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The widely used atrazine has been reported to exhibit extensive ecological hazards. Due to the biological accumulation, atrazine elicits widespread toxic effects on different organisms. However, true proof for the mechanism of atrazine-induced toxicity is lacking. To determine the potential mechanism by which atrazine exerted toxic effects, quails were treated with atrazine (0, 50, 250 and 500 mg/kg) by gavage administration for 45 days. Atrazine significantly increased the histological alterations and serum creatine kinase, lactate dehydrogenase and choline esterase levels. A marked disorder in ionic (Na+, K+, Ca2+ and Mg2+)contents and the decrease of ATPases (Na+-K+-ATPase, Ca2+-ATPase, Mg2+-ATPase and Ca2+-Mg2+-ATPase) activities were observed in the heart and liver of atrazine-exposed quails. Of note, it was also observed that atrazine suppressed the transcription of Na+, K+ transfer associated genes (Na+-K+-ATPase subunits) and Ca2+ transfer associated genes (Ca2+-ATPase subunits, solute carriers) in heart and liver. In conclusion, atrazine induced cardiac and hepatic damage via causing the ionic disorder, triggering the transcription of the ion transporters and leading the histopathological and functional alternations in the heart and liver of quails. This study demonstrated atrazine significantly induced the ionic disorder via decreasing the ATPases activities and disturbing the transcription of the ion transporters.

A novel mechanism underlies atrazine toxicity in quails (Coturnix Coturnix coturnix): triggering ionic disorder via disruption of ATPases