Search results for "Mitochondria"
showing 10 items of 1306 documents
Humanin: A mitochondria-derived peptide with emerging properties.
2020
Age affects the metabolic rate of insect brain.
1984
Abstract Brains of adult insects can be isolated and studied vitro. In female blowflies the oxygen uptake of the brain is age dependent. A steady increase is followed by a precipitous decrease around the middle of the life span. These changes are accompanied by alterations of mitochondrial structure and deposits of lipofuscin-like material.
PGC-1α, Inflammation, and Oxidative Stress: An Integrative View in Metabolism
2020
Peroxisome proliferator-activated receptor-γ coactivator (PGC)-1α is a transcriptional coactivator described as a master regulator of mitochondrial biogenesis and function, including oxidative phosphorylation and reactive oxygen species detoxification. PGC-1α is highly expressed in tissues with high energy demands, and it is clearly associated with the pathogenesis of metabolic syndrome and its principal complications including obesity, type 2 diabetes mellitus, cardiovascular disease, and hepatic steatosis. We herein review the molecular pathways regulated by PGC-1α, which connect oxidative stress and mitochondrial metabolism with inflammatory response and metabolic syndrome. PGC-1α regula…
Differential cysteine depletion in respiratory chain complexes enables the distinction of longevity from aerobicity.
2010
Mitochondrially encoded proteins in long-lived animals exhibit a characteristic anomaly on the amino acid usage level: they abstain from the use of cysteine in a lifespan-dependent fashion. Here, we have further investigated this phenomenon by analyzing respiratory chain complex subunits individually. We find that complex I cysteine depletion is the almost exclusive carrier of the cysteine-lifespan correlation, whereas complex IV cysteine depletion is uniform in all aerobic animals, unrelated to longevity, but even more pronounced than complex I cysteine depletion in the longest-lived species. In nuclear encoded subunits of the respiratory chain, we find lifespan-independent cysteine deplet…
Molecular bases of the treatment of Alzheimer's disease with antioxidants: prevention of oxidative stress
2004
Alzheimer's disease is associated with a systemic oxidative stress situation which can be followed in vivo by determining biomarkers such as plasma lipoperoxides and TBARS levels and the oxidation degree of glutathione in red blood cells. It has been observed that Alzheimer's patients show an increased level of plasma TBARS, which indicates a higher free radical oxidation of plasma unsaturated phospholipids, and an increased oxidation of red blood cells glutathione, which indicates oxidative stress in peripheral cells. This latter, glutathione oxidation, was found to correlate statistically with the cognitive status of the patients. Treatment with vitamin E resulted in an improved cognitive…
Telmisartan as metabolic modulator: a new perspective in sports doping?
2011
The World Antidoping Agency (WADA) has introduced some changes in the 2012 prohibited list. Among the leading innovations to the rules are that both 5-aminoimidazole-4-carboxamide-1-[beta]-D-ribofuranoside (peroxisome proliferator�activated receptor-[delta] [PPAR-[delta]]-5' adenosine monophosphate-activated protein kinase [AMPK] agonist) and GW1516 (PPAR-[delta]-agonist) are no longer categorized as gene doping substances in the new 2012 prohibited list but as metabolic modulators in the class �Hormone and metabolic modulators.� This may also be valid for the angotensin II receptor blocker telmisartan. It has recently been shown that telmisartan might induce similar biochemical, biological…
Mitochondrial function in liver disease.
2006
Oxidative stress is involved in the pathogenesis and progression of different liver diseases, such as alcoholic liver disease and biliary cirrhosis. The increased mitochondrial production of O2(-) at complexes I and III, and consequently of H2O2 and other reactive oxygen species (ROS), triggered by NADH overproduction seems the major cause of mitochondrial and cellular oxidative stress and damage in chronic alcoholism. The mitochondrial oxidative stress renders hepatocytes susceptible to ethanol- or acetaldehyde-induced mitochondrial membrane permeability transition (MMPT) and apoptosis. Nitrosative stress contributes to cell death by peroxynitrite formation. The expression of the death rec…
Glutathione-dependent formaldehyde dehydrogenase (ADH3) and low km mitochondrial aldehyde dehydrogenase (ALDH2). New evidence for differential expres…
2011
Epidemiological and experimental studies support the involvement of lipid peroxidation (LPO) in retinal diseases. In addition to other pathogenic mechanisms not fully understood, the possibility remains that peroxidic aldehydes, acting as cytotoxic chemicals, mediate in the progression of chronic ocular disorders.To test proper mechanisms involved in removing peroxidic aldehydes from the retina, in an attempt to understand long-lasting changes induced by LPO, the oxidative and antioxidant enzymatic activities, as well as the retinal distribution and activity of glutathione-dependent formaldehyde dehydrogenase (ADH3) and low km mitochondrial aldehyde dehydrogenase (ALDH2), were studied and c…
Mitochondrial aldehyde dehydrogenase (ALDH-2)--maker of and marker for nitrate tolerance in response to nitroglycerin treatment.
2008
The hemodynamic and anti-ischemic effects of nitroglycerin (GTN) are rapidly blunted as a result of the development of nitrate tolerance. Long-term nitrate treatment also is associated with decreased vascular responsiveness caused by changes in intrinsic mechanisms of the tolerant vasculature itself. According to the oxidative stress concept, increased vascular superoxide and peroxynitrite production as well as an increased sensitivity to vasoconstrictors secondary to activation of protein kinase C as well as vascular NADPH oxidases contribute to the development of tolerance. Recent experimental work has defined new tolerance mechanisms, including inhibition of the enzyme that bioactivates …
Alkylation at the active site of the D-3-hydroxybutyrate dehydrogenase (BDH), a membrane phospholipid-dependent enzyme, by 3-chloroacetyl pyridine ad…
1997
The structure of the rat liver's D-3-hydroxybutyrate dehydrogenase (BDH) active site has been investigated using an affinity alkylating reagent, the 3-chloroacetyl pyridine adenine dinucleotide (3-CAPAD). This NAD+ analogue reagent strongly inactivates the enzyme following a concentration- and time-dependent process with a stoichiometry of approximately 1. The reagent reacts at the coenzyme binding site as revealed by the efficient protection by NADH. The effect of 3-CAPAD is stronger with the enzyme into its natural membrane environment than with the lipid-free purified apoBDH or with the reconstituted apoBDH-mitochondrial phospholipid complex. The pH-dependent effect on the inactivation p…