Assessing the impact of sub-chronic polyethylene terephthalate nanoplastic exposure on male reproductive health in mice.

Abstract

The widespread use of polyethylene terephthalate (PET) in food and beverage packaging raises concerns about its potential health effects, particularly when PET-derived nanoplastics (PET-NPs) are released into the environment. This study investigates the reproductive toxicity of PET-NPs in male mice. Mice were exposed to PET-NPs at doses of 0.1 mg/day and 0.5 mg/day for 28 days, and the testes index, sperm count, sperm morphology, Reactive Oxygen Species (ROS) production, DNA integrity, histopathology, and spermatogenesis were evaluated. PET-NP exposure resulted in a significant decrease in sperm concentration and an increase in abnormal spermatozoa-particularly blunt-headed sperm and sperm with neck and tail anomalies- and elevated ROS levels in testicular tissue in a dose-dependent manner (p < 0.05). Additionally, PET-NPs induced DNA strand breaks, as demonstrated by the COMET assay (p < 0.05). Histopathological analysis revealed disorganization of the germinal epithelium, vacuolization, reduced sperm density, and increased interstitial spaces, accompanied by a significant decline in spermatogenic activity, as assessed by Johnsen scoring. These findings strongly suggest that the observed adverse effects on male reproductive health, including sperm abnormalities, DNA damage, and impaired spermatogenesis, are primarily driven by ROS-induced oxidative stress. The observed changes provide clear evidence of the adverse effects of subchronic exposure to PET nanoplastics on male reproductive health, highlighting the inherent risks associated with nanoplastic exposure and offering crucial insights for public health awareness and regulatory considerations.