Atrazine triggers hepatic oxidative stress and apoptosis in quails (Coturnix C. coturnix) via blocking Nrf2-mediated defense response

- ATZ exposure presented hepatotoxicity in quails.
- ATZ induced apoptosis by oxidative stress and mitochondrial dysfunction.
- Below 250 mg/kg ATZ exposure activated the Nrf2 signaling pathway to protect liver.
- Over 500 mg/kg ATZ exposure blocked the Nrf2-mediated defense response.

The bioaccumulation and environmental persistence of atrazine (ATZ) poses a severe hazard to animal ecosystem. Quail has strong sensitivity to environmental pollutant, thus it is one of the most important ecological pollution indicator. However, true proof for the effects of ATZ exposure on the liver of quails is lacking. To evaluate the liver injury and the role of Nrf2-mediated defense responses during ATZ exposure, male quails were treated with ATZ (0, 50, 250 and 500 mg/kg) by oral gavage for 45 days. Histopathological and ultrastructural changes, oxidative stress indices, apoptosis-related factors and Nrf2 pathway were detected. ATZ caused irreparable mitochondrial damage and destroyed morphophysiological integrity of the quail liver. Lower level ATZ (<250 mg/kg) activated Nrf2 signaling pathway to protect liver against oxidative stress and apoptosis via enhancing antioxidative activity. Higher level ATZ (>500 mg/kg) induced oxidative stress and apoptosis through decrease of non-enzymatic antioxidant, antioxidant enzymes and anti-apoptosis factors and increase of apoptosis factors expressions. Taken together, our results suggested that ATZ-induced hepatotoxicity in quails was associated with blocking Nrf2-mediated defense response.

295