Polystyrene nanoplastics (PS-NPs), a pervasive component of plastic pollution, have emerged as a significant environmental and health threat due to their microscopic size and bioaccumulative properties. This review systematically explores the biological effects and mechanisms of PS-NPs on cellular systems, encompassing oxidative stress, mitochondrial dysfunction, DNA damage, inflammation, and disruptions in autophagy. Notably, PS-NPs induce multiple forms of cell death, including apoptosis, ferroptosis, necroptosis, and pyroptosis, mediated through distinct yet interconnected molecular pathways. The review also highlights various factors that influence the cytotoxicity of PS-NPs, such as particle size, surface modifications, co-exposure with other pollutants, and protein corona formation. These complex interactions underscore the extensive and potentially hazardous impacts of PS-NPs on cellular health. The findings presented here emphasize the need for continued research on the mechanisms underlying PS-NP toxicity and the development of effective strategies for mitigating their effects, thereby informing regulatory frameworks aimed at minimizing environmental and biological risks.

Bisphenol A (BPA), a widespread environmental contaminant used in plastics and resins, poses significant health risks due to its endocrine-disrupting properties and potential for inducing intestinal toxicity. This study explored the toxicological effects of BPA on the small intestine of rats, focusing on the duodenum, jejunum, and ileum. Histopathological evaluation revealed that the duodenum experienced the most severe structural damage, including villous atrophy, epithelial shedding, and mitochondrial degeneration. BPA exposure disrupted oxidative stress homeostasis by reducing superoxide dismutase activity and increasing malondialdehyde levels, along with upregulating antioxidant-related genes like GPX2 and HO-1 upregulated, indicating lipid peroxidation and oxidative damage. Inflammatory markers such as IL-1 and NFκB were significantly upregulated, highlighting an active inflammatory response and epithelial cell apoptosis. BPA also altered lipid metabolism, with increased expression of lipogenic genes such as SREBP-1c and FAS, indicating metabolic dysregulation. Fecal microbiota analysis revealed reduced α-diversity, enrichment of pathogenic taxa like Escherichia-Shigella, and depletion of beneficial genera such as Lachnospiraceae NK4A136 group, exacerbating gut inflammation and barrier dysfunction. These findings suggest that BPA-induced small intestinal damage is driven by oxidative stress, inflammation, and gut dysbiosis, with the duodenum and jejunum being the more vulnerable segments.

Background: We have looked at antimony (Sb) as a new neurotoxin which causes neuronal apoptosis in animal studies. At the population level, however, there is no direct evidence for a relationship between Sb exposure and cognitive performance. Method: The study comprehensively assessed the correlation between urinary antimony levels and cognitive test scores in 631 creatinine-corrected older persons using data from the National Health and Nutrition Examination Survey (NHANES) from 2011 to 2014. Results: Using logistic regression, the study looked at the prevalence of cognitive impairment at different levels of urine antimony concentrations and found that, after controlling for covariates, higher doses of urinary antimony were positively associated with cognitive function compared to controls, odds ratio (ORs) with 95% confidence interval (CI) were 0.409 (0.185–0.906) and 0.402 (0.186–0.871) respectively. Restricted cubic spline curves showed a non-linear and dose-specific correlation between urinary antimony and cognitive performance, with lower doses associated with better cognitive performance, while higher doses may be associated with cognitive impairment. Conclusions: Our data provide evidence for a correlation between Sb and cognitive function at the population level, although the specific mechanisms need to be investigated further.