Transcriptome and proteome analyses reveal the mechanisms involved in polystyrene nanoplastics disrupt spermatogenesis in mice.

Nanoplastics have been demonstrated to be reproductively toxic to mammals. However, the mechanisms of nanoplastics induce reproductive damage in mammals, especially their effects on spermatogenesis, remain elusive. Herein, we explored the effects and underlying mechanisms of polystyrene nanoplastics (PS-NPs) on the testicular development of male mice after 28 days of exposure, representing the first systematic study of PS-NPs-induced male reproductive injury by integrating histomorphology, transcriptomics and proteomics. PS-NPs decreased the sperm concentration, sperm motility, and disrupted the structure of the seminiferous tubules of the mice. Besides, transcriptome and proteome analyses revealed that PS-NPs disrupted spermatogenesis by inhibiting the transcription of Prm3 / Tnp1 / Aurkc / Mea1 / Mettl14 and the expression of Pmfbp1/Ggn/Fsip2. Furthermore, PS-NPs enabled Hsd3b5 protein expression to reduce dihydrotestosterone levels, and affected sperm flagellar assembly by decreasing the expression of Dnah8 / Tekt5 / Rsph6a. Moreover, PS-NPs induced testicular cell apoptosis by up-regulating the expression of cathepsins (B/F/H). In addition, PS-NPs destroyed tight junctions by reducing the expression of the Claudin family (3/5/15). In conclusion, PS-NPs can disrupt spermatogenesis by altering the expression patterns of transcriptome and proteome, inducing testicular cell apoptosis and destroying tight junctions. [Display omitted] • PS-NPs disrupt spermatogenesis by inhibiting the expression of Prm3/Aurkc/Pmfbp1. • PS-NPs enable Hsd3b5 protein expression to reduce dihydrotestosterone levels. • PS-NPs affect sperm flagellum by decreasing the expression of Dnah8/Tekt5 / Rsph6a. • Cathepsins (B/F/H) are involved in PS-NPs-induced testicular cell apoptosis. • PS-NPs destroy tight junction via suppressing the expression of Claudins (3/5/15). [ABSTRACT FROM AUTHOR]