Search

Microplastics and pesticides are identified as two environmental pollutants that have an adverse impact on the environment. The knowledge about the combined exposure of pesticides and microplastics may facilitate further assessment of their ecotoxicity. In this study, we investigated joint effects of microplastic and dufulin on bioaccumulation, oxidative stress and metabolic profile of the earthworm. Bioaccumulation analysis showed that the bio-soil accumulation factor of dufulin in earthworms reached its maximum value on the 14th day, and microplastics could significantly increase the bioaccumulation of dufulin in earthworms. Biochemical analysis showed that the oxidative damage of earthworms could be observed on the 14th day of the exposure to dufulin, while the oxidative damage of earthworms could be observed on the 7th day of the combined exposure to microplastics and dufulin, and it could still be observed on the 14th day. 1H-NMR-based metabolomics revealed that the exposure of dufulin significantly altered the relative abundances of 14 metabolites and two metabolic pathways, but the combined exposure of dufulin and microplastics significantly changed the relative abundances of 21 metabolites and three metabolic pathways. It could be seen that microplastics could aggravate the oxidative damage and the interference with the metabolic profile caused by dufulin to earthworms. The results of this study could provide effective information for the risk assessment of dufulin and microplastic in environmental safety.

The widespread application of bisphenols (BPs) makes them ubiquitous in the natural environment and poses many potential risks. In this study, we examined the effects of perinatal exposure to BPA and its 3 alternatives (BPS, BPF, and BPAF) on lipid and glucose homeostasis in female mice adolescent offspring. Specifically, BPA exposure promoted the expression of hepatic lipid synthesis and fatty acid accumulation genes, resulting in a significant increase in 2 free fatty acids contents. BPS exposure caused an increase in 6 free fatty acids and triglyceride contents through promoting the expression of fatty acid synthesis, triglyceride synthesis and fatty acid accumulation genes and inhibiting the expression of fatty acid β-oxidation genes. Interestingly, BPAF exposure showed completely opposite effects on hepatic lipid metabolism compared to BPS exposure. 9 free fatty acids and triglycerides contents in the liver were significantly reduced. In particular, BPF exposure caused decreases in 2 free fatty acids contents, but no significant changes were found in the genes for lipid metabolism. In addition, unlike BPA and BPF exposure, BPS and BPAF exposure also resulted in significant increases in glucose and glycogen contents in the liver by activation of Fxr-Shp pathway and glycolysis, and inhibition of gluconeogenesis. The results showed that compared to BPA and BPF exposure, BPS and BPAF exposure significantly regulated the expression of genes related to glucose and lipid metabolism and severely interfered with hepatic lipid and glucose homeostasis. This suggested that we should thoroughly evaluate the potential health risks of BPA and its alternatives.

In this study, we used a 1H NMR based metabolomics strategy combined with gene expression analysis to determine the combined effects of gestational exposure of mice to BPA (10 μg/kg body weight by subcutaneous injection) and arsenic (10 ppb sodium arsenite in drinking water). Results showed that exposure to either BPA or, arsenic or their combination induced age-dependent metabolic disruptions in male mice offspring, and the combined exposure could exacerbate the metabolic changes induced by either BPA or arsenic alone. Moreover, this combined exposure influenced both glucose tolerance and insulin tolerance in mice, along with changing the expression of genes involved in lipid and glucose homeostasis. Specifically, the combined exposure to BPA and arsenic promoted the uptake of glucose and fatty acid from serum to liver, and genes involved in glycogenesis, glucogenesis, and fatty acid oxidation were activated in the liver in the combined exposure group. Taken together, these experimental results highlight the importance of considering the combined toxicity of environmental pollutants at levels relevant to human exposure, especially during the early life stages of mammals.

Neonicotinoids are increasingly being used for pest control, and their potential health risks are now receiving attention. In this study, the toxic effects of three neonicotinoids (dinotefuran, nitenpyram and acetamiprid) were evaluated in ICR mice. After 30 days of exposure to neonicotinoids (1/200 LD50), oxidative stress levels, biochemical parameters, free fatty acids contents, and 1H NMR-based hepatic metabolomics were tested. All treatment groups showed signs of amino acid metabolism disorders especially elevated branched chain amino acids and phenylalanine. Furthermore, animals exposed to neonicotinoids had elevated lipid levels, which induced oxidative stress. Overall, we found that oxidative stress is a common toxic effect of exposure to neonicotinoids. In addition, lipid accumulation induced by amino acid metabolism disorder may be the cause of oxidative stress. Our results further our understanding of the toxicological effects of neonicotinoids on mammals.

Ubiquitous exposure to the neonicotinoid insecticide nitenpyram has raised concerns about its potential toxicity. In this study, we explored its health effects on the female offspring of mice that had been exposed during pregnancy. We found that exposure of pregnant mice to nitenpyram resulted in decreased levels of serum triglycerides, total cholesterol, and glucose in female offspring, and additional research uncovered gut microbiota disturbances, accompanied by abnormal fecal metabolic profiles. Based on Pearson correlation analysis, we found that decreased abundance of Lactobacillus may play the most critical role, and changes in gut bacterial purine metabolism, BCAAs metabolism, and the TCA cycle are all closely related to the abundance of Lactobacillus. In summary, these results help explain the observed serum biochemical abnormalities and provide new insights into the intergenerational toxicity of nitenpyram.

Hexaconazole and epoxiconazole are the worldwidely used fungicides. However, limited information is known about the toxicological effects of their enantiomers on aquatic organisms. In this study, zebrafish were separately exposed to 100 and 1000 μgL−1 hexaconazole and epoxiconazole enantiomers for 21 d 1H NMR-based metabolomics analysis showed that the exposure of low and high dose of hexaconazole enantiomers altered energy metabolism, lipid metabolism and amino acid metabolism of zebrafish, with the different metabolic profiles resulted from the same dose of (+)-hexaconazole and (−)-hexaconazole. Similar to hexaconazole enantiomers, the metabolic profiles, including the changes related to energy metabolism, lipid metabolism and amino acid metabolism, were demonstrated in low and high dose epoxiconazole enantiomers treatment groups. There are differences in the metabolic profiles of zebrafish between exposed to (+)-epoxiconazole and (−)-epoxiconazole of the same dose. The results of histological examination revealed that the exposure of both enantiomers for hexaconazole and epoxiconazole resulted in the similar histopathological changes. The exposure of hexaconazole and epoxiconazole enantiomers at low and high dose resulted the vacuolization and swell in the liver of the female and male zebrafish. Compared to female zebrafish, more liver damage was found in male zebrafish in the hexaconazole enantiomers exposure groups. The reduction of spermatids was observed in hexaconazole and epoxiconazole enantiomers treatment groups of both doses. Hexaconazole enantiomers exposure of low and high dose resulted the increase in the number of mature eggs, while such effect was not observed in epoxiconazole enantiomers exposure groups. Hexaconazole and epoxiconazole enantiomers exposure resulted in no changes in brains of female and male zebrafish. As a result, both triazole-based chiral bactericides, hexaconazole and epoxiconazole, have similar toxicological effects but their mechanisms of action are not exactly the same. The above results will play an important part in making the differences in toxic effects of hexaconazole and epoxiconazole enantiomers clear. What's more, it is an indispensable part for an integrated environmental risk assessment.