Cadmium (Cd) is a kind of toxic heavy metal and it can cause damage to organs and tissues. Selenium (Se) can antagonize some metal element toxicity including Cd. The present study was designed to investigate Cd-induced damage to chicken ovary by autophagy and the protective mechanism of Se on Cd-induced damage. Administration of Cd for 12 weeks led to energy metabolism disorder of the chicken ovarian tissues, which resulted in autophagy. In addition, the mRNA expression of glucose-related genes including hexokinase II (HK2), pyruvate kinase (PK), pyruvate dehydrogenase complex (PDHX), and succinate dehydrogenase (SDH) and the activities of ATPase, including Na+-K+-ATPase, Ca2+-ATPase, Mg2+-ATPase, were all downregulated remarkably compared with the control. However, combined with oral administration of Se at 2 mg/kg, the mRNA expression of glucose-related genes and the activities of ATPase increased. The mRNA expression of the autophagy-related genes by Cd treatment, including microtubule-associated protein light chain 3 (LC3), dynein, autophagy-related gene 5 (Atg5), and Beclin 1, was remarkably enhanced, whereas mammalian target of rapamycin (mTOR) was downregulated. However, besides mTOR, their levels displayed a downregulated trend beyond simultaneous Se treatment. The protein expression of autophagy genes was similar to those of mRNA. In conclusion, Cd toxicity affect energy metabolism and induce autophagy, which causes damage to chicken ovary, whereas Se could protect effectively this injury induced by Cd.
Keywords: Autophagy; Cadmium; Chicken ovary; Energy metabolism; Selenium.