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.

This study aimed to investigate the effects of dietary fumaric acid (FA) on growth performance, immune responses, immune organ index and antioxidant status in broilers under chronic heat stress (HS). A total of 200 21-day-old Ross 308 chicks were randomly assigned in a 2 × 2 factorial arrangement with two diets (basal diet or 10 g/kg FA diet) and two temperatures (thermoneutral or HS) for 21 days. On day 42, growth performance, immune organ index, immune function and antioxidative ability were determined. HS resulted in a significant reduction in final body weight (FBW), average daily feed intake (ADFI), average daily gain (ADG), antibody titres against sheep red blood cells (SRBC) and Newcastle disease virus, IgM, IgG, relative weights of spleen, thymus and bursa of Fabricius, but a significant increase in the feed conversion ratio (FCR), activities of total superoxide dismutase (T-SOD) and glutathione peroxidase (GPx) in the bursa, contents of malondialdehyde and total carbonyl (TC) in thymus and bursa (P < 0.05). Dietary supplementation of FA increased FBW, ADFI, ADG, antibody titres against SRBC, IgG, relative weights of spleen and bursa, activity of GPx in thymus and bursa, whereas it decreased the FCR and TC of thymus and bursa. These results suggest that dietary 10 g/kg FA had positive effects on growth performance and immune function through improving the antioxidative capacity of immune organs.

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.

Ninety-six thousand one-day-old AA broilers were randomly assigned to two groups, 5 replicates in each group, and 9,600 chickens for each replicate. In the control group, 0.3 part per million (ppm) inorganic selenium (Na 2 SeO 3) was added to the diets; while in the experimental group, 0.3 ppm organic selenium (Se-enriched yeast) was added to the same basal diets. The feeding experimental period was 42 days. The results show that: (1) Organic selenium could increase daily weight gain and feed intake by 8.92 (P<0.05) and 3.99% (P<0.05), and decrease survival rate and feed conversion by 0.93 (P<0.05) and 4.84% (P<0.05), indicating that the effects of organic selenium on broiler growth performance were better than that of inorganic selenium, except for survival rate. (2) Compared with the control, meat red color degree of chest and thigh muscles were increased by 13.98 (P<0.05) and 20.83% (P<0.05); the drip losses of chest and thigh muscles were decreased by 13.57 (P<0.05) and 24.92% (P<0.05), respectively. (3) Serum glutathione peroxidase (GPX) activity in experimental group were 155.83% higher than that in the control (P<0.05). These results indicate that the effects of organic selenium on enhancing body oxidation resistance were superior to that of inorganic selenium.

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Alpha lipoic acid (ALA), a natural lipophilic compound, plays an important role in regulating several metabolic pathways due to its antioxidant properties. This study aims to investigate whether ALA could be used as a feed additive to enhance the antioxidant capacity of the ovary tissue in hens exposed to heat stress (HS). One hundred and sixty 128-days-old female chickens were randomly assigned into four groups: the control group (Con), ALA treatment group (ALA), ALA and HS treatment group (ALA + HS), and HS treatment group (HS). The ALA and ALA + HS groups were fed a basal diet with 0.25% ALA, whereas the Con and HS groups were fed a basal diet only. Serum oestradiol, progesterone levels, biomarkers of antioxidant capacity, and endoplasmic reticulum (ER) stress markers were detected in the ovaries of heat-stressed chickens. HS decreased serum oestradiol and progesterone concentrations compared with the control group, whereas dietary ALA (0.25%) increased oestradiol and progesterone levels in the serum of heat-stressed hens. Malondialdehyde concentration in the ovary was higher in the HS group than that of the ALA + HS group. Compared with the HS group, ALA increased the enzymatic activities of superoxide dismutase, glutathione peroxidase, and catalase in the ovaries of ALA + HS group. Simultaneously, ALA enhanced the total antioxidative capacity of the ovaries of heat-stressed hens. Moreover, ALA also significantly inhibited the increased expression of glucose-regulated protein 78 and CCAAT/enhancer-binding protein homologous protein, which are two markers of ER stress, and heat shock protein 70, a key biomarker of heat stress, in the ovaries of the ALA + HS group as compared to those of the HS group. This work implied that dietary ALA supplementation improved the antioxidant capacity and attenuated the HS-induced reduction of serum oestradiol and progesterone levels and modulated the oxidative and ER stress, which are involved in the protective effect of ALA in hens exposed to hyperthermia.