groups had a significantly higher standard metabolic rate than that of the control group. Standard metabolic rate in the 500 μg/L experiment group did not differ from the control group. State III respiration rate of liver mitochondria decreased with an increase in cadmium concentration. The 125 μg/L, 250 μg/L, and 500 μg/L experiment groups had a significantly lower state III respiration rate than that of the control group. The activity of CCO in the 500 μg/L experiment group was significantly lower than that of the control group. These results suggest that at low cadmium concentrations, the southern catfish could continuously improve the standard metabolism to provide extra energy in response to the cadmium stress. Cadmium exposures caused damage to the structure and function of liver mitochondria and decreased the activity of mitochondria enzymes, which results in a decrease in the energy of the liver metabolism. The adjustment of the metabolism of liver mitochondria in southern catfish was inconsistent with the adjustment of individual standard metabolism.

Liver metabolic changes induced by conjugated linoleic acid in calorie-restricted rats.

Complexes like conjugated linoleic acid (CLA) reduce the percentage of body fat by increasing energy expenditure, fat oxidation, or both. The aim of this study was to verify if CLA is able to mimic caloric restriction (CR), and determine the effects of CLA on liver metabolic profile of young adult male Wistar rats. We divided 36 animals into the following groups: 1) Control; 2) CLA (1% of daily food intake, 21 days, orogastric intubation); 3) Restr (fed 60% of the diet offered to controls); and 4) CLA Restr. Liver tissues were processed for biochemical and molecular or mitochondrial isolation (differential centrifugation) and blood samples were collected for biochemical analyses. Treatment of the animals for 21 days with 1% CLA alone or combined with CR increased liver weight and respiration rates of liver mitochondria suggesting significant mitochondrial uncoupling. We observed a decrease in adipose tissue leading to insulin resistance, hyperinsulinemia, and hepatic steatosis due to increased liver cholesterol and triacylglycerol levels, but no significant effects on body mass. The expression of hepatic cellular connexins (43 and 26) was significantly higher in the CLA group compared with the Control or Restr groups. CLA does not seem to be a safe compound to induce mass loss because it upregulates the mRNA expression of connexins and induces hepatic mitochondrial changes and lipids disorders.

Lactation Affects Isolated Mitochondria and Its Fatty Acid Composition but Has No Effect on Tissue Protein Oxidation, Lipid Peroxidation or DNA-Damage in Laboratory Mice.

Linking peak energy metabolism to lifespan and aging remains a major question especially when focusing on lactation in females. We studied, if and how lactation affects in vitro mitochondrial oxygen consumption and mitochondrial fatty acid composition. In addition, we assessed DNA damage, lipid peroxidation and protein carbonyls to extrapolate on oxidative stress in mothers. As model system we used C57BL/6NCrl mice and exposed lactating females to two ambient temperatures (15 °C and 22 °C) while they nursed their offspring until weaning. We found that state II and state IV respiration rates of liver mitochondria were significantly higher in the lactating animals than in non-lactating mice. Fatty acid composition of isolated liver and heart mitochondria differed between lactating and non-lactating mice with higher n-6, and lower n-3 polyunsaturated fatty acids in the lactating females. Surprisingly, lactation did not affect protein carbonyls, lipid peroxidation and DNA damage, nor did moderate cold exposure of 15 °C. We conclude that lactation increases rates of mitochondrial uncoupling and alters mitochondrial fatty acid composition thus supporting the “uncoupling to survive” hypothesis. Regarding oxidative stress, we found no impact of lactation and lower ambient temperature and contribute to growing evidence that there is no linear relationship between oxidative damage and lactation.

Liver mitochondrial and whole-animal level metabolic compensation in a catfish during seasonal acclimatization

Abstract To examine whether metabolic compensation during seasonal acclimatization at the liver mitochondrial level is consistent with that at the whole-animal level, respiration rates of liver mitochondria and resting metabolic rates in winter- and summer-acclimatized southern catfish (Silurus meridionalis Chen) were measured. At 12.5, 17.5, 22.5, 27.5 and 32.5°C, the mean values of state 3 respiration rates were 12.21, 13.84, 18.96, 24.78 and 32.01 nmol O2 min-1 mg-1 mitochondrial protein in the winter group, and 8.56, 9.20, 17.32, 22.74 and 26.32 nmol O2 min-1 mg-1 in the summer group, respectively. At the five assay temperatures the resting metabolic rates were 24.86, 42.68, 61.59, 84.10 and 125.65 mg O2 h-1 kg-1 body mass in the winter group, and 22.89, 40.59, 52.94, 75.13 and 109.35 mg O2 h-1 kg-1 in the summer group, respectively. Total mitochondrial respiration rates in the liver organ were estimated based on state 3 respiration rates, mitochondrial protein content and organ mass, and the mean values were 72.96, 71.87, 112.47, 167.35 and 183.27 nmol O2 min-1 in the winter group, and were 47.89, 47.39, 105.67, 138.18 and 132.29 nmol O2 min-1 in the summer group, respectively. Metabolic compensation caused by seasonal acclimatization occurred at the liver mitochondrial level and compensation at the liver organ level was found to be more efficient because of an increase in metabolic capacity of mitochondria and a boost in organ mass. Metabolic compensation at the whole-animal level was not detected. During seasonal acclimatization, the effect of metabolic compensation at liver mitochondrial level is inconsistent with that at the whole-animal level in the southern catfish. This may be due to different degrees of regulation of metabolic mechanisms among various tissues and organs in an acclimatized organism.

Temperature dependence of rat liver mitochondrial respiration with uncoupling of oxidative phosphorylation by fatty acids. Influence of inorganic phosphate.

The respiration rate of liver mitochondria in the course of succinate oxidation depends on temperature in the presence of palmitate more strongly than in its absence (in state 4). In the Arrhenius plot, the temperature dependence of the palmitate-induced stimulation of respiration has a bend at 22 degrees C which is characterized by transition of the activation energy from 120 to 60 kJ/mol. However, a similar dependence of respiration in state 4 is linear over the whole temperature range and corresponds to the activation energy of 17 kJ/mol. Phosphate partially inhibits the uncoupling effect of palmitate. This effect of phosphate is increased on decrease in temperature. In the presence of phosphate the temperature dependence in the Arrhenius plot also has a bend at 22 degrees C, and the activation energy increases from 128 to 208 kJ/mol in the range from 13 to 22 degrees C and from 56 to 67 kJ/mol in the range from 22 to 37 degrees C. Mersalyl (10 nmol/mg protein), an inhibitor of the phosphate carrier, similarly to phosphate, suppresses the uncoupling effect of laurate, and the effects of mersalyl and phosphate are not additive. The recoupling effects of phosphate and mersalyl seem to show involvement of the phosphate carrier in the uncoupling effect of fatty acids in liver mitochondria. Possible mechanisms of involvement of the phosphate carrier in the uncoupling effect of fatty acids are discussed.

Reactive Oxygen Species Produced by Liver Mitochondria of Rats in Sepsis

Reactive oxygen species (ROS) can be generated in experimental shock states through several different mechanisms. We measured ROS production in metabolically active liver mitochondria from rats rendered septic by cecal ligation and puncture. By polarography, the State 4 and State 3 respiration rates of liver mitochondria isolated from septic animals were no different from control organelles. During oxidation of succinate, however, nonenzymatic hydroxylation of salicylic acid to 2,3-dihydroxybenzoic acid by mitochondria from septic rats was increased, indicating generation of hydroxyl radical (OH.). Inhibition of electron transport at Complex I with rotenone had no effect on this pattern of OH. production, but rotenone and cyanide abolished the differences in OH. formation between control and septic liver mitochondria. Measurements of H2O2 release suggested that septic mitochondria will increase rates of H2O2 production in the presence of succinate. Additional investigations revealed no difference in the release of iron between septic and control mitochondria. When referenced to respiration rate, both OH. and H2O2 production were greater in septic liver mitochondria. The reproducible effect of sepsis on generation of reactive oxygen species by liver mitochondria utilizing FAD-linked but not NAD-linked substrates suggests that enhanced mitochondrial oxidative stress in sepsis is related to alterations in the activity of Complex II of the electron transport chain.