Dietary restriction lowers endogenous levels of oxidative stress in different brain regions of adult mice.

Increase in the cellular burden of oxidative stress is critically involved in various pathological manifestations of aging, including age-related neurological disorders. Dietary restriction can lower reactive oxygen species formation, and thereby lower oxidative damage in the brain. The brain consists of a diverse group of neurons with varying functions. However, attenuating role of dietary restriction on oxidative stress in different regions of brain is not well known. In the present study we demonstrated that by restricting diet intake for a period of six months, mice lowered the endogenous levels of oxidative stress markedly by decreasing lipid peroxidation and protein carbonyl contents in cerebral cortex, hippocampus and striatum regions of the brain. Based on these results we suggest that dietary restriction can significantly reduce oxidative stress in various regions of the brain by virtue of lowering endogenous levels of reactive oxygen species, which might prove beneficial for preserving normal brain function with age.

Experimental excitotoxicity provokes oxidative damage in mice brain and attenuation by extract of Asparagus racemosus.

Excitotoxicity and oxidative stress are the major mechanisms of neuronal cell death in neurodegenerative disorders that occurs in both Alzheimer's and Parkinson's diseases. Reactive oxygen species (ROS) that are generated extracellularly and intracellularly by various mechanisms are among the major risk factors that initiate and promote neurodegeneration.Therefore, it is important to find the compound which retard or reverse the neuronal injury. We designed this study to investigate the potential of extract of Asparagus racemosus (AR) against kainic acid (KA)-induced hippocampal and striatal neuronal damage. The dose of AR extract given to experimental animals was based on the evaluation of its total antioxidant activity. Extract of AR displayed potent reductant of Fe(3+). The excitotoxic lesion in brain was produced by intra-hippocampal and intra-striatal injections of kainic acid (KA; 0.25 microg in a volume of 0.5 microl) to ketamine and xylazine (200 and 2 mg/kg b.w. respectively) anesthetized mice. The results showed impairment of hippocampus and striatal regions of brain after KA injection marked by an increase in lipid peroxidation and protein carbonyl content and decline in glutathione peroxidase (GPx) activity and reduced glutathione (GSH) content. The AR extract supplemented mice displayed an improvement in GPx activity and GSH content and reduction in membranal lipid peroxidation and protein carbonyl. We show that the minimizing effect of AR extract on oxidative damage in addition to the elevation of GPx activity and GSH content could eventually result in protective effect on the KA-induced excitotoxicity.

Superoxide anion radical generation as a temperature stress response in the gills of freshwater catfish Heteropneustes fossilis: role in mucus exudation under elevated temperature.

Temperature induced superoxide anion radical (O2-) generation in vivo has been demonstrated in the gills of Heteropneustes fossilis by electron spin resonance (ESR) spin trapping. Temperature exposures from 25 degrees C to 37 degrees C for various times (1-4 hr) caused generation of O2- in the gill. The acid mucopolysaccharide test was conducted in gill sections during elevated temperatures. The results showed an increased activity of mucopolysaccharide in gills which indicate an increased mucus secretion in gills during elevated temperatures. The detectable stable levels of O2- in the gill at 32 and 37 degrees C temperature exposures point towards a probable role for this radical in the exudation of mucus under elevated temperature.

Reactive oxygen species and oxidative DNA damage.

Reactive oxygen species (ROS) such as the superoxide anion radical (O2.-) hydrogen peroxide (H2O2) and hydroxyl radical (.OH) have been implicated in the pathophysiology of various states, including ischemia reperfusion injury, haemorrhagic shock, atherosclerosis, heart failure, acute hypertension and cancer. The free radicals, nitric oxide (NO) and O2.- react to form peroxynitrite (ONOO-), a potent cytotoxic oxidant. A potential mechanism of oxidative damage is the nitration of tyrosine residues of protein, peroxidation of lipids, degradation of DNA and oligonucleosomal fragments. Several mechanisms are responsible for the protection of the cells from potential cytotoxic damage caused by free radicals. Cells have developed various enzymatic and nonenzymatic defense systems to control excited oxygen species, however, a certain fraction escapes the cellular defense and may cause permanent or transient damage to nucleic acids within the cells, leading to such events as DNA strand breakage and disruption of Ca2+ metabolism. There is currently great interest in the possible role of ROS in causing DNA damage that leads to cancer and spontaneous mutations. A high rate of oxidative damage to mammalian DNA has been demonstrated by measuring oxidized DNA bases excreted in urine after DNA repair. The rate of oxidative DNA damage is directly related to the metabolic rate and inversely related to life span of the organism.