Aging is associated with a decline of cardiac function. The mitochondrial permeability transition (MPT) may be a factor in cardiac dysfunction associated with aging. We investigated the effect of aging and long-term treatment with melatonin (approximately 10 mg/kg b.w./day for 2 months), a known natural antioxidant, on the susceptibility to Ca(2+)-induced MPT opening and cytochrome c release in rat heart mitochondria. The mitochondrial content of normal and oxidized cardiolipin as a function of aging and melatonin treatment was also analyzed. Mitochondria from aged rats (24 month old) displayed an increased susceptibility to Ca(2+)-induced MPT opening, associated with an elevated release of cytochrome c, when compared with young control animals (5 month old). Melatonin treatment counteracted both these processes. Aging was also associated with an oxidation/depletion of cardiolipin which could be counteracted as well by melatonin. It is proposed that the increased level of oxidized cardiolipin could be responsible, at least in part, for the increased susceptibility to Ca(2+)-induced MPT opening and cytochrome c release in rat heart mitochondria with aging. Melatonin treatment counteracts both these processes, most likely, by preventing the oxidation/depletion of cardiolipin. Our results might have implications in the necrotic and apoptotic myocytes cell death in aged myocardium, particularly in ischemia/reperfusion injury.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1111/j.1600-079X.2010.00758.x | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Basic Science and Pathogenesis.
Alzheimers Dement
December 2024
Division of Geriatrics, Department of Internal Medicine, University of Sao Paulo Medical School, São Paulo, São Paulo, Brazil.
Background: Nitric oxide (NO) is involved in synaptic transmission and cerebral plasticity, playing a role in the memory process. However, in states of brain inflammation, hypoxia, or ischemia, there is induction of inducible nitric oxide synthase (iNOS) expression by astrocytes and pyramidal cells in the brain. Under conditions of chronic activation, there is a decoupling of iNOS dimers, leading to a massive generation of superoxide anion and peroxynitrite, O2.
View Article and Find Full Text PDFNeuroprotective effects of testosterone on sevoflurane-induced neurotoxicity in testosterone-deprived male mice.
Neuropharmacology
March 2025
Department of Anesthesiology, Tianjin Medical University General Hospital, Tianjin Institute of Anesthesiology, Tianjin, China. Electronic address:
This study aims to investigate whether androgen deprivation, simulating conditions of aging or disease-induced low testosterone levels, increases the susceptibility of male mice to sevoflurane neurotoxicity, and whether testosterone supplementation can reverse the toxic effects of sevoflurane. In here, young male mice were subjected to orchiectomy (ORC) to induce testosterone deprivation. Various techniques, including western blotting, immunofluorescence, Morris Water Maze, Golgi staining, and neuronal signal measurement, were used to evaluate the effects of sevoflurane on long-term (ORC 10 weeks) and short-term (ORC 2 weeks) testosterone deprivation, and assess whether testosterone (1 mg/kg 1 h before sevoflurane exposure) could mitigate sevoflurane-induced neurotoxicity.
View Article and Find Full Text PDFInositol 1,4,5-Trisphosphate Receptor 1 Gain-of-Function Increases the Risk for Cardiac Arrhythmias in Mice and Humans.
Circulation
December 2024
Department of Physiology and Pharmacology, Libin Cardiovascular Institute, University of Calgary, Canada (B.S., M. Ni, Y.L., Z.S., H.W., H.-L.Z., J.W., D.B., S.C., W.G., J.Y., S.T., J.P.E., R.W., S.R.W.C.).
Article Synopsis
- * Researchers identified 21 human ITPR1 GOF variants and created a mouse model with one of these variants (ITPR1-W1457G), which was found to be prone to stress-induced ventricular arrhythmias.
- * Both mouse models and human data suggest that ITPR1 GOF variants increase Ca handling abnormalities and arrhythmia risk, with 7 rare ITPR1 variants in a human database showing similar GOF behavior linked to cardiac
Impairment of Glucose Uptake Induced by Elevated Intracellular Ca in Hippocampal Neurons of Malignant Hyperthermia-Susceptible Mice.
Cells
November 2024
Department of Research, Mount Sinai Medical Center, Miami, FL 33140, USA.
Malignant hyperthermia (MH) is a genetic disorder triggered by depolarizing muscle relaxants or halogenated inhalational anesthetics in genetically predisposed individuals who have a chronic elevated intracellular Ca concentration ([Ca]) in their muscle cells. We have reported that the muscle dysregulation of [Ca] impairs glucose uptake, leading to the development of insulin resistance in two rodent experimental models. In this study, we simultaneously measured the [Ca] and glucose uptake in single enzymatically isolated hippocampal pyramidal neurons from wild-type (WT) and MH-R163C mice.
View Article and Find Full Text PDFTouch, light, wounding: how anaesthetics affect plant sensing abilities.
Plant Cell Rep
November 2024
Department of Biophysics, Faculty of Science, Palacký University, Šlechtitelů 27, 78371, Olomouc, Czech Republic.
Anaesthetics affect not only humans and animals but also plants. Plants exposed to certain anaesthetics lose their ability to respond adequately to various stimuli such as touch, injury or light. Available results indicate that anaesthetics modulate ion channel activities in plants, e.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!