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Basophils and Mast Cells in COVID-19 Pathogenesis.
The occurrence and spatial distribution of polybrominated diphenyl ethers (PBDEs) and novel brominated flame retardants (NBFRs) in seawater and surficial sediment samples (N = 19 and 45, respectively) from the South China Sea (SCS) in 2018 were investigated, and the correlation between BFRs and site parameters (total organic carbon, depth, etc.) were assessed by principal component analysis. The concentration ranges of ΣPBDEs in seawater and sediments were 0.90-4.40 ng/L and 0.52-22.67 ng/g dry weight (dw), respectively, while those of ΣNBFRs were 0.49-37.42 ng/L and 0.78-82.29 ng/g dw, respectively. BDE-209 and decabromodiphenyl ethane were the predominant BFRs, accounting for 38.65% and 36.94% in seawater and 26.71% and 68.42% in sediments, respectively. Notably, tris(2,3-dibromopropyl)isocyanurate and 2,4,6-tris(2,4,6-tribromophenoxy)-1,3,5-triazine, seldomly detected in aquatic matrices worldwide, were detected for the first time in the study area, and their relatively high levels and detection frequencies indicate the ubiquitous application of these NBFRs in the Pearl River Delta. Zhuhai and Jiangmen are the main sources of NBFRs in the SCS. Preliminary risk assessment on NBFRs using hazard quotient indicates low to medium risks to marine organisms at some sites. The occurrence of NBFRs in the SCS highlights the prioritization of more toxicological information on these compounds.It is highly likely that the toxicity of water accommodated fractions (WAF) will influence marine microalgae, and consequently lead to potential risk for the marine ecological environment. However, it was often neglected whether WAF can influence the transformation of relative compounds in organisms. The metabolism of amino acids (AAs) can be used to track physiological changes in microalgae because amino acids are the basis of proteins and enzymes. In this study, using marine Chlorophyta Platymonas helgolandica as the test organism, the effects of different concentrations of WAF on AA compositions and stable carbon isotope ratios (δ13C) of individual AAs of Platymonas helgolandica were investigated. The results showed that the WAF of #180 fuel oil had an obvious suppressing effect on the growth and chlorophyll a content of microalgae. The growth inhibitory rate at 96 h was 80.66% at a WAF concentration of 0.50 mg L-1 compared with the control. Furthermore, seven among the 16 AAs, including alanine, cysteine, proline, aspartic acid, lysine, histidine and tyrosine, had relatively high abundance. Under the glycolysis pathway, the cysteine abundance was higher than control, meaning that the biosynthesized pathway of alanine through cysteine as a precursor could be damaged. Phosphoenolpyruvate (PEP) was an important synthesis precursor of alanine (leucine) and aromatic AA family (Phenylalanine and tyrosine), and played an important role in δ13CAAs fractionation under the WAF stress. Under the TCA pathway, to protect cell metabolism activities under WAF stress, the δ13C value of threonine and proline abundance in microalgae with the increase in WAF stress. Therefore, δ13CAAs fractionation can be used as a novel method for toxicity evaluation of WAF on future.The mosquito Aedes aegypti is a primary vector for major arboviruses, and its control is mainly based on the use of insecticides. Caffeine and spent coffee grounds (CG) are potential agents in controlling Ae. aegypti by reducing survival and blocking larval development. In this study, we analyzed the effects of treatment with common CG (CCG with caffeine), decaffeinated CG (DCG with low caffeine), and pure caffeine on the survival, behavior, and morphology of the midgut of Ae. aegypti under laboratory conditions. Third instar larvae (L3) were exposed to different concentrations of CCG, DCG, and caffeine. All compounds significantly affected larval survival, and sublethal concentrations reduced larval locomotor activity, delayed development, and reduced adult life span. Damage to the midgut of treated larvae included changes in epithelial morphology, increased number of peroxidase-positive cells (more abundant in DCG-treated larvae), and caspase 3-positive cells (more abundant in CCG-treated larvae), suggesting that the treatments triggered cell damage, leading to activation of cell death. In addition, the treatments reduced the FMRFamide-positive enteroendocrine cells and dividing cells compared to the control. CG and caffeine have larvicidal effects on Ae. aegypti that warrant field testing for their potential to control mosquitoes.Inorganic arsenic, an environmental contaminant, has adverse health outcomes. Our previous studies showed that arsenic causes abnormal cardiac development in zebrafish embryos by downregulating Dvr1/GDF1 expression and that folic acid protects against these effects. this website However, the mechanism by which arsenic represses Dvr1/GDF1 expression remains unknown. Herein, we demonstrate that specificity protein 1 (Sp1) acts as a transcriptional activator of GDF1. Arsenic treatment downregulated Sp1 at both the mRNA and protein level and its downstream targets GDF1 and SIRT1. Chromatin immunoprecipitation analysis showed that the occupancy of Sp1 on the GDF1 or SIRT1 promoter was significantly reduced in response to arsenite. Further investigation showed that Sp1 overexpression inhibited the arsenic-mediated decrease in GDF1 and SIRT1, while Sp1 knockdown had the opposite effect. We found that expression of the oxidative adaptor p66shc was inversely related to that of SIRT1 and that the binding of SIRT1 to the p66shc promoter was sharply attenuated by arsenite treatment. SIRT1 overexpression attenuated p66shc expression but enhanced GDF1 protein expression, while SIRT1 depletion exerted the opposite effect. Both the antioxidants N-acetylcysteine and folic acid reversed the arsenic-mediated repression of Sp1, GDF1 and SIRT1. Moreover, wild-type p66shc overexpression enhanced the arsenic-mediated repression of Sp1, GDF1 and SIRT1, which was accompanied by an increase in intracellular reactive oxygen species (ROS) levels, while both overexpression of a dominant negative p66shcSer36Ala mutant and deficiency in p66shc reversed these effects. Taken together, our results revealed that arsenic suppresses GDF1 expression via the ROS-dependent downregulation of the Sp1/SIRT1 axis, which forms a negative feedback loop with p66shc to regulate oxidative stress. Our findings reveal a novel molecular mechanism underlying arsenic toxicity and provide new insight into the protective effect of folic acid in arsenic-mediated toxicity.
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