Hydrolysis of propyrisulfuron in water: Kinetics, influence of 34 environmental factors, transformation products identification, mechanisms and toxicities.

Propyrisulfuron is a novel sulfonylurea herbicide used for controlling annual grass and broad-leaved weeds in fields, but its fates and behaviors in environment are still unknown, which are of utmost importance for environmental protection. To reduce its potential environmental risks in agricultural production, the hydrolysis kinetics, influence of 34 environmental factors including 12 microplastics (MPs), disposable face masks (DFMs) and its different parts, 6 fertilizers, 5 ions, 3 surfactants, a co-existed herbicide of florpyrauxifen-benzy, humic acid and biochar, and the effect of MPs and DFMs on its hydrolysis mechanisms were systematically investigated. The main hydrolysis products (HPs), possible mechanisms, toxicities and potential risks to aquatic organisms were studied. Propyrisulfuron hydrolysis was an acid catalytic pyrolysis, endothermic and spontaneous process driven by the reduction of activation enthalpy, and followed the first-order kinetics. All environmental factors can accelerate propyrisulfuron hydrolysis to varying degrees except humic acid, and different hydrolysis mechanisms occurred in the presence of MPs and DFMs. In addition, 10 possible HPs and 7 possible mechanisms were identified and proposed. ECOSAR prediction and ecotoxicity testing showed that acute toxicity of propyrisulfuron and its HPs for aquatic organisms were low, but may have high chronic toxicity and pose a potential threat to aquatic ecosystems. The investigations are significantly important for elucidating the environmental fates and behaviors of propyrisulfuron, assessing the risks in environmental protection, and further providing guidance for scientific application in agro-ecosystem.

Molybdenum and/or cadmium induce NLRP3 inflammasome production by causing mitochondria-associated endoplasmic reticulum membrane dysfunction in sheep hepatocytes.

Accumulation of the heavy metals molybdenum (Mo) and cadmium (Cd) in the liver can induce organelle damage and inflammation, resulting in hepatotoxicity. The effect of Mo and/or Cd on sheep hepatocytes was investigated by determining the relationship between the mitochondria-associated endoplasmic reticulum membrane (MAM) and NLRP3 inflammasome. Sheep hepatocytes were divided into four groups: the control group, Mo group (600 µM Mo), Cd group (4 µM Cd) and Mo + Cd group (600 µM Mo+4 µM Cd). The results showed that Mo and/or Cd exposure increased the levels of lactate dehydrogenase (LDH) and nitric oxide (NO) in the cell culture supernatant, elevated the levels of intracellular Ca2+ and mitochondrial Ca2+, downregulated the expression of MAM-related factors (IP3R, GRP75, VDAC1, PERK, ERO1-α, Mfn1, Mfn2, ERP44), shortened the length of the MAM and reduced the formation of the MAM structure, eventually causing MAM dysfunction. Moreover, the expression levels of NLRP3 inflammasome-related factors (NLRP3, Caspase1, IL-1ß, IL-6, TNF-α) were also dramatically increased after Mo and Cd exposure, triggering NLRP3 inflammasome production. However, an IP3R inhibitor, 2-APB treatment significantly alleviated these changes. Overall, the data indicate that Mo and Cd coexposure leads to structural disruption and dysfunction of MAM, disrupts cellular Ca2+ homeostasis, and increases NLRP3 inflammasome production in sheep hepatocytes. However, the inhibition of IP3R alleviates NLRP3 inflammasome production induced by Mo and Cd.

Crosstalk between Mfn2-mediated mitochondria associated membranes disorder and autophagy induced by molybdenum and cadmium in sheep heart.

To investigate the crosstalk of mitochondria associated membranes (MAMs) disorder and autophagy co-induced by molybdenum (Mo) and cadmium (Cd) in sheep hearts. A total of 48 sheep were randomly divided into 4 groups: control group, Mo group, Cd group and Mo + Cd group. The intragastric administration lasted for 50 days. The results showed that Mo or/and Cd exposure could cause morphological damage, imbalance of trace elements and antioxidant function, Ca2+ concentration decreased markedly, and significantly increase the contents of Mo or/and Cd in myocardium. Additionally, the mRNA and protein levels of endoplasmic reticulum stress (ERS) related factors and mitochondrial biogenesis related factors were altered by Mo or/and Cd, as well as the content of ATP, inducing ERS and mitochondrial dysfunction. Meanwhile, Mo or/and Cd could lead to the alteration of expression level of MAMs-related genes and proteins, and the distance between mitochondria and endoplasmic reticulum (ER), resulting in MAMs disorder. Moreover, Mo or/and Cd exposure upregulated the mRNA and protein levels of autophagy related factors. In conclusion, our results revealed that Mo or/and Cd exposure caused ERS, mitochondrial dysfunction and structural MAMs disruption, ultimately leading to autophagy in sheep hearts, and the effects of Mo and Cd co-exposure were more obvious.