Sodium Arsenite-Induced Alteration in Hepatocyte Function of Rat with Special Emphasis on Superoxide Dismutase Expression Pathway and its Prevention by Mushroom Lectin

Abstract

This study was accomplished to exemplify the possible protective role of ascorbic acid and mushroom lectin against arsenic-induced cytotoxicity and impairment of superoxide dismutase (SOD) production pathway in hepatocytes of rat. Hepatocytes were isolated from rat and treated with sodium arsenite (AS), arsenic plus ascorbic acid (AS + AA) and arsenic plus mushroom lectin (AS + ML). A placebo control was also included. Arsenic treatment resulted in the depletion of cell proliferation, phagocytic activity (nitro blue tetrazolium index) and superoxide dismutase (SOD) activity, relative mRNA expression of superoxide dismutase 2 (SOD 2 ) and enhanced production of nitric oxide (NO). Ascorbic acid, a standard antioxidant, could normalize cellular perturbation and SOD production pathway relating to gene expression, whereas partially purified Pleurotus florida lectin (PFL), an edible mushroom containing protein complex, maintained cellular activity and prevented stress by normalizing phagocytic (NBT index) and SOD activities vis-à-vis relative gene expression. It could further defend NO production of hepatocytes. Mushroom lectin strongly prevented sodium arsenite-induced damage of SOD production pathway in hepatocytes, and its effect was also comparable to a standard antioxidant, i.e. ascorbic acid.

Ameliorative effect of water spinach, Ipomea aquatica (Convolvulaceae), against experimentally induced arsenic toxicity

“…super oxide radical, hydrogen peroxide and hydroxyl radical, is proposed to be the principle mechanism in As-intoxication [28]. ROS is not only responsible to induce peroxidative alteration of cellular lipids, carbonylation of proteins, fragmentation of DNA, reduction of cellular antioxidant molecules in the biological systems, but also affect the cell proliferation index by altering the signal transduction, cell cycle control, cellular differentiation and apoptosis [32]. The present study describes the protective role of AEIA against As toxicity employing suitable in vitro and in vivo preclinical assays.…”

Arsenic and nicotine co-exposure lead to some synergistic effects on oxidative stress and apoptotic markers in young rat blood, liver, kidneys and brain

“…Exposure to a low dose and for a shorter duration exhibits antioxidant properties [41] while, prolonged exposure to a higher dose generates free radicals resulting in oxidative stress and reduction in antioxidant enzymes [15] . Interestingly, not only these compounds generated free radicals during their metabolism but also altered the gene expression levels of anti-oxidant enzymes [52] , [1] , [3] , [69] …”

Effects of 4-nonylphenol on oxidant/antioxidant balance system inducing hepatic steatosis in male rat

“…SOD presents in three isoforms, copper-zinc-containing superoxide dismutase (Cu–Zn–SOD, SOD1), manganese containing superoxide dismutase (Mn–Zn–SOD, SOD2) and extracellular superoxide dismutase (Cu–Zn–SOD, SOD3). The SOD1 isoenzyme is the most abundant one in the cytoplasm [5] . Reduction of SOD1 activity in 4-NP-treated group in this study might be due to the enhanced production of superoxide radical anions.…”