Promising anti-oxidative therapeutic potentials of edible freshwater snail Bellamya bengalensis extract against arsenic-induced rat hepatic tissue and DNA damage

Epidemiological data suggest that arsenic ultimately results in cancer in different parts of the body. Several synthetic therapeutic agents manifest inadequate potency with severe side effects against arsenic toxicity. The flesh of B. bengalensis, has long been used as an ethno-medicine in case of arthritis, blood-impurities, impaired immune system, conjunctivitis and liver anomalies. This potent organism might be a natural choice against arsenic and several other toxicities. Our earlier studies on arsenic-exposed human can correlate carcinogenesis with DNA-damage. In an attempt to investigate the possible protective and therapeutic effect against arsenic induced hepatotoxicity, the extract of B. bengalensis was tested in arsenic intoxicated rat model. The time- and dose-dependent effect of arsenic toxicity was also tested in B. bengalensis. Sodium-meta-arsenite NaAsO2 (0.6 ppm/100g bw/day for 28 days, as earlier reported) was treated alone or in combination with the B. bengalensis water extract (BBE, 100 mg/100g bw) to rat and compared with vehicle treated control. In a separate experiment, the B. bengalensis was exposed to high concentration of NaAsO2 contaminated water (5 to 20 ppm for 1 to 9 days) in laboratory condition and their DNA quality was evaluated in relation to its possible oxidative threat. Any concentration of arsenic was incapable to initiate a significant DNA damage in B. bengalensis. Lipid peroxidation was increased in arsenic exposed B. bengalensis after longer duration of its exposure. Increase in reduced antioxidant like non-protein-soluble thiol (NPSH) is concordant with the decrease in lipid peroxidation and DNA stability in this organism. In rat experiment, the BBE supplementation strongly prevented arsenic-induced oxidative, necrotic and apoptotic damages to liver tissue/DNA by strengthening antioxidant systems, which has been shown in hepatic DNA-fragmentation, comet-assay, histo-architecture (hematoxylin/eosin), alkaline-phosphatase, serum-glutamate-pyruvate-transaminase and lactate-dehydrogenase (tissue-degeneration-marker) results. Only arsenic exposure decreased hepatic superoxide-dismutase (SOD) in-vivo and in-vitro (H2O2/arsenite redox-stress to dialyzed and concentrated, 6-8kd cutoff-Millipore liver cytosolic SOD), catalase, xanthine-oxidase, lactoperoxidase activities and the level of NPSH with a concomitant increase in malondialdehyde resulting in mutagenic DNA-breakage and apoptotic liver damage which has been decisively restrained in B. bengalensis extract. The present investigation offers strong evidence on the hepato-protective and medicinal efficiencies of BBE against oxidative stress induced by arsenic.