Heat stress (HS) causes testicular injury, resulting in decreased fertility. Alpha-lipoic acid (ALA) is a well-known antioxidant. The aim of this study was to investigate the protective effects of ALA on HS-induced testicular damage in chickens. Histological changes; biomarkers of oxidative stress, including glutathione peroxidase (GPx), superoxide dismutase (SOD), catalase (CAT), and malondialdehyde (MDA); markers of endoplasmic reticulum (ER) stress, including glucose-regulated protein 78 (GRP78) and CCAAT/enhancer binding protein homologous protein (CHOP); apoptosis-related modulators, including Bax, Bcl-2, and caspase 3, in testicular tissue and serum testosterone levels were evaluated in chickens under heat stress. Heat stress induces spermatogenic cell abnormalities in chicken testes. Compared to the HS group, the histomorphological abnormalities in testicular tissue were visibly ameliorated, with significant increases in the enzyme activities of GPx, SOD, and CAT, increased serum testosterone concentration, and decreased MDA levels in the ALA + HS group. Consistent with these results, compared with the HS group, the protein levels of GRP78, CHOP, caspase 3, and Bax were significantly decreased, whereas Bcl-2, StAR, and 3β-HSD protein levels were increased in the ALA + HS group. Collectively, these findings suggest that ALA significantly ameliorates the heat-induced histomorphological abnormalities in the testes and decreased testosterone production by potentiating the activities of anti-oxidative enzymes (GPx, SOD, and CAT), inhibiting ER stress-related apoptotic pathways (Bax, Bcl-2, and caspase 3), and increasing steroidogenic gene (StAR and 3β-HSD) expression in chickens.

Heat stress induces apoptosis in various cells. Selenium, an essential micronutrient, has beneficial effects in maintaining the cellular physiological functions. However, its potential protective action against chronic heat stress (CHS)-induced apoptosis in granulosa cells and the related molecular mechanisms are not fully elucidated. In this study, we investigated the roles of selenium in CHS-induced apoptosis in mouse granulosa cells and explored its underlying mechanism. The heat treatment for 6–48 h induced apoptosis, potentiated caspase 3 activity, increased the expression levels of apoptosis-related gene BAX and ER stress markers, glucose-regulated protein 78 (GRP78), and CCAAT/enhancer binding protein homologous protein (CHOP) in mouse granulosa cells. The treatment with ER stress inhibitor 4-PBA significantly attenuated the adverse effects caused by CHS. Selenium treatment significantly attenuated the CHS- or thapsigargin (Tg, an ER stress activator)-induced apoptosis, potentiation of caspase 3 activity, and the increased protein expression levels of BAX, GRP78, and CHOP. Additionally, treatment of the cells with 5 ng/mL selenium significantly ameliorated the levels of estradiol, which were decreased in response to heat exposure. Consistently, administering selenium supplement alleviated the hyperthermia-caused reduction in the serum estradiol levels in vivo. Together, our findings indicate that selenium has protective effects on CHS-induced apoptosis via inhibition of the ER stress pathway. The current study provides new insights in understanding the role of selenium during the process of heat-induced cell apoptosis.

Effects of dietary fumaric acid on the growth performance, immune response, relative weight and antioxidant status of immune organs in broilers exposed to chronic heat stress | Shaojun He, Qirun Yin, Yongjie Xiong, Deyi Liu, Hong Hu | Agricultural Journals

Heat stress (HS) induces oxidative stress in the liver and affects health and production attributes in poultry birds. Bamboo leaf flavonoid (BLF) is a natural plant flavonoid that is effective in controlling oxidative stress. Therefore, the aim of current study was to investigate the impact of BLF on growth performance, liver index, serum biochemical parameters of liver function, liver antioxidant enzyme activities, and expression of genes and proteins related to the liver Keap1-Nrf2 system in cyclic heat stress (CHS) broilers. Twenty-eight-day old Arbor Acres broilers (n = 200) were randomly assigned to 5 groups. TN group fed basal diet was reared in a thermoneutral environment (24 ± 1 °C); CHS, 400 mg/kg BLF + CHS, 800 mg/kg BLF + CHS, and 1600 mg/kg BLF + CHS groups were reared in high temperature conditions (33 ± 1 °C, 8 h/day), with the basal diet supplemented with 0, 400, 800, and 1600 mg/kg BLF. The results indicated that ADG and ADFI of broilers in 28 to 35d and 36 to 42d CHS groups were significantly lower compared to the TN group. BLF improves growth performance of CHS broilers by increasing ADG, ADFI and decreasing F:G. BLF improved live weight, liver weight, liver index and reduced serum AST, ALP, ALT, T-BIL levels and increased TP levels in CHS broilers. Meanwhile, BLF supplementation enhanced the activity of hepatic antioxidant enzymes, resulting in higher T-AOC, CAT, GSH-PX and T-SOD levels than those of CHS broilers, and significantly reduced MDA levels. In addition, BLF down-regulated the protein levels of Keap1 and P62, increased the expression levels of Nrf2 genes and proteins, and activated the expression of its downstream NQO1, HO-1, and SOD-1 antioxidant genes compared to CHS broilers. In summary, BLF regulates the expression of key genes and proteins in the Keap1-Nrf2 signaling pathway to alleviate liver injury in broilers by inhibiting oxidative stress, thereby promoting the growth performance of broilers with CHS.