الفهرس 
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Abstract
Humans are presently living in an era of plastics due to the acceleration of industrialization. Concerns about nanoplastics (NPs) are growing regarding their widespread distribution in the environment and harmful impacts on human health. However, little is known about whether and how polystyrene nanoplastics (PS-NPs) impact male fertility in mammals. Therefore, this study was conducted to evaluate the adverse effects of PS-NPs on reproductive capacity and progeny outcomes in male albino rats as a mammalian model.
This study first evaluated the median lethal dose (LD50) of PS-NPs in male rats, and then in the formal study, 24 male rats were divided into three groups (n = 8): group I, the control group, received distilled water; group II and group III received PS-NPs at doses of 3 mg/kg bw (equivalent to 1/833 LD50) and 10 mg/kg bw (equivalent to 1/250 LD50), respectively. All doses were administered by oral gavage daily for 60 days. The fertility test was conducted by cohabiting an untreated sexually mature female separately with a treated male (1:1) overnight for mating.
The study indicated that the LD50 of PS-NPs was determined to be 2500 mg/kg. PS-NPs administration induced significant alternations, mainly indicating mortality in the high-dose group and a significant elevation in body weight gain over the 8-week exposure period in both treated groups, with no significant effects on testis or epididymis weights. Moreover, PS-NPs administration altered sperm quality and quantity parameters, as evidenced by a significant decline in sperm count, motility, progression, viability, and the total number of normal sperm, coupled with a significant elevation in sperm morphological abnormalities. Furthermore, PS-NPs-induced endocrine disruption was indicated by reducing serum reproductive hormonal levels, as evidenced by a significant decline in luteinizing hormone (LH) and testosterone
(T) and altering serum thyroid hormonal activity, as indicated by
elevated thyroid stimulating hormone (TSH) activity and declined free circulating thyroid hormonal levels [free triiodothyronine (FT3) and free thyroxine (FT4)]. Furthermore, testicular homogenate analysis revealed that PS-NPs induced oxidative stress in a dose-dependent manner, as evidenced by a significant elevation in malondialdehyde (MDA) content coupled with a significant decline in concentrations of total antioxidant capacity (TAC) and superoxide dismutase (SOD) and an elevation in catalase (CAT) activity. The comet assay results indicated high levels of DNA damage in testicular tissues, confirming the genotoxic impact of PS-NPs, as indicated by a significant decrease in the percentage of DNA in the head, coupled by a significant increase in the percentage of DNA in the tail, tail length, tail moment, and olive moment. Histological examination of the testicular tissues of PS-NPs-treated rats showed a degenerative appearance and a morphometric change of the seminiferous tubules in a dose-dependent manner. Examination of pregnancy outcomes of paternally treated PS-NPs-fetuses showed an increase in the pre- and post-implantation loss indices, a decrease in the litter size, and a reduction in the fetal body weight and length. Moreover, various types of morphological and skeletal abnormalities were observed.
Altogether, the present findings provide novel perspectives on PS- NPs general toxicity with specific reference to male reproductive toxicity and fertility. Therefore, limitations should be set in PS-NPs usage in modern society regarding their long half-life in natural environments and toxicity on general health, especially reproductive health.