We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Polystyrene microplastics impaired the function of leydig cells via GRP78/PERK/CHOP mediated endoplasmic reticulum stress in vivo and in vitro
AI summary Read the abstract
This study found that polystyrene microplastics damaged Leydig cells, which are responsible for producing testosterone in males, in both mice and cell experiments. The microplastics triggered a stress response in a cell structure called the endoplasmic reticulum, leading to cell death through a specific molecular pathway involving GRP78, PERK, and CHOP proteins. These findings suggest a mechanism by which microplastic exposure could contribute to declining male reproductive health and testosterone levels.
The toxic effect of Polystyrene Microplastics (PS-MPs) on leydig cells were found in male mice, but the toxic mechanism was not clear. The PS-MPs exposure mice model and cell model were established in this study to explore the leydig cells toxic mechanism. In vivo study, the leydig cells toxicity in male mice was evaluated exposed to PS-MPs for 28 days. And found that the sperm density, mobility and testosterone (T) level decreased, and the sperm malformation rate and malondialdehyde level increased. PS-MPs exposure impaired the function of male reproduction. The results also showed that the levels of testosterone-producing proteins (StAR, P450scc,3β-HSD and CYP17A1) decreased, apoptosis signaling pathways (Bax/Bcl-2, Caspase-8 and Caspase-12) were activated and endoplasmic reticulum stress (GRP78/p-PERK/CHOP) occurred in male mice exposed to PS-MPs. In vitro study, TM3 cells (leydig cells) were treated with 50, 100 and 200 μg/mL of PS-MPs for 24 h. And we found that PS-MPs exposure reduced the cell viability and the level of T, increased reactive oxygen species (ROS) level in TM3 cells. PS-MPs exposure impaired the function of the leydig cells. Further testing revealed that PS-MPs could activate GRP78/p-PERK/CHOP pathway, aggrandized endoplasmic reticulum stress in the leydig cells, then increased apoptosis level, and induced testosterone synthase protein reduction. These could be reversed when exposed to ROS inhibitor or endoplasmic reticulum stress inhibitor. In conclusion, PS-MPs exposure induced the high level of ROS, activated the GRP78/p-PERK/CHOP signaling pathway, enhanced endoplasmic reticulum stress in leydig cells, then apoptosis level increased, which impaired the leydig cell function.
More Papers Like This
Polystyrene microplastics impair the functions of cultured mouse Leydig (TM3) and Sertoli (TM4) cells by inducing mitochondrial-endoplasmic reticulum damage
AI summary Read the abstract
Lab experiments showed that polystyrene microplastics damaged two key types of testicular cells in mice -- Leydig cells that produce testosterone and Sertoli cells that support sperm development -- by harming their mitochondria (the cell's energy centers) and stressing the endoplasmic reticulum. These findings suggest that microplastic exposure could contribute to male reproductive problems by disrupting hormone production and sperm development at the cellular level.
Male reproductive toxicity of polystyrene microplastics: Study on the endoplasmic reticulum stress signaling pathway
AI summary Read the abstract
Researchers exposed mice to polystyrene microplastics for 35 days and found significant male reproductive toxicity, including decreased sperm counts and motility, increased sperm abnormalities, and reduced testosterone levels. The microplastics caused structural damage to the seminiferous tubules and triggered endoplasmic reticulum stress in testicular tissue. The study suggests that microplastic exposure may impair male reproductive health through stress-related signaling pathways in the testes.
Exposure to nanoplastics induces mitochondrial impairment and cytomembrane destruction in Leydig cells
AI summary Read the abstract
Researchers exposed mouse Leydig cells (which produce testosterone) to 20-nanometer polystyrene nanoplastics in the lab and found that the particles entered the cells and caused dose-dependent damage. The nanoplastics triggered oxidative stress, destroyed mitochondria, disrupted cell membranes, and reduced testosterone production. This study adds to growing evidence that nanoplastics could harm male reproductive health by directly damaging the cells responsible for making testosterone.
Chronic Polystyrene Microplastic Exposure Reduces Testosterone Levels in Mice through Mitochondrial Oxidative Stress and BAX/BCL2-Mediated Apoptosis
AI summary Read the abstract
This mouse study found that oral exposure to polystyrene microplastics for four weeks significantly lowered testosterone levels by damaging the cells in the testes that produce it. The microplastics caused mitochondrial damage, oxidative stress, and triggered cell death in these testosterone-producing cells. These findings suggest that chronic microplastic exposure could contribute to declining male hormone levels and fertility issues.
Chronic exposure to polystyrene microplastics induced male reproductive toxicity and decreased testosterone levels via the LH-mediated LHR/cAMP/PKA/StAR pathway
AI summary Read the abstract
Mice exposed to polystyrene microplastics in their drinking water for 180 days showed significant reproductive damage, including reduced testosterone, lower sperm quality, and changes in testicular structure. The researchers identified a specific hormonal pathway through which microplastics suppress testosterone production in the cells that make it. This long-term, low-dose study is particularly relevant because the exposure levels are closer to what humans might experience in everyday life.
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.