The effects of aluminium (Al) on thyroid function were evaluated in adult Wistar 
rats intraperitoneally (i.p) injected with 7 mg Al (as lactate)/kg body weight 
(b.w) per day during a six week period. The time-course kinetics of Na(125)I (3 
μCi per 100 g b.w, i.p) was analysed by measuring gamma-radioactivity of 
thyroid, serum, serum protein precipitate and bile, at times ranging from 2 to 
96 h post-dosing. In Al-treated group the (125)I(-) thyroid uptake at 24 h 
(15,840 ± 570 vs. 18,030 ± 630 dpm/mg, P<0.05) as well as the rate of (125)I(-) 
release from the gland, calculated as the slope of the plot between 24 and 96 h 
(84 ± 8 vs. 129 ± 11 dpm/mg/h, P<0.05) were significantly reduced as compared to 
control. The biliary (125)I(-) excretion was not modified at all studied times. 
The Al content and lipid peroxidation (69.1 ± 8.5 vs. 53.2 ± 7.0 nmol MDA/g wet 
weight, P<0.05) of thyroid tissue were increased in Al-treated rats. The serum 
concentrations of total thyroxine (T4, 3.78 ± 0.14 vs. 4.68 ± 0.12 μg/dL, 
P<0.05) and total triiodothyronine (T3, 47 ± 4 vs. 66 ± 5 ng/dL, P<0.05) were 
decreased by effect of Al, but free-T4 (1.05 ± 0.05 vs. 1.04 ± 0.04 ng/dL, NS) 
and thyrotropin (TSH, 2.7 ± 0.4 vs. 2.6 ± 0.5 ng/ml, NS) remain unchanged. In 
spite of the Al could indirectly affect thyroid iodide uptake and hormones 
secretion by a mechanism involving the induction of an oxidative stress state, 
however, these changes could be managed by the hypothalamus-pituitary-thyroid 
endocrine axis. We can conclude that in adult rats the Al would not act as a 
thyroid disruptor.