Journal of Basic and Clinical Physiology and Pharmacology · 2006 · 29 citations · 12 references
Life SciencesPharmacologyToxicologyClinical BiochemistryAntioxidant DefenseLipid PeroxidationNeuroprotectionOxidative Stress PhysiologyPulmonary ToxicologyReactive Oxygen SpeciesAntioxidant Defense MechanismsAntioxidant Defense SystemsAscorbic Acid PhysiologyAscorbic Acid TreatmentCellular Antioxidant DefenseNickel Pulmonary ToxicityPlasma Ascorbic Acid LevelsPulmonary Oxidative Stress
We studied the effect of oral supplementation with L-ascorbic acid (50 mg /100 g body weight (BW) on nickel sulfate (2.0 mg/ 100 g BW, i.p)-induced lipid peroxidation and histopathology in the lung of Wister strain male albino rats. Lipid peroxide and glutathione levels and the activities of the antioxidant enzymes, superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px), were estimated. Nickel sulfate administration significantly increased the level of lipid peroxides and decreased all antioxidant enzyme activities. Nickel sulfate treatment also induced (a) loss of normal characteristics and architectural organization, (b) inflammation in bronchioles, (c) alveolar congestion, (d) alveolar cell hyperplasia, and (e) congestion in the lumen. The simultaneous administration of L-ascorbic acid and nickel sulfate improved both lipid peroxidation and the histopathology of lung when compared with rats receiving nickel sulfate alone. The results indicate that L-ascorbic acid prevents nickel-induced alteration of antioxidant defense mechanisms and histopathology of lung tissue.
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Konstantin Salnikow, Steven P. Donald, Richard K. Bruick et al. · Journal of Biological Chemistry · 2004 · 321 citations · Full text