Search

Numerous studies have found that high Selenium (Se) influences the pancreas in animals. Considerable studies suggest that Se status plays an important role in the pancreatic function and regulation of blood glucose in chicks. However, true proof for the effects of the supranutritional Se status on the chicken pancreas through modulating the selenotranscriptome is lacking. 1 day-old chicks were fed a basal diet and Se (0.15 mg, 3.0 mg, or 5.0 mg Se per kg of diet) for 8 weeks. The blood glucose level, tissue Se content, redox homeostasis and mRNA level of the selenoproteome in the pancreas were measured. The supranutritional Se status (3.0 mg kg−1) decreased the blood glucose level and increased the pancreatic antioxidant capacity. The excess Se status (5.0 mg kg−1) increased the blood glucose and Se content and decreased the pancreatic antioxidant capacity. The dietary Se status affected the mRNA levels of 24 selenoproteins and the selenoprotein synthesis related transcription factors in the pancreas. The dietary Se level could modulate the growth performance via affecting the blood glucose level and pancreatic function. Se contributions to chicken growth and the regulation of blood glucose are associated with pancreatic redox homeostasis via a modulated selenotranscriptome in chickens.

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 500mg/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 (250mg/kg) activated Nrf2 signaling pathway to protect liver against oxidative stress and apoptosis via enhancing antioxidative activity. Higher level ATZ (500mg/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.

The aim of this study was to evaluate the possible chemoprotective role of lycopene (LYC) against atrazine (ATR)-induced ionic disorder and hepatotoxicity in mice. Male kunming mice were treated with LYC (5mg/kg) and/or ATR (50mg/kg or 200mg/kg) by lavage administration for 21days. Ionic disorder was assessed by determining the Na(+), K(+) and Ca(2+) content and the alteration in ATP enzymes (ATPases) including Na(+)-K(+)-ATPase, Ca(2+)-ATPase, Mg(2+)-ATPase and Ca(2+)-Mg(2+)-ATPase and the mRNA levels of ATPase's subunits in liver. ATR caused the increases of alanine aminotransferase and aspartate aminotransferase activities and histological changes. LYC pretreatment significantly protected liver against ATR-caused alternation. The significant effect of ATR and LYC on the K(+) and Mg(2+) content in liver was not observed, but ATR increased hepatic Na(+)-K(+)-ATPase activity and decreased Mg(2+)-ATPase and Ca(2+)-Mg(2+)-ATPase activity. The mRNA expressions of Na(+)-K(+)-ATPase subunits were regulated significantly by ATR. A significant increase of Ca(2+) content and seven down-regulated mRNA expressions of Ca(2+)-ATPase subunits and a decrease of Ca(2+)-ATPase activity were observed in the ATR-treated mice. Notably, LYC modulated these ATR-induced alterations of ATPase activity and mRNA expression of their subunits. These results suggest that ATR presents hepatotoxicity via regulating hepatic ATPase's activities and their subunit transcriptions and inducing ionic disorder. LYC protects liver against ATR-induced hepatotoxicity, significantly. LYC modulated hepatic ionic homeostasis disturbance via regulation of ATPase activities and their subunits' (1a1, 1b3, 1b4 and 2b4) transcriptions. In summary, these effects play a critical role of LYC-mediated chemoprevention against ATR-induced hepatotoxicity.