We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Endogenous hydrogen sulfide counteracts polystyrene nanoplastics-induced mitochondrial apoptosis and excessive autophagy via regulating Nrf2 and PGC-1α signaling pathway in mouse spermatocyte-derived GC-2spd(ts) cells
AI summary Read the abstract
Researchers investigated how polystyrene nanoplastics damage reproductive cells in mice and whether endogenous hydrogen sulfide can provide protection. The study found that nanoplastics induced mitochondrial damage, excessive autophagy, and cell death in spermatocyte-derived cells, while hydrogen sulfide counteracted these effects by regulating oxidative stress defense pathways.
Nanoplastics (NaPs) has reported to accumulate in the testes and cause degeneration in the seminiferous tubules. Additionally, exogenous hydrogen sulfide (HS) is proposed to enhance tolerance to oxidative stress. The current work aimed to investigate the mechanisms of NaPs-induced reproductive toxicity in vitro and probable reproductive protection by endogenous HS. We firstly found that 80 nm fluorescent NaPs could enter into GC-2spd(ts) cells by fluorescent inverted microscope. In addition, we demonstrated that NaPs-induced could induce ROS-dependent mitochondrial apoptosis and autophagy in vitro. Our results showed that the HS donor NaHS ameliorated NaPs-triggered mitochondrial apoptosis and autophagy in GC-2spd(ts) cells. Moreover, NaPs treatment did not change the interaction between nuclear factor erythroid-derived 2-related factor (Nrf2) and Kelch-like ECH associated protein 1 (Keap1), while inhibiting nuclear accumulation of Nrf2 protein was observed. Meanwhile, NaHS weakened this interaction, subsequently improving antioxidant ability via increasing the protein levels of heme oxygenase-1 (HO-1) and NAD(P)H dehydrogenase quinone 1 (NQO1). Further, invitro experiments showed that NaPs-induced reproductive toxicity associated with reducing PGC-1α. Meanwhile, NaPs-induced higher expression PGC-1α was further enhanced by NaHS co-treatment. Together, this study highlight that exogenous HS should be an essential therapeutic approach to alleviate NaPs-induced reproductive toxicity via regulating Nrf2/PGC-1α signal.
More Papers Like This
Exogenous Hydrogen Sulfide Mitigates Oxidative Stress and Mitochondrial Damages Induced by Polystyrene Microplastics in Osteoblastic Cells of Mice
AI summary Read the abstract
Researchers found that polystyrene microplastics induced oxidative stress, mitochondrial damage, and altered gene expression in mouse bone-forming cells, while exogenous hydrogen sulfide treatment mitigated these toxic effects by modulating key signaling pathways.
Nrf2-mediated ferroptosis of spermatogenic cells involved in male reproductive toxicity induced by polystyrene nanoplastics in mice
AI summary Read the abstract
When polystyrene nanoplastics were injected into the bloodstream of mice, they accumulated in the testes and caused significant damage to sperm-producing cells through a process called ferroptosis, a type of iron-dependent cell death. The nanoplastics disrupted a key protective pathway (Nrf2) that normally prevents this type of cell death. These findings suggest that nanoplastic exposure could harm male fertility by directly damaging the cells responsible for producing sperm.
Keap1-Nrf2 pathway up-regulation via hydrogen sulfide mitigates polystyrene microplastics induced-hepatotoxic effects
AI summary Read the abstract
Researchers investigated whether hydrogen sulfide could protect against liver damage caused by polystyrene microplastics in mice. They found that hydrogen sulfide activated the Keap1-Nrf2 antioxidant defense pathway, which reduced oxidative stress and inflammation in liver tissues exposed to microplastics. The study suggests that the Keap1-Nrf2 pathway plays a protective role against microplastic-induced hepatotoxicity and that hydrogen sulfide could be a potential therapeutic agent.
Investigating polystyrene nanoplastics-induced reproductive toxicity in vitro: Focus on Nrf2-PKM2-autophagy signaling pathway
AI summary Read the abstract
This lab study investigated how polystyrene nanoplastics damage male reproductive cells, finding they triggered autophagy (cellular self-digestion) and disrupted key proteins in a signaling pathway important for sperm cell survival. The findings suggest nanoplastics could impair male fertility by causing programmed cell death in testicular cells. This adds to growing evidence that plastic nanoparticles can harm reproductive health.
Integrated transcriptomic and metabolomic analysis reveals the underlying mechanisms for male reproductive toxicity of polystyrene nanoplastics in mouse spermatocyte-derived GC-2spd(ts) cells
AI summary Read the abstract
Researchers used integrated transcriptomic and metabolomic analysis to investigate how polystyrene nanoplastics affect mouse spermatocyte cells. They found that nanoplastic exposure disrupted lipid metabolism, triggered oxidative stress, and activated cell death pathways in the reproductive cells. The study suggests that nanoplastic exposure may pose risks to male reproductive health by interfering with critical metabolic and gene expression processes in developing sperm cells.
Research digests by email
When a large batch of papers lands in the Atlas, we read through it and send a short write-up of what stood out.