Tag Archives: mitochondrial respiration
Sex differences in respiration and redox homeostasis of heart mitochondria in rats on high-fructose diet
O. Ivanova1, N. Gorbenko1, O. Borikov2, T. Kiprych1, K. Taran1
1SI “V. Danilevsky Institute for Endocrine Pathology Problems
of the NAMS of Ukraine”, Kharkiv, Ukraine;
2V. N. Karazin Kharkiv National University, Kharkiv, Ukraine;
*e-mail: ivolga3006@ukr.net
Received: 05 April 2024; Revised: 27 May 2024;
Accepted: 25 July 2024; Available on-line: 04 September 2024
Sex hormones play a leading role in the sexual dimorphism of mitochondrial dysfunction and oxidative stress that are associated with Metabolic Syndrome (MetS) and considered as possible causes of cardiovascular disease. The aim of the work was to determine mitochondrial respiration and redox homeostasis in the heart mitochondria of high-fructose diet-fed (НFD) rats depending on sex. MetS was induced in Wistar rats by 8 weeks intake of fructose (200 g/l) with drinking water. The experiment was performed on 30 rats divided into five groups: control males, control females, HFD-fed males, HFD- fed females with intact ovaries, ovariectomized HFD-fed females. Heart mitochondria were isolated and indicators of redox homeostasis as well as mitochondrial oxygen consumption rate were determined. Heart mitochondria of intact female rats were characterized by a lower intensity of lipid peroxidation, a higher activity of antioxidant defense system and state 3 respiration in comparison with control males. HFD was shown to induce more expressed oxidative stress due to significant inhibition of enzymatic and non-enzymatic components of antioxidant defese and more pronounced dysregulation of mitochondrial respiration in the heart mitochondria of ovariectomized females as compared to males. This data may partially explain the greater cardiovascular risk in women with low estrogen sufficiency and justify the necessity of new sex-specific prevention and treatment of cardiovascular risk approaches.
Effect of long-term ethanol consumption and a high-fat diet on mitochondrial respiration in rat pancreatic acinar cells and hepatocytes
O. O. Bilonoha*, H. M. Mazur, B. O. Manko,
O. R. Kulachkovsky, V. V. Manko
Ivan Franko National University of Lviv, Lviv, Ukraine;
*e-mail: olha.bilonoha@lnu.edu.ua
Received: 26 March 2024; Revised: 09 May 2024;
Accepted: 25 July 2024; Available on-line: 04 September b2024
Chronic alcohol consumption may cause pancreatitis and alcohol-related liver diseases. Both adaptation and damage of liver mitochondria in animals on chronic ethanol and high-fat diets were demonstrated. It is currently not clear if ethanol or its metabolites such as fatty acid ethyl esters can cause mitochondrial damage to the pancreas. The present study aimed to evaluate the effect of chronic ethanol administration in combination with a high-fat diet on mitochondrial respiration in both pancreatic acinar cells and hepatocytes of rats. Wistar male rats on a high-fat diet (35% calories) were administered ethanol (6 g/kg body weight) by oral gavage for 14 days. Pancreatic acini cells and hepatocytes were isolated with collagenase digestion. The respiration of isolated cells was studied with a Clark electrode. Ethanol administration to rats kept on a high-fat diet was followed by a rapid loss of animal weight during the first 5 days of the experiment and diminished secretory response of pancreatic acini to acetylcholine, however, no changes in acinar cells ultrastructure, basal, oligomycin-insensitive or FCCP-uncoupled respiration were found. Meanwhile ethanol caused a significant (~40%) increase in basal and maximal FCCP-uncoupled respiration rate of isolated hepatocytes. In conclusion, chronic ethanol administration to rats on a high-fat diet does not cause mitochondrial damage in the pancreas, while mitochondria of the liver adapt to ethanol by increasing respiration rate.