The effect of arsenic compounds depends on the chemical form and is specific for certain organs. The lack of specific biological indicators for the effects of each arsenic species makes it difficult to differentiate their toxicity. Five prospective biological indicators of system ic toxicity were examined at time points ranging from 15 m in to 24 h using male Sprague-Dawley rats, B6C3F1 mice, Golden-Syrian hamsters, and Hartley guinea pigs, following intraperitoneal dosing with 0.1 and 1 mg/kg sodium arsenite. Rats and mice were also dosed with 1 mg/kg sodium arsenate. Total blood arsenic levels were determined in all animal species to show that exposure occurred and as an index of the severity of the change is an indicator of toxicity. Total blood arsenic levels were increased in all animal species. This increase was dose, arsenic species, and animal dependent. Renal pyruvate dehydrogenase activity was significantly decreased at early time points in mice, hamsters, and guinea pigs, and at later time points in rats dosed with arsenite. Rats and mice dosed with arsenate also exhibited PDH decrease at early time points. Blood hematocrit and glucose were increased in the rat and guinea pig, respectively, after arsenite administration. Creatinine and urea nitrogen were found to be unresponsive to arsenic in most animal species. Data suggested that the mouse and secondly the hamster appear to be the most appropriate animal models for the study of acute arsenic toxicity. the acute toxicity of DMA is lower than that of the inorganic (Marafante et al., 1985). Each of these arsenic species has commercially and each has its own toxicity. Assigning toxic a particular species has been complicated by the finding that can, in some cases, metabolize one arsenic species to other et al., 1999). Environmental inorganic arsenic compounds metabolized, sometimes to other toxic intermediates (Cullen et Exposure to gallium arsenide (Webb et al., 1986) and exposure (Fowler & Weissberg, 1974) lead to pulmonary and blood toxicity, The arsenic species that induce toxicity in either case are not known. The development of biological indicators that differentiate As(III), As(V), and AsH3toxicity could make it possible to the mechanisms of toxicity of some arsenic compounds. An indicator of arsenic exposure would show significant upon very-low-dose exposure and would respond quantitatively manner to each different chemical species of arsenic.