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MCA is a halogen-free flame retardant. It can cause damage to other tissues such as the kidneys and liver. [https://www.selleckchem.com/products/erastin.html selleck chemicals llc] However, the effects on the circadian rhythm and thyroid in adult mice have not been studied. In this article, adult male mice received MCA at concentrations of 0, 10, 20, 30 mg/kg. The results showed that the time spending on wheel-running and rest bouts changed in different period after MCA exposure. link2 MCA disrupted the T3 and T4 hormone homeostasis and decreased the expression of thyroid hormone synthesis genes. The histological morphology of the thyroid gland was damaged. It was suggested that MCA exposure caused circadian rhythm disorder and thyroid dysfunction.Disruption of cholinergic neurotransmission can affect cognition, but little is known about whether low-to-moderate fluoride exposure affects cholinergic system and its effect on the prevalence of dental fluorosis (DF) and intelligence quotient (IQ). A cross-sectional study was conducted to explore the associations of moderate fluoride exposure and cholinergic system in relation to children's DF and IQ. We recruited 709 resident children in Tianjin, China. Ion selective electrode method was used to detect fluoride concentrations in water and urine. Cholinergic system was assessed by the detection of choline acetyltransferase (ChAT), acetylcholinesterase (AChE) and acetylcholine (ACh) levels in serum. Compared with children in the first quartile, those in fourth quartile the risk of either developing DF or IQ less then 120 increased by 19% and 20% for water and urinary fluoride. The risk of having both increased by 58% and 62% in third and fourth quartile for water fluoride, 52% and 65% for urinary fluoride. Water fluoride concentrations were positively associated with AChE and negatively associated with ChAT and ACh, trends were same for urinary fluoride except for ACh. The risk of either developing DF or having non-high intelligence rose by 22% (95%CI 1.07%, 1.38%) for the fourth quartile than those in the first quartile of AChE, for having the both, the risk was 1.27 (95%CI 1.07, 1.50), 1.37 (95%CI 1.17, 1.62) and 1.44 (95%CI 1.23, 1.68) in second, third and fourth quartiles. The mediation proportion by AChE between water fluoride and either developing DF or IQ less then 120 was 15.7%. For both to exist, the proportion was 6.7% and 7.2% for water and urinary fluoride. Our findings suggest low-to-moderate fluoride exposure was associated with dysfunction of cholinergic system for children. AChE may partly mediate the prevalence of DF and lower probability of having superior and above intelligence.Although rivers are one of the dominant pathways by which microplastics reach the oceans, reports on remote rivers are rare. Dafeng River is located in Guangxi Province, China, is an important water source and a habitat of a coastal dolphin, Sousa chinensis, which is a first-class national protected animal in China. In this study, we determined the distribution and characteristics of microplastics in the surface water, sediment, and fish of the river. During the dry and rainy seasons, the microplastics content of the surface water ranged from 3 × 10-4-2.5 × 10-3 items/L (7 × 10-4-0.12 items/m2) and 4 × 10-5-9 × 10-4 items/L (2 × 10-3-2.8 × 10-2 items/m2), while those in the sediment samples ranged from 9.4 to 50.3 items/kg (dry weight) and 0.0-21.3 items/kg, respectively. The pollution level during the dry season was approximately two to three times higher than that during the rainy season (P surface water in terms of items/kg. The level of microplastics pollution in the Dafeng River was relatively low; however, that in aquatic organisms was more severe. Our work highlights the requirement for concern towards microplastics pollution in the organisms of remote rivers.Hydrological management of the Three Gorges Dam has resulted in the interception of heavy metals in the Three Gorges Reservoir (TGR). However, the exposure to heavy metals and health risks among local residents remained poorly understood. Here we collected 208 biomarker samples (hair) and 20 food species from typical regions in the TGR to assess the exposure levels of three toxic metals (Cr, Pb and As) in residents of the TGR, and subsequently investigated their health risk via dietary intake. Results indicated that hair Cr and As levels were below the reference value for normal people and threshold of skin lesions, respectively, whereas about 22% hair Pb exceeded the reference for clinical medicine, indicating a potential Pb exposure of local residents. Smoking habit and fish consumption were found to be predictors for hair Pb. In addition, the concentrations of heavy metals in all investigated food samples were below the limits of contaminants in food in China, except for Pb in the sweet potato and fish. The estimated daily intake of metals (DIMs) revealed that the intakes of Cr and As from studied food were under the recommended thresholds of Cr and As. However, the intake of Pb via diet exceeded the limit of the prevalence of chronic kidney disease and closed to the threshold for cardiovascular, which was probably associated with the high Pb concentrations of fish and sweet potato. Overall, residents around the TGR were at low exposure to Cr and As, but Pb exposure may need more attention.Bixafen, a pyrazole-carboxamide fungicide, is a potent toxicant that may elicit multiple adverse effects in non-target organisms. However, knowledge of the mechanisms involved in developmental defects caused by bixafen in aquatic organisms remains limited. In this study, the effects of bixafen on retinal development were evaluated in embryo-larval zebrafish. We exposed zebrafish embryos to 0, 0.1, and 0.3 μM bixafen. Exposure of zebrafish embryos to bixafen caused severe retinal defects, including extreme microphthalmia and a significantly increased cell density of the ganglion cell layer (GCL). Compared with the controls, the expression levels of rod and cone photoreceptor marker genes (rho, opn1sw2, opn1mw1, opn1lw1, and opn1sw1) in the outer nuclear layer (ONL) were significantly downregulated after bixafen exposure. Furthermore, bixafen caused significantly increased expression levels in the GCL marker ath5 and decreased expression levels in the inner nuclear layer (INL) markers prox1a, vsx1, and sox2. Accordingly, we observed a significantly increased rate of cell apoptosis in the retina after bixafen exposure. Taken together, our data demonstrate that bixafen exhibits retinal developmental toxicity to zebrafish embryos/larvae, and thus, it may pose a significant environmental threat to aquatic organisms.Acute exposure to cadmium (Cd) causes vacuolar degeneration in buffalo rat liver 3 A (BRL 3 A) cells. The present study aimed to determine the relationship between Cd-induced microtubule damage and intracellular vacuolar degeneration. Western blotting results showed that Cd damaged the microtubule network and downregulated the expression of microtubule-associated proteins-kinesin-1 heavy chain (KIF5B), γ-tubulin, and acetylated α-tubulin in BRL 3 A cells. Immunofluorescence staining revealed that Cd inhibited interactions between α-tubulin and microtubule-associated protein 4 (MAP4) as well as KIF5B. Increasing Cd concentrations decreased the levels of the lipid kinase, PIKfyve, which regulates the activity of endosome-lysosome fission. Immunofluorescence and transmission electron microscopy revealed vacuole-like organelles that were late endosomes and lysosomes. The PIKfyve inhibitor, YM201636, and the microtubule depolymerizer, nocodazole, aggravated Cd-induced endosome-lysosome enlargement. Knocking down the kif5b gene that encodes KIF5B intensified the enlargement of endosome-lysosomes and expression of early endosome antigen 1 (EEA1), Ras-related protein Rab-7a (RAB7), and lysosome-associated membrane glycoprotein 2 (LAMP2). Nocodazole, YM201636, and the knockdown of kif5b blocked autophagic flux. We concluded that Cd-induced damage to the microtubule network is the main reason for endosome-lysosome enlargement and autophagic flux blockage in BRL 3 A cells, and kinesin-1 plays a critical role in this process.Selenium (Se) is a beneficial trace element for certain animals including humans, while remaining controversial for plants. High Se concentration in soil is toxic to plants especially at seedling stage of the plants. Although, arbuscular mycorrhizal fungi (AMF) are important for plant stress resistance; but the mechanisms by which AMF alleviate Se stress in crop seedlings are unclear. Therefore, we investigated the potential strategies of AMF symbiosis to alleviate Se stress in maize (Zea mays) from plants and soil perspectives. Results showed that Se stress (Se application level &gt; 5 mg kg-1) significantly inhibited leaf area, shoot dry weight, and root dry weight of maize (P less then 0.05). In contrast, AM symbiosis significantly improved root morphology, increased nitrogen and phosphorus nutrition, promoted shoot growth, inhibited the transport of Se from soil/roots to shoots, and then diluted the concentration of Se in shoots (32.65-52.80%). In general, the response of maize growth to AMF was mainly observed in shoots rather than roots. In addition, AMF inoculation significantly increased the easily extractable glomalin-related soil protein and organic matter contents and decreased the availability of soil Se to the plant. Principal component analysis showed that AMF promoted growth and nutrition uptake of maize was the most dominant effect of Se stress alleviation, followed by the decrease of soil Se availability, limiting Se transport from soil/roots to shoots. Moreover, the expression of Se uptake-related ion transporter genes (ZmPht2, ZmNIP2;1, and ZmSultr1;3) in maize roots were down-regulated upon AM symbiosis which resultantly inhibited the uptake and transport of Se from soil to maize roots. Thus, AMF could impede Se stress in maize seedlings by improving plant and soil characteristics.Di(2-ethylhexyl) phthalate (DEHP) is a ubiquitous pollutant that results in hepatotoxicity. link3 However, an understanding of the systematic mechanism of hepatic injury caused by DEHP remains limited. Here, we performed a comprehensive metabolomics and transcriptomics analyses to describe hepatic responses of rats to long-term DEHP exposure and, together with pathology and functional injury of liver, systematically analyzed the pathogenesis and mechanisms of liver damage. SD rats were exposed to 0 and 600 mg/kg/day DEHP for 12 weeks. Thereafter, biochemical indicators and histopathological changes regarding liver function were detected. Metabolomics and transcriptomics profiles of rat liver samples were analyzed using a UPLC-MS/MS system and Illumina Hiseq 4000, respectively. DEHP induced hepatocyte structural alterations and edema, depressed monooxygenase activity, decreased antioxidant activities, aggravated oxidative damage, blocked the tricarboxylic acid cycle and respiratory chain, and disturbed glucose homeostasis in the liver. These findings indicate that reactive oxygen species play a major role in these events. Overall, this study systematically depicts the comprehensive mechanisms of long-term DEHP exposure to liver injury and highlights the power of metabolomics and transcriptomics platforms in the mechanistic understanding of xenobiotic hepatotoxicity.