We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
N-Acetyl-L-Cysteine Ameliorates BPAF-Induced Porcine Sertoli Cell Apoptosis and Cell Cycle Arrest via Inhibiting the ROS Level
Summary
Researchers investigated how bisphenol AF, a plastic-derived environmental contaminant, affects testicular Sertoli cells in pigs. The study found that high concentrations of BPAF triggered cell death, cell cycle arrest, and elevated levels of reactive oxygen species, while reducing antioxidant defenses. Evidence indicates that the antioxidant N-acetyl-L-cysteine could block these harmful effects, suggesting that BPAF-induced damage operates through oxidative stress pathways.
Bisphenol AF (BPAF) is a newly identified contaminant in the environment that has been linked to impairment of the male reproductive system. However, only a few studies have systematically studied the mechanisms underlying BPAF-induced toxicity in testicular Sertoli cells. Hence, this study primarily aims to explore the toxic mechanism of BPAF on the porcine Sertoli cell line (ST cells). The effects of various concentrations of BPAF on ST cell viability and cytotoxicity were evaluated using the Counting Kit-8 (CCK-8) assay. The results demonstrated that exposure to a high concentration of BPAF (above 50 μM) significantly inhibited ST cell viability due to marked cytotoxicity. Flow cytometry analysis further confirmed that BPAF facilitated apoptosis and induced cell cycle arrest in the G2/M phase. Moreover, BPAF exposure upregulated the expression of pro-apoptotic markers BAD and BAX while downregulating anti-apoptotic and cell proliferation markers BCL-2, PCNA, CDK2, and CDK4. BPAF exposure also resulted in elevated intracellular levels of reactive oxygen species (ROS) and malondialdehyde (MDA), alongside reduced activities of the antioxidants glutathione (GSH), catalase (CAT), and superoxide dismutase (SOD). Furthermore, the ROS scavenger N-acetyl-L-cysteine (NAC) effectively blocked BPAF-triggered apoptosis and cell cycle arrest. Therefore, this study suggests that BPAF induces apoptosis and cell cycle arrest in ST cells by activating ROS-mediated pathways. These findings enhance our understanding of BPAF's role in male reproductive toxicity and provide a foundation for future toxicological assessments.
Sign in to start a discussion.
More Papers Like This
Polystyrene microplastics induce apoptosis and necroptosis in swine testis cells via ROS/MAPK/HIF1α pathway
Researchers exposed swine testis cells to polystyrene microplastics and found that the particles reduced cell viability and triggered both programmed cell death and necroptosis. The damage was driven by excessive production of reactive oxygen species that activated stress signaling pathways. Since pigs are physiologically similar to humans, the findings raise concerns about potential reproductive health effects of microplastic exposure in mammals.
Polystyrene microplastics induce apoptosis in chicken testis via crosstalk between NF-κB and Nrf2 pathways
Researchers found that polystyrene microplastics caused testicular damage in chickens through crosstalk between inflammatory and antioxidant defense pathways. Exposure to microplastics through drinking water disrupted the blood-testis barrier, triggered oxidative stress by inhibiting the Nrf2 pathway, activated inflammatory signaling through NF-kB, and ultimately induced cell death in testicular tissue.
The Protective Role of L-Cysteine in the Regulation of Blood–Testis Barrier Functions—A Brief Review
This review examines how the amino acid L-cysteine helps protect the blood-testis barrier, a critical structure that shields developing sperm cells from harmful substances including environmental contaminants like microplastics. Researchers found that L-cysteine supports barrier integrity through its antioxidant properties and by regulating the proteins that hold barrier cells together. The findings suggest that L-cysteine supplementation could potentially help maintain male reproductive health in the face of increasing environmental pollutant exposure.
Evaluation of possible attenuative role of chrysoeriol against polyethylene microplastics instigated testicular damage: A biochemical, spermatogenic and histological study
Researchers investigated whether the plant compound chrysoeriol could protect against testicular damage caused by polyethylene microplastics in a rat model. The study found that microplastic exposure reduced antioxidant enzyme activity and increased inflammation markers, while co-administration of chrysoeriol showed a protective effect by mitigating oxidative stress and preserving sperm quality.
Epigallocatechin-gallate ameliorates polystyrene microplastics-induced oxido-inflammation and mitochondria-mediated apoptosis in testicular cells via modulation of Nrf2/HO-1, /mTOR/Atg-7, and Cx-43/NOX-1 levels
Researchers found that polystyrene microplastics caused oxidative stress, inflammation, and reduced sperm quality in rats, but that treatment with EGCG — a compound found in green tea — reversed most of these harmful effects by restoring antioxidant defenses and reducing cell death pathways in testicular tissue.