Enantioselective bioaccumulation and toxicological effects of chiral neonicotinoid sulfoxaflor in rats.

Sulfoxaflor is a widely used fourth-generation neonicotinoid pesticide, which has been detected in biological and environmental samples. Sulfoxaflor can potentially be exposed to humans via the food chain, thus understanding its toxic effects and enantioselective bioaccumulation is crucial. In this study, toxicokinetics, bioaccumulation, tissue distribution and enantiomeric profiles of sulfoxaflor in rats were investigated through single oral exposure and 28-days continuous exposure experiment. Sulfoxaflor mainly accumulated in liver and kidney, and the (-)-2R,3R-sulfoxaflor and (-)-2S,3R-sulfoxaflor had higher enrichment than their enantiomers in rats. The toxicological effects were evaluated after 28-days exposure. Slight inflammation in liver and kidney were observed by histopathology. Sphingolipid, amino acid, and vitamin B6 metabolism pathways were significantly disturbed in metabonomics analysis. These toxicities were in compliance with dose-dependent effects. These results improve understanding of enantioselective bioaccumulation and the potential health risk of sulfoxaflor.

Multifaceted Effects of Subchronic Exposure to Chlorfenapyr in Mice: Implications from Serum Metabolomics, Hepatic Oxidative Stress, and Intestinal Homeostasis.

As chlorfenapyr is a commonly used insecticide in agriculture, the health risks of subchronic exposure to chlorfenapyr remained unclear. This study aimed to extensively probe the health risks from subchronic exposure to chlorfenapyr at the NOAEL and 10-fold NOAEL dose in mice. Through pathological and biochemical examinations, the body metabolism, hepatic toxicity, and intestinal homeostasis were systematically assessed. After 12 weeks, a 10-fold NOAEL dose of chlorfenapyr resulted in weight reduction, increased daily food intake, and blood lipid abnormalities. Concurrently, this dosage induced hepatotoxicity and amplified oxidative stress in hepatocytes, a finding further supported in HepG2 cells. Moreover, chlorfenapyr resulted in intestinal inflammation, evidenced by increased inflammatory factors (IL-17a, IL-10, IL-1ß, IL-6, IL-22), disrupted immune cells (RORγt, Foxp3), and compromised intestinal barriers (ZO-1 and occludin). By contrast, the NOAEL dose presented less toxicity in most evaluations. Serum metabolomic analyses unveiled widespread disruptions in pathways related to hepatotoxicity and intestinal inflammation, including NF-κB signaling, Th cell differentiation, and bile acid metabolism. Microbiomic analysis showed an increase in Lactobacillus, a decrease in Muribaculaceae, and diminished anti-inflammatory microbes, which further propelled the inflammatory response and leaded to intestinal inflammation. These findings revealed the molecular mechanisms underlying chlorfenapyr-induced hepatotoxicity and intestinal inflammation, highlighting the significant role of the gut microbiota.

Influence of co-exposure to sulfamethazine on the toxicity and bioaccumulation kinetics of chlorpyrifos in zebrafish (Danio rerio).

Pesticides and antibiotics are frequently present in aquatic environment which may pose potential risks to aquatic organisms. However, the interaction of pesticides and antibiotics in co-exposure model remains unclear. Here, the effects of the co-exposure of sulfamethazine (SMZ) on the toxicity and bioaccumulation of the organophosphorus insecticide chlorpyrifos (CPF) in zebrafish (Danio rerio) were explored. The 96-h LC50 of chlorpyrifos to zebrafish was 1.36 mg/L and sulfamethazine at 1 mg/L slightly increased the acute toxicity with the 96-h LC50 of 1.20 mg/L which was not significant. The 30-day co-exposure of chlorpyrifos with sulfamethazine at 1 mg/L aggravated the oxidative stress, decreased CarE and AChE activity, and increased CYP450 activity significantly. Furthermore, the co-exposure reduced the accumulation of chlorpyrifos and sulfamethazine while prolonged their depuration duration. The results demonstrated the exposure risk of chlorpyrifos to zebrafish may be enhanced in the presence of sulfamethazine.

The toxic effects of combined exposure of chlorpyrifos and p, p'-DDE to zebrafish (Danio rerio) and tissue bioaccumulation.

Pesticides are widely used and frequently detected in the environment. The evaluation on the toxic effects of the co-exposure of two or more pesticides or related metabolites could reflect the real situation of the exposing risks. In this study, zebrafish was used as a model to investigate the potential toxic interactions of chlorpyrifos and 1,1-dichloro-2,2-bis(p-chlorophenyl)ethylene (p,p'-DDE) on the survival rate, oxidative stress response and neurotoxicity, as well as their bioaccumulation and distribution in tissues. Co-exposure of chlorpyrifos and p,p'-DDE resulted in significant additive acute toxic effects on adult zebrafish with model deviation ratio (MDR) = 1.64. Both 7-day short-term at 1% LC50 and 35-day long-term at 0.5% LC50 co-exposure of chlorpyrifos with p,p'-DDE (50 and 100 µg/L) significantly reduced the survival rate of zebrafish colony to 75 and 82.5%. Co-exposure of chlorpyrifos and p,p'-DDE contributed to increased activity of antioxidant enzyme CAT, SOD and GST and excessive MDA generation, and decreased activity of CarE, CYP450 and AChE, compared with either single exposure of them. In co-exposure, the bioaccumulation of chlorpyrifos and p,p'-DDE was significantly different from the single exposure group. Overall, this study unraveled the potential toxic interaction of chlorpyrifos and p,p'-DDE on zebrafish and provided reference for environmental risk assessment of pesticide mixture.

Photolysis of N-chlorourea and its effect on urea removal in a combined pre-chlorination and UV254 process.

Urea is one of the most important nitrogenous organic pollutants in water, and its removal attracts attention because of a growing concern related to water eutrophication. Urea has previously been considered to be largely unaffected by the UV-chlorine process. However, N-chlorourea, an intermediate of urea chlorination, has been shown to absorb ultraviolet radiation, and as such its photolysis is possible. Experiments were conducted to quantify the kinetics of N-chlorourea degradation under UV254 irradiation. The results showed that about 92% of N-chlorourea was degraded under UV254 irradiation. Ammonia and nitrate were detected as the primary nitrogen containing products of the photolysis of N-chlorourea. Solution pH ranging from 3.0 to 7.5 influenced the distribution of these products but not on the degradation rate. Based on these data, a possible pathway of photodegradation of N-chlorourea under UV254 is proposed. The degradation of urea was also achieved by the photolysis of N-chlorourea during the combined pre-chlorination and UV254 process. Insights gained in this study may be useful for exploring the potential of combined pre-chlorination and UV254 process on urea removal in water treatment.