Search results for "Active oxygen"

Diabetic Retinopathy and Oxidative Stress

2014

Abstract Diabetic retinopathy (DR) is the leading cause of acquired blindness in working age adults worldwide. Biochemical changes in DR contribute to both the microscopic structural and functional changes in the retina. All these alterations result in macroscopic retinal damage that can be assessed by funduscopy. The overproduction of reactive oxygen species (ROS) in the mitochondria is considered a causal link between elevated glucose and biochemical abnormalities in the pathophysiology of DR. Moreover, oxidatively induced pathways also seem to provide positive feedback to ROS production, resulting in a vicious cycle. ROS can directly damage lipids, proteins and DNA, leading to cell death…

G6PD Overexpression Protects Mice Against Associated Oxidative Stress and Delays the Occurrence of Frailty

2016

To assess the impact of lifelong overexpression of G6PD on reactive oxygen species (ROS)-derived damage and the prevention of frailty, we measured the levels of macromolecular oxidative damage in young and old mice and the we tested the neuromuscular fitness and the grip strength in old mice. Old G6PD-Tg male and female mice showed diminished accumulation of DNA oxidation (measured as 8-hydroxyguanosine or 8-OHdG) in liver and brain. Old females also showed reduced lipid oxidation (measured as malondialdehyde or MDA) in the liver. Old G6PD-Tg males, but not females, presented a small but significant increase in brain protein carbonylation. In accordance with these findings, liver from 2-yea…

Implication of eNOS Uncoupling in Cardiovascular Disease

2017

Under physiological conditions, nitric oxide (NO) is produced in the vasculature mainly by the endothelial nitric oxide synthase (eNOS). Endothelial NO relaxes blood vessels, inhibits platelet activity, and protects against atherosclerosis. Under pathological conditions such as hypertension, diabetes, and hypercholesterolemia, eNOS may become uncoupled. Uncoupled eNOS generates superoxide at the expense of NO and contributes substantially to oxidative stress and endothelial dysfunction. Major mechanisms of eNOS uncoupling include deficiency of the eNOS cofactor tetrahydrobiopterin, deficiency of the eNOS substrate L-arginine, and eNOS S-glutathionylation. Reversal of eNOS uncoupling may rep…

Hemorrhagic Shock and Antioxidants: Influence of Timing on Survival

2001

Evidence of oxidative stress in very long chain fatty acid--treated oligodendrocytes and potentialization of ROS production using RNA interference-di…

2011

X-linked adrenoleukodystrophy (X-ALD) and pseudo neonatal adrenoleukodystrophy (P-NALD) are neurodegenerative demyelinating diseases resulting from the functional loss of the peroxisomal ATP-binding cassette transporter D (ABCD1) and from single peroxisomal enzyme deficiency (Acyl-CoA oxidase1: ACOX1), respectively. As these proteins are involved in the catabolism of very long chain fatty acids (VLCFA: C24:0, C26:0), X-ALD and P-NALD patients are characterized by the accumulation of VLCFA in plasma and tissues. Since peroxisomes are involved in the metabolism of reactive oxygen species (ROS) and nitrogen species (RNS), we examined the impact of VLCFA on the oxidative status of 158N murine o…

Increased susceptibility of microcytic red blood cells to in vitro oxidative stress.

1995

Oxidative damage to erythrocytes in thalassaemia has been related to generation of free radicals by an excess of denaturated alpha- or beta-globin chains, intracellular iron overload and low concentration of normal haemoglobin (HGB). Two good indicators of such oxidative damage are the high red blood cell (RBC) malonyldialdehyde (MDA) production detected following exogenous oxidant stress and the decrease of pyrimidine 5'-nucleotidase (P5N), the most sensitive enzyme to SH-group damage in vivo. Conflicting data, however, have so far accumulated in the literature concerning differences in oxidative damage between the different forms of thalassaemia and iron deficiency anaemia (IDA). In the p…

Prevention of 7-Ketocholesterol-Induced Overproduction of Reactive Oxygen Species, Mitochondrial Dysfunction and Cell Death with Major Nutrients (Pol…

2020

The brain, which is a cholesterol-rich organ, can be subject to oxidative stress in a variety of pathophysiological conditions, age-related diseases and some rare pathologies. This can lead to the formation of 7-ketocholesterol (7KC), a toxic derivative of cholesterol mainly produced by auto-oxidation. So, preventing the neuronal toxicity of 7KC is an important issue to avoid brain damage. As there are numerous data in favor of the prevention of neurodegeneration by the Mediterranean diet, this study aimed to evaluate the potential of a series of polyphenols (resveratrol, RSV

Sterigmatocystin-induced cytotoxicity via oxidative stress induction in human neuroblastoma cells.

2020

Abstract Sterigmatocystin (STE) is a mycotoxin produced by fungi of the genus Aspergillus. Considering that the effect of STE on neuronal system has not been well studied, the aim of the present study consists to investigate the cytotoxic effects of STE in human neuroblastoma (SH-SY5Y) cells. Moreover, the role of oxidative stress and intracellular defense systems was assessed by evaluating reactive oxygen species (ROS) generation, lipid peroxidation (LPO) and antioxidant no-enzymatic (GSH) levels and enzymatic (GPx, GST, CAT and SOD) activity. Our results revealed that STE decreased cell viability in a dose and time-dependent manner. Furthermore, after 24 h of exposure, STE induced an incr…

Development of an in vitro neuroblastoma 3D model and its application for sterigmatocystin-induced cytotoxicity testing

2021

Abstract Given the increasing importance of establishing better risk assessments for mycotoxins, novel in vitro tools for the evaluation of their toxicity are mandatory. In this study, an in vitro 3D spheroid model from SH-SY5Y cells, a human neuroblastoma cell line, was developed, optimized and characterized to test the cytotoxic effects caused by the mycotoxin sterigmatocystin (STE). STE induced a concentration- and time-dependent cell viability decrease in spheroids. Spheroids displayed cell disaggregation after STE exposure, increasing in a dose-dependent manner and over time. STE also induced apoptosis as confirmed by immunofluorescence staining and Western blot. Following the decrease…

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…