Search results for " STRESS"
showing 10 items of 3936 documents
Mitochondrial oxidative stress and CD95 ligand: A dual mechanism for hepatocyte apoptosis in chronic alcoholism
2002
Apoptosis plays an important role in the progression of alcohol-induced liver disease to cirrhosis. Oxidative stress is an early event in the development of apoptosis. The major aim of this study was to study the conditions in which oxidative stress occurs in chronic alcoholism and its relationship with apoptosis of hepatocytes. We have found that oxidative stress is associated with chronic ethanol consumption in humans and in rats, in the former independently of the existence of alcohol-induced liver disease. Ethanol or acetaldehyde induces apoptosis in hepatocytes isolated from alcoholic rats, but not in those from control rats. Inhibition of aldehyde dehydrogenase, but not of cytochrome …
The Relationship between Alcohol–induced Apoptosis and Oxidative Stress in the Liver
2005
This chapter discusses the relationship of apoptosis and oxidative stress induced by alcohol in the liver. Oxidative stress is involved in the pathogenesis and progression of alcohol-induced liver disease. Chronic alcoholism always causes oxidative stress independently of the presence of liver disease. Two key mechanisms are responsible for it: (1) the mitochondrial respiratory chain and (2) cytochrome P450 2El activity. Increased production of reactive oxygen species at complexes I and III together with NADH overproduction would be the major cause for mitochondrial oxidative stress in chronic alcoholism. Reactive Oxygen Species (ROS) cause oxidative damage, which may lead to cell death by …
Oxidative stress in diabetic retinopathy
2020
Diabetic retinopathy (DR) is the leading cause of acquired blindness in working adults worldwide. Biochemical changes in DR contribute to both the microscopic structural and functional changes in the retina. All these alterations result in retinal damage that can be assessed by funduscopy, optical coherence tomography (OCT), and angioOCT. Reactive oxygen species (ROS) overproduction in the mitochondria is considered a causal link between elevated glucose and biochemical abnormalities in the pathophysiology of DR. Moreover, oxidative-induced pathways also seem to provide positive feedback to ROS production, resulting in a vicious cycle. ROS can directly damage lipids, proteins, and DNA, lead…
2021
Cardiovascular diseases (CVDs) rank the leading cause of morbidity and mortality globally. Obesity and its related metabolic syndrome are well-established risk factors for CVDs. Therefore, understanding the pathophysiological role of adipose tissues is of great importance in maintaining cardiovascular health. Oxidative stress, characterized by excessive formation of reactive oxygen species, is a common cellular stress shared by obesity and CVDs. While plenty of literatures have illustrated the vascular oxidative stress, very few have discussed the impact of oxidative stress in adipose tissues. Adipose tissues can communicate with vascular systems, in an endocrine and paracrine manner, throu…
Oxidative stress in osteoarticular diseases
2016
Epigenetics, oxidative states and diabetes
2020
Abstract Although controlling a wide range of physiological cell functions, redox states unbalance during inflammation toward oxidative stress. Specific regions of our genome are extremely sensitive to both oxygen and reactive oxygen species, therefore modulating gene transcription in response to this specific epigenetic effect. Additional epigenetic mechanisms may include the alteration of the methylation states of DNA, protein and lipid nitration or modulation of specific microRNAs. A crucial role in finely tuning redox states is also played by mitochondria, where oxidative phosphorylation is epigenetically controlled. Diabetes, the most considerable “epigenetic” clinical disorder, exacer…
Electrochemical sensor for evaluating oxidative stress in airway epithelial cells
2021
Cigarette smoke exposure induces oxidative stress within the airways. Increased oxidative burden contributes to the pathogenesis of chronic lung disorders and is associated with aging and chronic inflammation. Airway epithelial cells highly contribute to Reactive Oxygen Species (ROS) generation within injured and inflamed lung tissues. Among ROS, hydrogen peroxide (H2O2) can be monitored in the extracellular space. Herein, we present an amperometric/voltammetric sensor based on gold nanoparticles and graphene oxide able to detect H2O2 with good sensitivity and selectivity. Using this sensor, H2O2 release was measured in conditioned medium from primary bronchial epithelial cells (PBEC), bron…
Oxidative Stress and DNA Damage in Obesity-Related Tumorigenesis
2014
Reactive oxygen species induce oxidative modification of critical macromolecules. Oxygen derived free radicals may act as potential cytotoxic intermediates inducing inflammatory and degenerative processes, or as signal messengers for the regulation of gene expression. This dual effect mainly depends on the availability of free radicals in terms of concentration, as well as on the environmental characteristics in which they are produced. The formation of free radicals has been proposed to be the linking factor between certain metabolic disturbances and cancer. Circulating mononuclear cells of patients with high cholesterol levels, insulin resistance, metabolic syndrome or obesity present low…
Long term p38-a deficiency up-regulates antioxidant enzymes through compensatory NF-?B activation
2015
p38a MAPK may function as a mediator of reactive oxygen species signaling and thus p38a is considered a sensor of oxidative stress. In liver-specific p38a knock-out (KO) adult mice we previously found glutathione depletion and down-regulation of antioxidant enzymes. Our aim was to assess the influence of long-term p38a deficiency on oxidative stress and on the regulation of antioxidant enzymes in liver of old mice. To this end, wild type or liver-specific KO mice after weaning, at 4-6 months of age, or at 24 months of age were used. Reduced glutathione (GSH) and oxidized glutathione levels were determined by mass spectrometry, gene expression of antioxidant enzymes was determined by RT-PCR,…
Uncoupling of Endothelial Nitric Oxide Synthase in Cardiovascular Disease and its Pharmacological Reversal
2010
Publisher Summary This chapter discusses the role of oxidative stress in vascular dysfunction and atherogenesis, and strategies for its prevention. Endothelial dysfunction and oxidative stress have been identified as a common denominator of many cardiovascular risk factors. They support pro-inflammatory, prothrombotic, proliferative, and vasoconstrictor mechanisms that are involved in the initiation, progression, and complications of atherosclerosis. The pathophysiologic causes of oxidative stress involve changes in a number of different enzyme systems. Increased production of ROS by uncoupled eNOS is likely to contribute significantly to vascular oxidative stress and endothelial dysfunctio…