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61,005 resultsShowing papers similar to Synergistic assault of DEHP and MPs: Unmasking the ER stress-triggered autophagic injury male fertility
ClearPPARγ 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.
The single and combined effects of decabromodiphenyl ethane and mixed microplastics on male mice reproductive toxicity
Researchers investigated the combined reproductive toxicity of mixed microplastics and the flame retardant DBDPE in male mice over seven weeks. The study found that DBDPE alone decreased sex hormone levels and sperm count, and when combined with microplastics, the effects on testicular damage, sperm malformation, and oxidative stress were compounded, suggesting that microplastics may amplify the toxicity of co-occurring chemical contaminants.
Polystyrene nanoparticles enhance the adverse effects of di-(2-ethylhexyl) phthalate on male reproductive system in mice
Researchers investigated the combined reproductive toxicity of polystyrene nanoparticles and the plasticizer DEHP in male mice over 35 days. The study found that co-exposure to nanoparticles and DEHP produced enhanced adverse effects on sperm quality and testicular tissue compared to either substance alone, suggesting nanoplastics may amplify the endocrine-disrupting effects of plasticizers.
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.
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.
Enhanced reproductive toxicities induced by phthalates contaminated microplastics in male mice (Mus musculus)
Researchers investigated the combined reproductive toxicity of phthalate-contaminated microplastics in male mice over a 30-day exposure period. They found that microplastics enhanced the accumulation of phthalates in the liver and gut, and the combination significantly worsened reproductive damage including reduced sperm quality and testicular tissue changes. The study suggests that microplastics may amplify the harmful effects of chemical contaminants they carry by increasing their bioavailability in the body.
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.
Male reproductive toxicity of polystyrene microplastics: Study on the endoplasmic reticulum stress signaling pathway
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.
Polystyrene-microplastics and DEHP co-exposure induced DNA damage, cell cycle arrest and necroptosis of ovarian granulosa cells in mice by promoting ROS production
Researchers found that co-exposure to polystyrene microplastics and DEHP (a common plastic additive) caused more damage to mouse ovarian cells than either pollutant alone, triggering excessive oxidative stress that led to DNA damage, cell cycle arrest, and cell death. These findings suggest that microplastics combined with their chemical additives may pose a synergistic threat to female reproductive health.
Individual and combined effects of microplastics and diphenyl phthalate as plastic additives on male goldfish: A biochemical and physiological investigation
Male goldfish exposed to both microplastics and the plasticizer chemical DPP (diphenyl phthalate) together showed significant liver damage, disrupted fat and sugar metabolism, and hormonal imbalances including decreased testosterone and increased estrogen. The combined exposure was more harmful than either pollutant alone, demonstrating how microplastics and their chemical additives can work together to disrupt the endocrine system.
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.
Combined effect of polystyrene microplastics and cadmium on rat blood-testis barrier integrity and sperm quality
Researchers exposed male rats to polystyrene microplastics and cadmium, both separately and together, and found that both substances damaged testicular tissue, disrupted the blood-testis barrier, and reduced sperm quality. Notably, the combined exposure was less severe than cadmium alone, likely because microplastics absorbed some cadmium in the gut and reduced its bioavailability. The study also found for the first time that microplastics trigger autophagy in reproductive cells as a protective response.
The endoplasmic reticulum-mitochondrial crosstalk involved in nanoplastics and di(2-ethylhexyl) phthalate co-exposure induced the damage to mouse mammary epithelial cells
Researchers found that nanoplastics combined with DEHP, a common plastic softener, caused severe damage to mouse mammary (breast) gland cells by disrupting communication between two key cell structures: the endoplasmic reticulum and mitochondria. The combined exposure was worse than either substance alone, triggering cell death, inflammation, and oxidative stress. This is concerning because people are typically exposed to both nanoplastics and plastic additives like DEHP simultaneously through food and consumer products.
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.
Synergistic endocrine disruption and cellular toxicity of polyethylene microplastics and bisphenol A in MLTC-1 cells and zebrafish
When zebrafish and testicular cells were exposed to polyethylene microplastics and the chemical bisphenol A (BPA) together, the combination caused significantly worse reproductive harm than either pollutant alone, including reduced cell survival and disrupted hormone-producing gene activity. This matters because people are commonly exposed to both microplastics and BPA through food packaging, and their combined effect on reproductive health may be greater than expected.
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.
Chemical Cocktail: Understanding PSNP and DBP Impact on Testicular Health of Swiss albino mice
A 60-day study in male mice found that polystyrene nanoplastics and the common plasticizer di-n-butyl phthalate (DBP) each impaired sperm quality and testicular structure, but combining the two caused even greater damage — including tubular degeneration, oxidative stress, and structural lesions — than either substance alone. This suggests that real-world simultaneous exposures to nanoplastics and chemical additives they carry could pose compounded reproductive health risks.
Combined exposure of PS-MPs with NaF induces Sertoli cell death and dysfunction via ferroptosis and apoptosis
This study found that polystyrene microplastics combined with sodium fluoride caused far worse damage to testicular cells in mice than either substance alone. The combination triggered both ferroptosis (iron-dependent cell death) and apoptosis (programmed cell death) in Sertoli cells, which are essential for sperm production. Since both fluoride and microplastics are common environmental contaminants, their combined effect on male reproductive health is a growing concern.
Novel insights into male reproductive toxicity: autophagy-dependent ferroptosis triggered by polylactic acid nanoplastics and copper sulfate
Researchers exposed mice to polylactic acid nanoplastics combined with copper sulfate and found that the combination caused significant testicular damage through a process linking autophagy to ferroptosis, a form of iron-dependent cell death. The combined exposure was more damaging than either substance alone, disrupting sperm production and testicular tissue structure. The study suggests that nanoplastics from biodegradable plastics may amplify the reproductive toxicity of environmental heavy metals.
Polystyrene microplastics impair the functions of cultured mouse Leydig (TM3) and Sertoli (TM4) cells by inducing mitochondrial-endoplasmic reticulum damage
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.
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.
Polystyrene nanoplastics aggravate reproductive system damage in obese male mice by perturbation of the testis redox homeostasis
Researchers found that polystyrene nanoplastics worsened reproductive damage in male mice already fed a high-fat diet, reducing sperm quality and testosterone production beyond what obesity alone caused. The nanoplastics disrupted the protective blood-testis barrier and increased oxidative stress in reproductive tissues. The study suggests that nanoplastic exposure combined with obesity may create compounding risks to male fertility.
Combined Enterohepatic Toxicity of Polystyrene Microplastics and Di(2-ethylhexyl) Phthalate in Mice: Gut Microbiota-Dependent Synergistic Effects
Researchers investigated the combined toxicity of polystyrene microplastics and the plasticizer DEHP in mice, focusing on gut-liver axis effects. They found that co-exposure worsened harmful outcomes compared to either pollutant alone, with gut microbiota playing a key mediating role in the synergistic toxicity. The study suggests that microplastics and their associated chemical additives may interact to amplify health risks through disruption of the gut-liver connection.
Combined ecotoxicity of polystyrene microplastics and Di-(2-ethylhexyl) phthalate increase exposure risks to Mytilus coruscus based on the bioaccumulation, oxidative stress, metabolic profiles, and nutritional interferences
Researchers exposed hard-shelled mussels to a common plastic additive (DEHP) and polystyrene microplastics together, and found that the microplastics increased how much DEHP accumulated in the animals' digestive organs. The combined exposure disrupted the mussels' antioxidant defenses and altered their metabolic processes more than either pollutant alone. The study suggests that microplastics can amplify the harmful effects of chemical pollutants in marine organisms.