Enhanced hepatic metabolic perturbation of polystyrene nanoplastics by UV irradiation-induced hydroxyl radical generation

The environmental behavior of and risks associated with nanoplastics(NPs)have attracted considerable attention.However,compared to pristine NPs,environmental factors such as ultraviolet(UV)irradiation that lead to changes in the toxicity of NPs have rarely been studied.We evaluated the changes in morphology and physicochemical properties of polystyrene(PS)NPs before and after UV irradiation,and compared their hepatotoxicity in mice.The results showed that UV irradiation caused particle size reduction and increased the carbonyl index(CI)and negative charge on the particle surface.UV-aged PS NPs(aPS NPs)could induce the generation of hydroxyl radicals(·OH),but also further promoted the generation of·OH in the Fenton reaction system.Hepatic pathological damage was more severe in mice exposed to aPS NPs,accompanied by a large number of vacuoles and hepatocyte balloon-like changes and more marked perturbations in blood glucose and serum lipoprotein,alanine aminotransferase and aspartate aminotransferase levels.In addition,exposure to PS NPs and aPS NPs,especially aPS NPs,triggered oxidative stress and significantly damaged the antioxidant capacity of mice liver.Compared with PS NPs,exposure to aPS NPs increased the number of altered metabolites in hepatic and corresponding metabolic pathways,especially glutathione metabolism.Our research suggests that UV irradiation can disrupt the redox balance in organisms by promoting the production of·OH,enhancing PS NPs-induced liver damage and metabolic disorders.This study will help us understand the health risks of NPs and to avoid underestimation of the risks of NPs in nature.

An insight into aggregation kinetics of polystyrene nanoplastics interaction with metal cations

Once inevitably released into the aquatic environment,polystyrene nanoplastics(PS-NPs)will present complicated environmental behaviors,of which the aggregation is a key process determining their environmental fate and impact.In this study,the aggregation kinetics of different sizes(30 nm and 100 nm)of PS-NPs with metal cations(Na^(+),K^(+),Ca^(2+),Mg^(2+)and Pb^(2+))at different solution pH(3,6 and 8)were investigated.The results showed that the aggregation of PS-NPs increased with cation concentration.Taking Pb^(2+)as an example,the adsorption behavior of cations onto PS-NPs was determined by transmission electron microscopy(TEM)and energy dispersive X-ray(EDX)spectroscopy,which demonstrated Pb^(2+)could be adhered onto the surface of PS-NPs with the effect of charge neutralization.The critical coagulation concentrations(CCC)of smaller PS-NPs were higher than that of larger PS-NPs for monovalent cations,whereas a different pattern is observed for divalent cations.It was suggested that there were other factors that DLVO theory does not consider affect the stability of NPs with different particle sizes.In addition,it should be noted that PS-NPs had the capacity of adsorbing large amounts of heavy metal cations and carried them transport to a long distance,and the corresponding ecological risks need to further elucidate.

Polystyrene nanoplastic exposure actives ferroptosis by oxidative stress-induced lipid peroxidation in porcine oocytes during maturation

Background Polystyrene nanoplastics(PS-NPs)are becoming increasingly prevalent in the environment with great advancements in plastic products,and their potential health hazard to animals has received much attention.Several studies have reported the toxicity of PS-NPs to various tissues and cells;however,there is a paucity of information about whether PS-NPs exposure can have toxic effects on mammalian oocytes,especially livestock.Herein,porcine oocytes were used as the model to investigate the potential effects of PS-NPs on mammalian oocytes.Results The findings showed that different concentrations of PS-NPs(0,25,50 and 100μg/m L)entering into porcine oocytes could induce mitochondrial stress,including a significant decrease in mitochondrial membrane potential(MMP),and the destruction of the balance of mitochondrial dynamic and micromorphology.Furthermore,there was a marked increase in reactive oxygen species(ROS),which led to oocyte lipid peroxidation(LPO).PS-NPs exposure induced abnormal intracellular iron overload,and subsequently increased the expression of transferrin receptor(TfRC),solute carrier family 7 member 11(SLC7a11),and acyl-CoA synthetase long-chain family member 4(ACSL4),which resulted in ferroptosis in oocytes.PS-NPs also indu ced oocyte maturation failure,cytoskeletal dysfunction and DNA damage.Cotreatment with 5μmol/L ferrostatin-1(Fer-1,an inhibitor of ferroptosis)alleviated the cellular toxicity associated with PS-NPs exposure during porcine oocyte maturation.Conclusions In conclusion,PS-NPs caused ferroptosis in porcine oocytes by increasing oxidative stress and altering lipid metabolism,leading to the failure of oocyte maturation.