Lactational exposure to polystyrene nanoplastics is associated with hepatorenal alterations, oxidative stress, and apoptosis-associated changes in male rat offspring

The widespread environmental prevalence of polystyrene nanoplastics (PSNPs) poses a significant challenge to global health, particularly regarding the risks associated with early-life exposure to these pollutants. This study investigated the hepatic and renal effects of maternal lactational exposure to PSNPs on male rat offspring. Lactating dams were exposed to different concentrations of PSNPs. Male offspring were evaluated at post-weaning (PND30) and early adulthood (PND60). The evaluations included serum biochemical analyses of alanine aminotransferase, aspartate aminotransferase, urea, and creatinine, histopathological assessment, morphometric analysis, and immunohistochemical evaluation of p53 and BCL-2 immunoreactivity. Our findings revealed that lactational exposure to PSNPs was associated with structural and metabolic alterations in both the liver and kidneys. Histomorphometric analyses showed significant structural alterations, which were corroborated by histopathological observations of cellular damage. Biochemical assays showed alterations in serum markers of hepatic and renal function, as marked by elevated serum markers. The PSNP exposure was also associated with an oxidative imbalance, evidenced by increased total oxidant status and oxidative stress index levels and reduced total antioxidant capacity in hepatic and renal tissues. Immunohistochemical analysis showed increased p53 immunoreactivity and decreased BCL-2 immunoreactivity, indicating apoptosis-associated molecular alterations in hepatic and renal tissues. These deleterious effects were observed at both PND30 and PND60, with alterations in biochemical, histopathological, oxidative stress, and apoptosis-related parameters. These results suggest that lactational exposure to PSNPs is associated with hepatorenal alterations in male rat offspring, with treatment-related changes detected at both PND30 and PND60. Because only male offspring were examined, the present findings cannot be generalized to female offspring. Further studies including both sexes are warranted to determine whether sex-dependent differences influence susceptibility to PSNP-induced developmental toxicity.