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Abstract
Occupational exposure to thallium (Tl+) 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 Tl in rat brain regions
after a subchronic administration (30 days) of sublethal doses of Tl (I) acetate:
0.8 mg/kg (1/40 of LD(50)), 1.6 mg/kg (1/20 of LD(50)), we measured the concentrations
of Tl by atomic absorption spectrophotometry. A possible role of oxidative injury
in the pattern of toxicity exerted by Tl 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 Tl 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 Tl 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 Tl, whereas all regions from rats treated with 1.6 mg/kg Tl 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 Tl, which are associated with regional susceptibility of the brain
to this metal.