Taurine provides antioxidant defense against NaF-induced cytotoxicity in murine hepatocytes.

Abstract

Fluoride is an environmental and industrial pollutant that affects various organs in humans and animals. The present study was conducted to investigate the protective role of taurine (2-aminoethane sulphonic acid) against fluoride-induced cytotoxicity in murine hepatocytes. Sodium fluoride (NaF) was used as the source of fluoride for this particular study. Dose-dependent studies suggest that incubation of hepatocytes with NaF (100mM) for 1h significantly decreased the cell viability as well as intracellular antioxidant power. Increased activities of alanine transaminase (ALT) and alkaline phosphatase (ALP) due to the same dose of toxin exposure confirmed membrane damage. Toxin-induced increased level of intracellular reactive oxygen species (ROS) was confirmed by intracellular ROS production assay using a fluorescent probe 2',7'-dichlorofluorescein diacetate (DCF-DA). In addition, the activities of the antioxidant enzymes like superoxide dismutase (SOD), catalase (CAT) and glutathione-S-transferase (GST) were also decreased by toxin treatment at the previous dose. The same treatment also reduced the level of glutathione (GSH) and total thiols, elevated the level of oxidized glutathione (GSSG) and increased the level of lipid peroxidation end products, protein carbonyl content and extent of DNA fragmentation. Incubation of hepatocytes with taurine, both prior to and in combination with NaF, altered all the NaF-induced parameters. A known antioxidant, vitamin C was taken to compare the cytoprotective activity of taurine against fluoride poisoning. Combining all, the results suggest that taurine protects mouse hepatocytes against fluoride-induced cytotoxity.

• Authors: Joydeep Das, Jyotirmoy Ghosh, Prasenjit Manna, Parames C Sil
• Journal: Pathophysiology : the official journal of the International Society for Pathophysiology (Pathophysiology) Vol. 15 Issue 3 Pg. 181-90 (Oct 2008) ISSN: 0928-4680 [Print] Switzerland
• PMID: 18676123 (Publication Type: Journal Article)