The long-term effects of the herbicide atrazine on the dopaminergic system following exposure during pubertal development

Atrazine (2-chloro-4-ethylamino-6-isopropylamino-s-triazine) is used worldwide as a herbicide, and its presence in the environment has resulted in documented human exposure. Atrazine has been shown to cause dopaminergic neurotoxicity. The juvenile period is particularly vulnerable to environmental agents, but only few studies have investigated the long-term effects of atrazine following exposure during the pubertal development. Therefore, we evaluated the effects of a 41-day exposure to atrazine on the dopaminergic system in rats. Sprague-Dawley rats were treated orally with atrazine at 25 or 50 mg/kg bw, daily from postnatal day 22 to 62. The content of dopamine (DA) was examined in striatum samples by HPLC-FL, and the mRNA and protein expression of tyrosine hydroxylase (TH), orphan nuclear hormone (Nurr1), dopamine transporter (DAT) and vesicular monoaminetransporter 2 (VMAT2) were examined in samples of the ventral mid-brain by use of fluorescence PCR and Western-blot analysis when the rats reached the age of one year. Exposure of juvenile rats to the high dose of atrazine led to reduced levels of DA and mRNA of Nurr1 in one-year-old animals. This study shows that the long-term adverse effects of atrazine on the dopaminergic system have a special relevance after juvenile exposure.