Exposure to nanoplastics induces mitochondrial impairment and cytomembrane destruction in Leydig cells.

Plastic particle pollution poses an emerging threat to ecological and human health. Laboratory animal studies have illustrated that nano-sized plastics can accumulate in the testis and cause testosterone deficiency and spermatogenic impairment. In this study, TM3 mouse Leydig cells were in vitro exposed to polystyrene nanoparticles (PS-NPs, size 20 nm) at dosages of 50, 100 and 150 µg/mL to investigate their cytotoxicity. Our results demonstrated that PS-NPs can be internalized into TM3 Leydig cells and led to a concentration-dependent decline in cell viability. Furthermore, PS-NPs stimulation amplified ROS generation and initiated cellular oxidative stress and apoptosis. Moreover, PS-NPs treatment affected the mitochondrial DNA copy number and collapsed the mitochondrial membrane potential, accompanied by a disrupted energy metabolism. The cells exposed to PS-NPs also displayed a down-regulated expression of steroidogenesis-related genes StAR, P450scc and 17ß-HSD, along with a decrease in testosterone secretion. In addition, treatment with PS-NPs destructed plasma membrane integrity, as presented by increase in lactate dehydrogenase release and depolarization of cell membrane potential. In summary, these data indicated that exposure to PS-NPs in vitro produced cytotoxic effect on Leydig cells by inducing oxidative injury, mitochondrial impairment, apoptosis, and cytomembrane destruction. Our results provide new insights into male reproductive toxicity caused by NPs.

Maternal exposure to polystyrene nanoplastics during gestation and lactation induces hepatic and testicular toxicity in male mouse offspring.

Nanoplastics have raised considerable concerns since their ubiquity in the environment and potential hazard to health. It has been proven that polystyrene nanoparticles (PS-NPs) can be maternally transferred to the offspring. In this study, mice were exposed gestationally and lactationally to PS-NPs (size 100 nm) at different doses (0.1, 1 and 10 mg/L) to investigate the trans-generational poisonousness. Our data illustrated that maternal PS-NPs exposure in pregnancy and lactation resulted in a decline in birth and postnatal body weight in offspring mice. Furthermore, high-dose PS-NPs reduced liver weight, triggered oxidative stress, caused inflammatory cell infiltration, up-regulated proinflammatory cytokine expression, and disturbed glycometabolism in the liver of male offspring mice. In addition, pre- and postnatal PS-NPs exposure diminished testis weight, disrupted seminiferous epithelium and decreased sperm count in mouse offspring. Moreover, PS-NPs induced testicular oxidative injury, as presented by increased malondialdehyde generation and altered superoxide dismutase and catalase activities in the testis of offspring mice. These findings declared that maternal exposure to PS-NPs in pregnancy and lactation can cause hepatic and testicular toxicity in male mouse pups, which put forward new understanding into the detrimental effects of nanoplastics on mammalian offspring.