Oral administration of KBrO3 induced DNA degradation in intestinal tissue of treated animals. This was seen in the comet assay which showed increased level of DNA single strand breaks and alkali labile sites in the mucosal cells of the intestine. DNA-protein cross-links which impede the activities of proteins involved in DNA replication, transcription and repair, were also significantly enhanced in KBrO3 treated rats. The pre-treatment of PCI-32765 animals with taurine reduced the level of KBrO3-induced DNA damage and DPC formation probably by its anti-mutagenic action as has been reported earlier in other systems. Histological observations of the duodenum strongly support the biochemical results. The intestine from KBrO3 treated animals showed extensive intestinal damage. The lumen was full of debris, inflammatory cells and intestinal villi had lost their contour and prominence of mucus secreting cells was observed, both in the remnant of villi as well as in the intestinal crypts. These changes were greatly reduced by prior administration of taurine, probably by neutralising the excessive formation of ROS and thereby reducing the morphological and cellular damage. The protection offered by taurine against KBrO3-induced gastrointestinal toxicity as seen here is probably due to the diminution in KBrO3-induced OS due to its AO property. Unlike polyphenolic antioxidants, taurine itself does not directly quench classical ROS and free radicals like H2O2, superoxide anion and hydroxyl radical but its metabolic precursor, hypotaurine, has been shown as an efficient radical scavenger. Taurine is widely believed to act as an AO for which several reasons have been proposed. First, taurine regulates the levels of various endogenous AO. It enhances the synthesis of GSH and also stimulates the activity of G6PD, an enzyme that generates NADPH which is required by glutathione reductase to convert oxidised glutathione into GSH. Second, taurine protects cells from injury and subsequent necrosis by preventing Ca2+ overload via Na2+/Ca2+ exchanger. Third, taurine conjugates with MDA, the end product of LPO, thereby stabilising the lipid bilayer and making the membranes lipids less vulnerable to ROS induced toxic insult. Fourth, due to its strongly negatively charged sulfonic group, taurine can conjugate redox active CP-690550 metals like Fe2+ and Cu2+, reducing their reaction with H2O2, a process which generates the damaging hydroxyl radical. Fifth, taurine has been shown to prevent the diversion of electrons from respiratory chain to other acceptors such as oxygen, thereby inhibiting the accumulation of ROS like superoxide anion. Finally, taurine can act as an organic osmolite by increasing tissue osmolarity and conferring more flexibility to the cell membrane. Either one or more of these mechanisms may be involved in protecting the intestine from toxicity induced by KBrO3. In summary, our results show that OS induced by KBrO3 contributes to the development of intestinal toxicity.