Effect of Salmonella typhimurium enterotoxin (S-LT) on lipid peroxidation and cell viability levels of isolated rat enterocytes.

Reactive oxygen species (ROS) are potent mediators of inflammatory disorders and may be of pathophysiological importance in S. typhimurium induced tissue damage. This study was carried out to investigate if ROS play a role in mediating the enterocyte damage during in vitro exposure to Salmonella typhimurium enterotoxin (S-LT). The ROS generation was detected by measuring the changes in the enterocyte arachidonic acid (AA) metabolism (measured indirectly by estimating the level of enterocyte damage in the absence and presence of the cyclooxygenase inhibitor, indomethacin) and xanthine oxidase activity. The enterocyte damage was estimated by measuring the changes in the level of lipid peroxidation and cell viability. The results obtained showed that the exposure of isolated rat enterocytes to S-LT resulted in an increased XO activity; an increased arachidonic acid metabolism, dose and time dependent increase in the level of lipid peroxidation and decreased cell viability. Lipid peroxidation decreased and cell viability increased in the presence of the antioxidant enzymes superoxide dismutase (SOD) or catalase. Thus the in vitro exposure of the enterocytes to S-LT is accompanied by an increased generation of ROS which may induce the lipid peroxidation of the enterocyte membrane thereby leading to a loss of cell viability.