Antimony is a hard, brittle metal that has extensive uses in industry. Antimony-containing compounds are used in the manufacture of paints, ceramics, pyrotechnics, fire retardants and glass. The National Institute for Occupational Safety and Health estimates that more than 250,000 individuals in the United States are exposed to antimony compounds at work. Antimony-containing compounds produce cardiac functional alterations and toxicity in both experimental animals and humans. Previously, we reported that potassium antimonyl tartrate (PAT) induced oxidative stress and was directly toxic to cultured neonatal rat cardiac myocytes. Little is known, however, regarding the biochemical effects of nonlethal concentrations of PAT on cardiac myocytes. Numerous studies have reported the induction of stress or heat shock proteins in a wide variety of cellular systems following exposure to metals. Heat-shock proteins are a ubiquitous group of proteins that are synthesized in response to heat and other environmental stress and are thought to afford protection against cell toxicity. The stress protein heme oxygenase is especially susceptible to induction by metals. Drummond and Kappas demonstrated that PAT as well as other antimony-containing compounds were potent inducers of heme oxygenase in the liver and kidney of rats, but the effects of PAT on the heart were not examined. In the present study, sublethal concentrations of PAT were examined in neonatal rat cardiac myocytes for PAT-induced changes in cellular glutathione levels, heme oxygenase and stress protein expression. Our results indicate that an 18 hr exposure to low concentrations of PAT (5-25 uM) increases cellular glutathione levels, heat shock protein 70 and heme oxygenase activity in cardiac myocytes in a concentration-dependent manner.
The Toxicologist. Society of Toxicology 35th Annual Meeting, March 10-14,1996, Anaheim, California