Lipid peroxidation is generally thought to be a major mechanism of cell injury in aerobic organisms subjected to oxidative stress. All cellular membranes are especially vulnerable to oxidation due to their high concentration of polyunsaturated fatty acids. However, birds have special adaptations for preventing membrane damage caused by reactive oxygen species. This study examines fatty acid profiles and susceptibility to lipid peroxidation in liver and heart mitochondria obtained from Adelie penguin (Pygoscelis adeliae). The saturated fatty acids in these organelles represent approximately 40-50% of total fatty acids whereas the polyunsaturated fatty acid composition was highly distinctive, characterized by almost equal amounts of 18:2 n-6; 20:4 n-6 and 22:6 n-3 in liver mitochondria, and a higher proportion of 18:2 n-6 compared to 20:4 n-6 and 22:6 n-3 in heart mitochondria. The concentration of total unsaturated fatty acids of liver and heart mitochondria was approximately 50% and 60%, respectively, with a prevalence of oleic acid C18:1 n9. The rate C20:4 n6/C18:2 n6 and the unsaturation index was similar in liver and heart mitochondria; 104.33 +/- 6.73 and 100.09 +/- 3.07, respectively. Light emission originating from these organelles showed no statistically significant differences and the polyunsaturated fatty acid profiles did not change during the lipid peroxidation process.
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http://dx.doi.org/10.1556/ABiol.59.2008.2.5 | DOI Listing |
Int J Mol Sci
January 2025
Department of Microbiology & Immunology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117597, Singapore.
This review describes our current understanding of the role of the mitochondria in the repurposing of the anti-diabetes drugs metformin, gliclazide, GLP-1 receptor agonists, and SGLT2 inhibitors for additional clinical benefits regarding unhealthy aging, long COVID, mental neurogenerative disorders, and obesity. Metformin, the most prominent of these diabetes drugs, has been called the "Drug of Miracles and Wonders," as clinical trials have found it to be beneficial for human patients suffering from these maladies. To promote viral replication in all infected human cells, SARS-CoV-2 stimulates the infected liver cells to produce glucose and to export it into the blood stream, which can cause diabetes in long COVID patients, and metformin, which reduces the levels of glucose in the blood, was shown to cut the incidence rate of long COVID in half for all patients recovering from SARS-CoV-2.
View Article and Find Full Text PDFInt J Mol Sci
December 2024
Department of Senior Citizen Service Management, National Taichung University of Science and Technology, Taichung 40343, Taiwan.
A diabetic heart is characterized by fibrosis, autophagy, oxidative stress, and altered mitochondrial functions. For this review, three databases (PubMed, EMBASE, and Web of Science) were searched for articles written in English from September 2023 to April 2024. Studies that used exercise training for at least 3 weeks and which reported positive, negative, or no effects were included.
View Article and Find Full Text PDFMitochondrion
January 2025
Departamento de Biología Celular Fisiología e Inmunología Universidad de Córdoba Campus de Excelencia Internacional Agroalimentario ceiA3 Córdoba Spain. Electronic address:
Cytochrome b reductase 3 (CYB5R3) overexpression upregulates mitochondrial biogenesis, function, and abundance in skeletal muscle and kidneys, and mimics some of the salutary effects of calorie restriction, with the most striking effects being observed in females. We aimed to investigate the mitochondrial adaptations prompted by CYB5R3 overexpression in the heart, an organ surprisingly overlooked in studies focused on this long-lived transgenic model despite the critical role played by CYB5R3 in supporting cardiomyocytes mitochondrial respiration. Given that CYB5R3 effects have been found to be sex-dependent, we focused our research on both males and females.
View Article and Find Full Text PDFLife Sci
January 2025
Department of Cardiology, Affiliated Hospital of Nantong University, Jiangsu 226001, China. Electronic address:
Doxorubicin (DOX), a chemotherapeutic agent utilized in the management of cancer, provokes cardiotoxicity although effective remedy is lacking. Given that DOX provokes oxidative stress and cell death in cardiomyocytes, this study evaluated the possible involvement of cuproptosis, a newly identified form of cell death, in DOX-instigated cardiac remodeling and contractile dysfunction, alongside the impact of the heavy metal scavenger metallothionein (MT) on DOX cardiomyopathy. Cardiac-specific MT transgenic and wild-type (WT) mice were treated with DOX (5 mg/kg/wk.
View Article and Find Full Text PDFAppl Biochem Biotechnol
January 2025
Department of Pharmacology, Faculty of Veterinary Medicine, Assiut University, Assiut, 71516, Egypt.
Doxorubicin (DOX) is a commonly used chemotherapeutic medication for treating malignancies, although its cardiotoxicity limits its use. There is growing evidence that alteration of the mitochondrial fission/fusion dynamic processes accompanied by excessive reactive oxygen species (ROS) production and alteration of calcium Ca homeostasis are potential underlying mechanisms of DOX-induced cardiotoxicity (DIC). Metformin (Met) is an AMP-activated protein kinase (AMPK) activator that has antioxidant properties and cardioprotective effects.
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