CENTRAL AND PERIPHERAL ALTERATION OF THE CHOLINERGIC ENZYMES ACTIVITIES OF THE RAT IN RESPONSE TO REPEATED AND ACUTE THALLIUM EXPOSURE

Abstract

Many of the reported symptoms of thallium toxicity are effects known to be mediated by the autonomic nervous system through the cholinergic pathway. The present study examines the effect of acute and repeated exposure to thallium on the activity of the cholinergic enzym es, acetyl cholinesterase (AChE) and choline acetyltransferase (ChAT), in various brain regions, segments of the gastrointestinal (GI) tract, and regions of the urinary bladder. Adult male Sprague-Dawley rats were injected (ip) with either saline, 0.1, 1.0, or 5.0 mg/kg of thallium acetate, daily for 5 days (for the repeated study) or a single dose of 25 mg/kg (for the acute study). The activity of the cholinergic enzymes was measured at either 24 or 48 h after the last dose. The highest dose of thallium (5 mg/kg) was fatal at 48 h after the last injection (6 rats out of 8 died). At lower doses, repeated thallium exposure caused a decrease in AChE activity in som e brain regions (nucleus accum bens and hypothalamus) and urinary bladder regions and an increase in AChE activity in the striatum and m idbrain regions. The effect of a single dose of 25 mg/kg was m ore pronounced, resulting in a significant decrease in AChE activity in the hypothalamus, nucleus accumbens, and the duodenal segment of the GI tract as well as in the two regions of the urinary bladder. Thallium exposure, especially in the high single dose, resulted in a significant increase in ChAT activity 24 h after injection in the nucleus accumbens, brain stem, ileum and duodenum segments of the GI tract, and both regions of the urinary bladder. Thus, the altered activities of the cholinergic enzymes reported here in response to thallium exposure may support a role for the cholinergic system in som e pathological conditions associated with thallium toxicity.