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Fluorochloridone (FLC), a pyrrolidone herbicide, has been recognized as a hazardous chemical. The in vitro adverse effects of FLC on the reproduction of livestock have not been assessed. This study was conducted to explore the cytotoxicity and toxicological mechanisms of FLC on cultured goat Sertoli cells. The results showed that FLC exposure significantly decreased goat Sertoli cell viability (p < 0.05) and induced oxidative stress. And FLC treatment promoted apoptosis and initiation of autophagy. Interestingly, FLC inhibited lysosomal biogenesis and blocked autophagic flux in goat Sertoli cells. The expression levels of autophagy-related proteins Atg5, LC3II, and p62 were significantly increased (p < 0.05) in FLC-treated goat Sertoli cells compared with the control. Importantly, FLC-induced ROS accumulation further causes mitochondrial dysfunction and disturbs mitophagy. FLC significantly decreased (p < 0.05) the expression levels of OPA1, MFN2, p-Drp1, FIS1, PINK1, and Parkin in goat Sertoli cells. Moreover, pretreatment with N-acetyl-l-cysteine (NAC, an antioxidant) significantly reduced (p < 0.01) FLC-induced ROS accumulation and reversed the disorder of autophagy levels. Our results indicated that FLC-induced toxicity in primary goat Sertoli cells was characterized by ROS accumulation, inducing oxidative stress, inhibiting lysosomal biogenesis, blocking autophagic flux, and promoting mitochondrial dysfunction, resulting in apoptosis via the mitochondrial pathway., Competing Interests: Declaration of competing interest The authors have declared that no competing interest exists., (Copyright © 2023 Elsevier Inc. All rights reserved.)

Oxidative stress is a common cause of male infertility. Sertoli cells are one of the target cells of oxidative injury, which leads to impaired testicular function. Follicle-stimulating hormone (FSH) is critical in Sertoli cell function. However, the role of FSH in the response of goat Sertoli cells to H 2 O 2 -induced oxidative stress has not been studied yet. To investigate this response, we established an oxidative stress model using goat Sertoli cells. FSH pretreatment significantly enhanced the decreased cell viability (p < 0.05) caused by oxidative injury and inhibited autophagic flux. FSH significantly increased p62 mRNA and protein levels (p < 0.01). Further investigations revealed that FSH also increased the expression level and nuclear translocation of Nrf2 in Sertoli cells (p < 0.01), which resulted in increased antioxidant enzyme activity (p < 0.05). In contrast, treatment with siNrf2 and sip62 abolished this protective effect of FSH. These findings suggest that FSH protects Sertoli cells against oxidative stress via the p62-Nrf2 pathway, and that p62 accumulation maintains persistent activation of Nrf2. Thus, p62 and Nrf2 are required for FSH-mediated protective role in H 2 O 2 -induced Sertoli cell injury. The findings reveal new mechanisms by which FSH protects against oxidative injury in goat Sertoli cells., Competing Interests: Declaration of competing interest The authors declare that they have no conflict of interest., (Copyright © 2022 Elsevier Inc. All rights reserved.)

Although the follicle-stimulating hormone (FSH) plays a vital role in male reproduction, the molecular relationships among FSH, autophagy, and the secretory function of Sertoli cells remain largely undetermined. In this study, we sought to investigate the effects of FSH on dairy goat Sertoli cell autophagy and the role of autophagy in protein clearance. FSH treatment of primary Sertoli cells was found to enhance the expression level of LC3-II, reduce p62 degradation and the number of lysosomes, and downregulate the levels of LAMP2 protein and lysosomal gene mRNAs. Further analyses revealed that starvation-induced autophagy promotes the translocation of transcription factor EB (TFEB) from the cytoplasm to nucleus and its binding to the promoter region of LAMP2, whereas FSH suppresses the nuclear translocation of TFEB. Moreover, we found that the FSH-mediated inhibition of autophagy extends the biological half-lives of androgen-binding protein (ABP), glial-derived neurotrophic factor (GDNF), and stem cell factor (SCF) and promotes the secretion of these proteins. Collectively, these observations indicate that FSH inhibits autophagy by reducing lysosomal biogenesis, which is associated with the suppression of TFEB nuclear translocation via activation of the PI3K/Akt/mTOR pathway, thereby extending the biological half-lives and enhancing the expression of ABP, GDNF, and SCF in dairy goat Sertoli cells., (Copyright © 2021 Elsevier B.V. All rights reserved.)

Background Objective Materials and methods Results Discussion and conclusion Reproductive aging can adversely affect male fertility and the health of offspring. The aging process is accompanied by impaired autophagy. Recent studies have shown that Trehalose plays an important role in the prevention of various diseases by regulating autophagy. However, the roles of Trehalose in testicular aging and reproductive decline remain to be clarified.The present study aimed to evaluate the protective effects of Trehalose on testes in an aging mouse model.In this study, an in vivo aging model in mice by administering D‐galactose was established to explore the protective effect of Trehalose on testicular aging. We examined histological changes and related indicators of apoptosis, autophagy, mitochondrial biogenesis, and sperm quality.D‐galactose treatment induced oxidative stress, apoptosis, and impairment of autophagy of testicular cells in mouse testes. Trehalose administration significantly reduced germ cell apoptosis and DNA damage caused by D‐galactose‐induced oxidative stress. Notably, Trehalose activated autophagy activity and improved mitochondrial function in testicular cells. Furthermore, Trehalose treatment increased the expression level of the tight junction protein ZO‐1, and accelerated clearance of damaged mitochondria in Sertoli cells, indicating that Trehalose ameliorated Sertoli cell function in D‐galactose‐induced aging testes.These findings suggest that Trehalose administration activated the autophagy activity in testicular cells and improved mitochondrial function, thereby effectively preventing testicular aging. Trehalose and its activated autophagy are crucial for preventing testicular aging, thus restoring autophagy activity by administering Trehalose could be a promising means to delay aging. [ABSTRACT FROM AUTHOR]

Zearalenone (ZEA), one of the non-steroidal estrogen mycotoxin, can cause male reproductive damage and genotoxicity in mammals. Testicular oxidative injury is an important factor causing male sterility. Testicular Sertoli cells are essential for spermatogenesis and male fertility. At present, the mechanism of oxidative injury in dairy goat Sertoli cells after exposure to ZEA remains unclear. This study explored the effects of ZEA on oxidative stress and autophagy in dairy goat Sertoli cells. It was found that treatment of primary Sertoli cells with 25, 50 and 100 μmol/L ZEA for 24 h can promote ROS production, decrease cell viability, antioxidant enzyme activity and mitochondrial membrane potential, induce caspase-dependent cell apoptosis and autophagy activity. ZEA-induced autophagy was confirmed by LC3-I/LC3-II transformation. More importantly, N-acetylcysteine (NAC) pretreatment can remarkably inhibit ZEA-induced oxidative stress, apoptosis and autophagy in Sertoli cells by eliminating ROS. In conclusion, this study indicates that ZEA induces oxidative stress and autophagy in dairy goat Sertoli cells by promoting ROS production. [Display omitted] • ZEA induced ROS production and oxidative stress in goat Sertoli cells. • ZEA induced apoptosis in Sertoli cells. • ZEA promoted lysosome biogenesis and induced autophagy. [ABSTRACT FROM AUTHOR]

Abstract Heat stress damaged spermatogenesis and semen quality, however, the exact molecular mechanism is not clear. The objective of this study was to determine the effects of elevated ambient temperature and local testicular heating on the expressions of heat shock protein 70 and androgen receptor in boar testes. A growing body of evidence demonstrated that germ cell apoptosis can be aggravated by heat stress and androgen deprivation, and at normal temperature, withdrawal of androgen led to germ cell apoptosis. There were no reports that heat stress damaged spermatogenesis has relationship with androgen. In this study, adult boars (Landrace, n = 9) were used and randomly divided into: control group (CON), 20–27 °C; environmental hyperthermia group (EH), 37–40 °C, 3 h/d 42 d; and local testicular heating group (LTH), 42 °C 1 h. After heat treatments, all boars were castrated and the testes were harvested. qRT-PCR and Western Blot results showed that the mRNA and protein levels of heat shock protein 70 and androgen receptor were significantly increased after heat treatments. Immunohistochemistry results showed that heat stress caused a redistribution of heat shock protein 70 from the cytoplasm to the nucleus, and androgen receptor was mainly expressed in Sertoli cells. These results indicated that heat stress promoted the inhibition of heat shock protein 70 on the androgen receptor, suggesting that the possible mechanism of heat stress damaged spermatogenesis and semen quality was that heat stress reduced the sensitivity of testicular cells to androgen by up-regulating heat shock proteins. [ABSTRACT FROM AUTHOR]