Search results for "oxidative phosphorylation"
showing 10 items of 284 documents
Oxidative halogenation of substituted pyrroles with cu(II). Part II. Bromination of some ethyl 3-pyrrolecarboxylates and corresponding acids
1990
Ethyl 3-pyrrolecarboxylates and their corresponding acids are brominated with copper(II) bromide. The reaction afforded at 0°, with high-yield nuclear monobromination.
Aryl radicals by copper(II) oxidation of hydrazines: A new method for the oxidative and reductive arylation of alkenes
1989
Abstract A new source of aryl radicals interesting from the preparative point of view has been found in the reaction of arylhydrazines and copper(II) sulfate. The process allows selectively both the reductive and oxidative arylation of alkenes.
2014
Nitric oxide (NO) derived from the endothelial NO synthase (eNOS) has antihypertensive, antithrombotic, anti-atherosclerotic and antiobesogenic properties. Resveratrol is a polyphenol phytoalexin with multiple cardiovascular and metabolic effects. Part of the beneficial effects of resveratrol are mediated by eNOS. Resveratrol stimulates NO production from eNOS by a number of mechanisms, including upregulation of eNOS expression, stimulation of eNOS enzymatic activity and reversal of eNOS uncoupling. In addition, by reducing oxidative stress, resveratrol prevents oxidative NO inactivation by superoxide thereby enhancing NO bioavailability. Molecular pathways underlying these effects of resve…
The role of mitochondria in sterigmatocystin-induced apoptosis on SH-SY5Y cells
2020
Mitochondria are cellular organelles involved in many crucial functions, such as generation of energy (ATP) and initiation of apoptosis. The aim of the present study was to evaluate the role of mitochondria in the toxicity induced by sterigmatocystin (STE), a mycotoxin produced by fungi of the genus Aspergillus, on SH-SY5Y cells. Our results showed that STE exposure decreased cell viability in a time- and concentration-dependent manner by MTT assay and caused mitochondrial dysfunction, as highlighted by the increase of STE cytotoxicity in cells forced to rely on mitochondrial oxidative phosphorylation. Furthermore, intracellular ATP depletion and increased mitochondrial reactive oxygen spec…
Redox modulation of Rubisco conformation and activity through its cysteine residues
2008
Treatment of purified Rubisco with agents that specifically oxidize cysteine-thiol groups causes catalytic inactivation and increased proteolytic sensitivity of the enzyme. It has been suggested that these redox properties may sustain a mechanism of regulating Rubisco activity and turnover during senescence or stress. Current research efforts are addressing the structural basis of the redox modulation of Rubisco and the identification of critical cysteines. Redox shifts result in Rubisco conformational changes as revealed by the alteration of its proteolytic fragmentation pattern upon oxidation. In particular, the augmented susceptibility of Rubisco to proteases is due to increased exposure…
Relationship Between Oxidative Stress, ER Stress, and Inflammation in Type 2 Diabetes: The Battle Continues
2019
Type 2 diabetes (T2D) is a metabolic disorder characterized by hyperglycemia and insulin resistance in which oxidative stress is thought to be a primary cause. Considering that mitochondria are the main source of ROS, we have set out to provide a general overview on how oxidative stress is generated and related to T2D. Enhanced generation of reactive oxygen species (ROS) and oxidative stress occurs in mitochondria as a consequence of an overload of glucose and oxidative phosphorylation. Endoplasmic reticulum (ER) stress plays an important role in oxidative stress, as it is also a source of ROS. The tight interconnection between both organelles through mitochondrial-associated membranes (MAM…
Retracted: Targeting Mitochondria as Therapeutic Strategy for Metabolic Disorders.
2019
Mitochondria are critical regulator of cell metabolism; thus, mitochondrial dysfunction is associated with many metabolic disorders. Defects in oxidative phosphorylation, ROS production, or mtDNA mutations are the main causes of mitochondrial dysfunction in many pathological conditions such as IR/diabetes, metabolic syndrome, cardiovascular diseases, and cancer. Thus, targeting mitochondria has been proposed as therapeutic approach for these conditions, leading to the development of small molecules to be tested in the clinical scenario. Here we discuss therapeutic interventions to treat mitochondrial dysfunction associated with two major metabolic disorders, metabolic syndrome, and cancer. …
Atherogenic dyslipidemia and oxidative stress: a new look
2009
Although results from in vitro studies and clinical trials demonstrate strong associations between oxidative stress and cardiovascular risk, to date still no convincing data are available to suggest that treatment with antioxidants might reduce vascular events. Oxidative modifications of low-density lipoproteins (LDL) represent an early stage of atherosclerosis, and small, dense LDL are more susceptible to oxidation than larger, more buoyant particles. Oxidized LDL are independent predictors of subclinical and clinical atherosclerosis. Recent studies suggested that novel therapeutic strategies may take into account the removal of such particles from circulation. Future research is required …
Glucose 6-P dehydrogenase delays the onset of frailty by protecting against muscle damage.
2021
Background: Frailty is a major age-associated syndrome leading to disability. Oxidative damage plays a significant role in the promotion of frailty. The cellular antioxidant system relies on reduced nicotinamide adenine dinucleotide phosphate (NADPH) that is highly dependent on glucose 6-P dehydrogenase (G6PD). The G6PD-overexpressing mouse (G6PD-Tg) is protected against metabolic stresses. Our aim was to examine whether this protection delays frailty. Methods: Old wild-type (WT) and G6PD-Tg mice were evaluated longitudinally in terms of frailty. Indirect calorimetry, transcriptomic profile, and different skeletal muscle quality markers and muscle regenerative capacity were also investigate…
Biochemical adaptations in middle-distance runners: an assessment of blood and anthropometric parameters
2014
In order to understand the mechanism underlying the physiological adaptation of purely aerobic workout, we investigated the effect of 2 months of training on nine males (17-22 year-old) middle distance running agonistic athletes. Blood sample was collected in the morning to analyze: hematological parameters, lipid profile, liver function enzymes [glutamate oxaloacetate transaminase, glutamate pyruvate transaminase, gamma-glutamyl transferase (γ-GT)] and skeletal and myocardial markers of muscle damage [creatin kinase (CK) and creatin kinase MB (CK-MB)]. Endurance training, as it implies high oxygen consumption, should increase reactive oxygen species, but it has been shown that exercise lea…