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61,005 resultsShowing papers similar to Combined effect of polystyrene microplastics and cadmium on rat blood-testis barrier integrity and sperm quality
ClearThe simultaneous administration of microplastics and cadmium alters rat testicular activity and changes the expression of PTMA, DAAM1 and PREP
Researchers examined the combined effects of microplastics and cadmium on testicular function in rats. The study found that simultaneous exposure caused testicular damage including impaired tissue structure, increased cell death, reduced testosterone, and altered expression of proteins involved in sperm cell development. The study suggests that microplastics may partially reduce cadmium bioavailability through adsorption, resulting in combined effects that were more severe than microplastics alone but less harmful than cadmium alone.
Maternal Exposureto Combined Cadmium and PolystyreneNanoplastics Induces Offspring Testicular Dysplasia via MitochondrialReactive Oxygen Species Overactivating the Peroxisome Proliferator-ActivatedReceptor α‑Mediated Autophagy Signaling Pathway
Maternal exposure to combined polystyrene nanoplastics and cadmium during pregnancy caused testicular dysplasia in offspring via mitochondrial reactive oxygen species overactivating the PPARα-mediated autophagy pathway, with combined exposure more harmful than either alone.
Synergistic effect of PS-MPs and Cd on male reproductive toxicity: Ferroptosis via Keap1-Nrf2 pathway
A mouse study found that microplastics and the heavy metal cadmium work together to cause more severe damage to male reproductive organs than either pollutant alone. The combination triggered a form of cell death called ferroptosis by disrupting a key protective pathway in the body. This is the first study to show this synergistic reproductive harm, suggesting that microplastics can make other environmental toxins more dangerous.
Combined effects of polystyrene nanoplastics and lipopolysaccharide on testosterone biosynthesis and inflammation in mouse testis
Researchers found that polystyrene nanoplastics combined with bacterial toxins (LPS) caused worse damage to mouse testicles than either substance alone, reducing sperm count, lowering testosterone levels, and increasing inflammation. Since microplastics in the environment can carry bacteria and their toxins, this combination exposure is realistic. The findings suggest that nanoplastic pollution could amplify the reproductive harm caused by bacterial infections in males.
Maternal Exposure to Combined Cadmium and Polystyrene Nanoplastics Induces Offspring Testicular Dysplasia via Mitochondrial Reactive Oxygen Species Overactivating the Peroxisome Proliferator-Activated Receptor α-Mediated Autophagy Signaling Pathway
Researchers investigated the combined effects of maternal exposure to polystyrene nanoplastics and cadmium on offspring in a mouse model. The study found that co-exposure caused testicular developmental abnormalities in offspring through mitochondrial oxidative stress and disrupted autophagy signaling, suggesting that nanoplastics may amplify the reproductive toxicity of co-occurring environmental contaminants.
Impact of polystyrene microplastic exposure at low doses on male fertility: an experimental study in rats
Researchers exposed adult male rats to varying doses of polystyrene microplastics and found dose-dependent declines in semen quality along with disrupted reproductive hormone levels. Higher doses caused increased oxidative stress, mitochondrial damage, and inflammatory responses in testicular tissue. The study suggests that even relatively low doses of microplastic exposure may have adverse effects on male reproductive health in animal models.
Dose-Dependent Effect of Polystyrene Microplastics on the Testicular Tissues of the Male Sprague Dawley Rats
Male rats exposed to increasing doses of polystyrene microplastics showed dose-dependent testicular damage including disrupted spermatogenesis and altered hormone levels, suggesting potential reproductive toxicity from microplastic accumulation.
Polystyrene nanoplastics aggravated dibutyl phthalate-induced blood-testis barrier dysfunction via suppressing autophagy in male mice
In a mouse study, polystyrene nanoplastics combined with dibutyl phthalate (a common plasticizer chemical) caused significantly worse damage to the blood-testis barrier than either substance alone. The nanoplastics carried the phthalate into the reproductive system, where the combination reduced sperm quality, impaired sperm development, and damaged the protective barrier around the testes. This research shows how nanoplastics can make other common plastic chemicals more dangerous to male fertility.
Co-exposure of cadmium and polystyrene nanoplastics: Induction pyroptosis and autophagy in mice testis
Researchers investigated the combined effects of cadmium and polystyrene nanoplastics on mouse testicular tissue. The study found that co-exposure produced more severe testicular damage than either substance alone, driven by the interplay between pyroptosis (inflammatory cell death) and autophagy. Inhibiting one of these cellular processes affected the other, suggesting they are closely interconnected in the toxicity response to nanoplastic and heavy metal co-exposure.
Low-dose polystyrene microplastics exposure impairs fertility in male mice with high-fat diet-induced obesity by affecting prostate function
Male mice exposed to low doses of microplastics had lower sperm quality and fewer offspring, and these effects were significantly worse when combined with a high-fat diet. The combination triggered inflammation and cell death in the prostate gland, reducing key nutrients in seminal fluid needed for sperm health. This suggests that microplastic exposure may be an overlooked factor in declining male fertility, especially for those with metabolic conditions like obesity.
Co-exposure to polystyrene nanoplastics and hexachlorocyclohexane induces enhanced human sperm toxicity in vitro
Scientists found that when human sperm are exposed to both tiny plastic particles (nanoplastics) and a pesticide chemical at the same time, it causes much more damage than either substance alone. The combination severely reduced sperm's ability to swim and function properly, which could contribute to male fertility problems. This suggests that the growing presence of microplastics in our environment might make other harmful chemicals even more dangerous to reproductive health.
Nanoplastic PS and cadmium co-exposure accelerates ferroptosis mediated by HIF-1α-related signaling in spermatogonium
Researchers exposed mouse sperm precursor cells to nanoplastics combined with cadmium and found that co-exposure caused significantly more cell damage than either contaminant alone. The combined treatment triggered a form of cell death called ferroptosis through a specific signaling pathway involving the gene HIF-1a. The study suggests that nanoplastics may worsen the reproductive toxicity of heavy metals commonly found alongside plastic pollution in the environment.
Co-exposure to polystyrene microplastics and microcystin-LR aggravated male reproductive toxicity in mice
Researchers found that exposing mice to a combination of polystyrene microplastics and microcystin-LR, a toxin produced by algae, caused more severe damage to male reproductive organs than either pollutant alone. The microplastics increased the amount of the toxin that accumulated in testicular tissue. The study suggests that the interaction between microplastics and other environmental contaminants may amplify reproductive health risks.
Determination of Biological and Molecular Attributes Related to Polystyrene Microplastic-Induced Reproductive Toxicity and Its Reversibility in Male Mice
Researchers exposed male mice to polystyrene microplastics through drinking water and found that the particles caused mitochondrial damage in testicular tissue, including reduced membrane potential and disrupted energy production. This mitochondrial dysfunction led to decreased sperm quality, likely driven by oxidative stress. Importantly, the study found that sperm quality recovered after one to two spermatogenic cycles without further exposure, suggesting that reproductive toxicity from microplastics may be reversible.
Polystyrene Microplastics Disrupt Spermatogenesis through Oxidative Stress in Rat Testicular Tissue
Male Wistar rats orally administered polystyrene microplastics showed excessive oxidative stress in testicular tissue across all exposure groups, with spermatogenesis impairment and reduced fertility correlating with dose, demonstrating reproductive toxicity in a mammalian model.
Polystyrene microplastics induced male reproductive toxicity in mice
Researchers exposed male mice to polystyrene microplastics of different sizes and found that the particles accumulated in testicular tissue and entered reproductive cells. After 28 days of exposure, sperm quality and testosterone levels declined, and tissue examination revealed disorganized sperm-producing cells and inflammation. The study suggests that microplastic exposure may pose risks to male reproductive health in mammals.
PS-MPs or their co-exposure with cadmium impair male reproductive function through the miR-199a-5p/HIF-1α-mediated ferroptosis pathway
Researchers found that polystyrene microplastics, especially when combined with cadmium, caused significant reproductive damage in male mice through a cell death pathway called ferroptosis. Smaller microplastic particles were more toxic than larger ones, and the combination of microplastics with cadmium amplified the harm beyond what either caused alone. The study identifies a specific molecular mechanism by which microplastics and heavy metals together may threaten male reproductive health.
Combined effect of polystyrene nanoplastic and di-n-butyl phthalate on testicular health of male Swiss albino mice: analysis of sperm-related parameters and potential toxic effects
This mouse study found that combined exposure to polystyrene nanoplastics and a common plasticizer chemical (DBP) caused worse damage to male reproductive health than either substance alone. The combination significantly reduced sperm quality, lowered antioxidant defenses, and damaged testicular tissue over 60 days. These findings are concerning because people are often exposed to both nanoplastics and plasticizer chemicals at the same time through food packaging and everyday products.
Polystyrene exacerbates cadmium‐induced mitochondrial damage to lung by blocking autophagy in mice
Researchers found that polystyrene microplastics exacerbated cadmium-induced mitochondrial damage in mouse lungs by blocking autophagy, revealing a synergistic toxicity mechanism when these two common environmental contaminants co-occur.
Polystyrene Microplastics Affect the Reproductive Performance of Male Mice and Lipid Homeostasis in Their Offspring
Researchers found that long-term exposure to environmentally relevant doses of polystyrene microplastics over 21 weeks significantly impaired reproductive function in male mice, including decreased testicle weight and sperm quality. The study also revealed transgenerational effects, with offspring showing disrupted lipid homeostasis.
Combined effects of polystyrene microplastics and cadmium on oxidative stress, apoptosis, and GH/IGF axis in zebrafish early life stages
Researchers exposed zebrafish embryos to polystyrene microplastics and cadmium, both alone and together, and found that the combination caused significantly worse effects than either pollutant individually. Co-exposure amplified oxidative stress, increased cell death in the spine and esophagus, and disrupted growth hormone pathways more severely than single exposures. The findings suggest that microplastics and heavy metals in waterways may interact to create heightened risks for developing fish.
Polystyrene microplastics induce male reproductive toxicity in mice by activating spermatogonium mitochondrial oxidative stress and apoptosis
A mouse study found that polystyrene microplastics significantly reduced sperm count and motility while increasing sperm deformities. The damage was caused by oxidative stress in the energy-producing mitochondria of sperm-forming cells, which triggered cell death -- raising concerns about microplastics' potential impact on male fertility.
Adverse effects and potential mechanisms of polystyrene microplastics (PS-MPs) on the blood-testis barrier
This review examines how polystyrene microplastics damage the blood-testis barrier, a critical structure that protects developing sperm cells from harmful substances. Microplastics can break down this barrier through oxidative stress, inflammation, and disruption of gut bacteria, allowing pollutants and immune cells to enter the reproductive system. These findings suggest that microplastic exposure may contribute to declining male fertility, a trend observed globally in recent decades.
PPARγ mediated lysosomal membrane permeabilization and lipophagy blockage were involved in microplastics and di (2-ethylhexyl) phthalate co-exposure induced immature testis injury
Mice exposed to both polystyrene microplastics and DEHP, a common plastic additive, suffered significantly worse testicular damage than those exposed to either substance alone. The combined exposure disrupted fat metabolism in reproductive cells by damaging lysosomes (cellular recycling centers) and blocking the normal breakdown of lipids. This is especially relevant to human health because people are typically exposed to microplastics and plastic additives like DEHP at the same time through everyday products.