Endogenous Hydrogen Sulfide Promotes Apoptosis via Mitochondrial Pathways in the Livers of Broilers with Selenium Deficiency Exudative Diathesis Disease.

Hydrogen sulfide (H2S), an endogenous gasotransmitter, plays an important role in apoptosis. Exudative diathesis (ED) disease is associated with dietary selenium (Se) deficiency in broilers. The liver is one of the target organs of Se deficiency; however, little is known about the effect of H2S on apoptosis via mitochondrial pathways in the livers of broilers with ED disease. In the present study, we aimed to investigate the correlation between endogenous H2S and mitochondrial-mediated apoptosis in the livers of broilers with ED disease, as induced by Se deficiency. One hundred twenty healthy, 1-day-old broilers were randomly assigned to one of two groups (60 each) based on diet: Basal diet (control group, 0.2 mg/kg Se) or a low-Se diet (-Se group, 0.033 mg/kg Se). At day 20, 15 broilers of a similar weight were sacrificed from the control group, while the same number of broilers were euthanatized from the -Se group when displaying typical symptoms of ED between days 18 and 25. The livers were collected, and apoptosis was measured using a TUNEL assay. Additionally, H2S concentration, the expression of H2S synthases of cystathionine γ-lyase (CSE), cystathionine ß-synthase (CBS), and 3-mercaptopyruvate sulfurtransferase (3-MST), as well as mitochondrial apoptosis-related genes of Bcl-2, Bax, Bak, Cyt-C, Caspase-9, Caspase-3, and p53, were examined in livers. The results indicated that Se deficiency could induce apoptosis in the livers of broilers. Swelling, fractures, and vacuolization were visible in the mitochondrial cristae in the livers of the -Se group. The expression of H2S synthase-related genes and H2S concentration was significantly enhanced (P < 0.05) in the livers of the -Se group compared to controls. Moreover, a low-Se diet downregulated (P < 0.05) the level of Bcl-2 and upregulated (P < 0.05) the levels of Bax, Bak, Cyt-C, Caspase-9, Caspase-3, and p53. These results suggest that an H2S increase in the livers of ED broilers, which was induced by Se deficiency, is related to apoptosis mediated by mitochondrial pathways.

Manganese-induced effects on testicular trace element levels and crucial hormonal parameters of Hyline cocks.

Manganese (Mn) is an essential element required for normal development and reproduction. However, little is known about the reproductive toxicity of Mn in birds. To investigate the Mn-induced toxicity on testicular trace element levels and crucial hormonal parameters on male reproduction in birds, 50-day-old male Hyline cocks were fed either a commercial diet or a Mn-supplemented diet. The changes in contents of copper (Cu), iron (Fe), zinc (Zn), and calcium (Ca) in testis were detected. Hormonal parameters were evaluated including the levels of testosterone (T), luteinizing hormone (LH), follicle-stimulating hormone (FSH), thyroid-stimulating hormone (TSH), triiodothyronine (T3), and thyroxine (T4) in the serum. The mRNA levels of luteinizing hormone receptor (LHR) and follicle-stimulating hormone receptor (FSHR) were determined in this study. The results showed that Mn was accumulated in testis, and the content of Cu, Fe, Zn, and Ca decreased. Exposure to Mn significantly lowered the content of T, LH, FSH, and the mRNA expression levels of LHR and FSHR. Levels of T3 and T4 appeared with a decreased tendency, and TSH presented no obvious regularity. It indicated that Mn exposure resulted in the disbalance of testicular trace elements and influenced hormone levels in the molecular level, which may be possible underlying reproductive toxicity mechanism induced by Mn.