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The simultaneous administration of microplastics and cadmium alters rat testicular activity and changes the expression of PTMA, DAAM1 and PREP
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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.
This paper confirms the damaging effects produced by MP and Cd on testicular activity in the rat. Oral treatment with both chemicals resulted in testicular damage, documented by biomolecular and histological alterations, particularly by impaired morphometric parameters, increased apoptosis, reduced testosterone synthesis, and downregulation of the steroidogenic enzyme 3β-HSD. We also demonstrated, for the first time, that both MP and Cd can affect the protein level of PTMA, a small peptide that regulates germ cell proliferation and differentiation. Interestingly, the cytoarchitecture of testicular cells was also altered by the treatments, as evidenced by the impaired expression and localization of DAAM1 and PREP, two proteins involved in actin- and microtubule-associated processes, respectively, during germ cells differentiation into spermatozoa, impairing normal spermatogenesis. Finally, we showed that the effect of simultaneous treatment with MP and Cd were more severe than those produced by MP alone and less harmful than those of Cd alone. This could be due to the different ways of exposure of the two substances to rats (in drinking water for Cd and in oral gavage for MP), since being the first contact in the animals' gastrointestinal tract, MP can adsorb Cd, reducing its bioavailability through the Trojan-horse effect.
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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.
Microplastics and Cadmium Co-Exposure Impairs Testicular Function via A Trojan Horse Mechanism: Protective Role of D-Aspartate
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In rats, exposure to microplastics and cadmium together damaged testicular tissue, lowered sperm quality and testosterone, and disrupted barriers protecting developing sperm cells, with combined exposure worse than microplastics alone. Rats also given D-aspartate showed reduced cell damage and oxidative stress, along with changes in proteins linked to sperm production.
Synergistic effect of PS-MPs and Cd on male reproductive toxicity: Ferroptosis via Keap1-Nrf2 pathway
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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.
The single and combined effects of decabromodiphenyl ethane and mixed microplastics on male mice reproductive toxicity
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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.
Prenatal microplastic exposure-induced testicular developmental toxicity and its long-term hazards in male rat offspring.
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Pregnant rats were given microplastics during pregnancy, and their male offspring had lower birth weights, smaller testicles, reduced testosterone and luteinizing hormone levels, fewer hormone-producing Leydig cells, and changes in sperm, effects that persisted from birth into adulthood.
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