Subchronic administration of sublethal doses of thallium to rats: effects on distribution and lipid peroxidation in brain regions

Occupational exposure to thallium (T1+) is known to be responsible for severe neurological manifestations in humans, including ataxia and paralysis; however, little is known yet about the precise mechanism of toxicity elicited by this heavy metal at sublethal doses and its brain distribution after chronic or subchronic exposures resulting from environmental contamination. In order to evaluate the levels of T1 in rat brain regions after a subchronic administration (30 days) of sublethal doses of T1 (I) acetate: 0.8 mg/kg (1/40 of LD50), 1.6 mg/kg (1/20 of LD50), we measured the concentrations of T1 by atomic absorption spectrophotometry. A possible role of oxidative injury in the pattern of toxicity exerted by T1 in the same brain regions, was also studied. Lipid peroxidation (LP) as a current marker of oxidative stress, was estimated by the generation of lipid fluorescent products. Higher concentrations of T1 were observed in brain tissue from adult rats treated with 1.6 mg/kg, as compared to those treated with 0.8 mg/kg. However, no differential distribution of T1 among regions was observed after administration of 0.8 mg/kg dose to rats, nor after 1.6 mg/kg dose. We also found significant changes in LP both in corpus striatum and cerebellum from rats treated daily with 0.8 mg/kg T1, whereas all regions from rats treated with 1.6 mg/kg T1 exhibited enhanced LP as compared to control. These findings suggest an active role of free radicals and oxidative events involved in the pattern of toxicity after exposure to sublethal doses of T1, which are associated with regional susceptibility of the brain to this metal. (C) 2000 Elsevier Science Ireland Ltd. All rights reserved.