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首页> 外文期刊>Comparative biochemistry and physiology. Toxicology & pharmacology: CBP >Diphenyl diselenide dietary supplementation protects against methylmercury-chloride-induced immunotoxicity in the head kidney and spleen of grass carp (Ctenopharyngodon idella) via regulation of purinergic signaling and the NLRP3 inflammasome
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Diphenyl diselenide dietary supplementation protects against methylmercury-chloride-induced immunotoxicity in the head kidney and spleen of grass carp (Ctenopharyngodon idella) via regulation of purinergic signaling and the NLRP3 inflammasome

机译:通过调节嘌呤能信号传导和NLRP3炎症,二苯基二烯酯膳食补充剂可保护甲基汞 - 氯化物诱导的草鲤(Ctenopharyncodon idella)的脾脏(Ctenopharyncodon idella)中的免疫毒性

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摘要

This study aimed to evaluate whether dietary supplementation with diphenyl diselenide (Ph2Se2) would prevent the impaired immune and inflammatory responses elicited by methylmercury chloride (CH3HgCl) via protective effects on purinergic signaling in fish immune organs. Tissue and lymphocytic nucleoside triphosphate diphosphohydrolase (NTPDase) activity for adenosine triphosphate (ATP) and adenosine diphosphate (ADP) was downregulated in the head kidney and spleen of grass carp (Ctenopharyngodon idella) exposed to CH3HgCl. Concomitantly, adenosine deaminase (ADA) activity was upregulated. Further, nucleotide-binding oligomerization domain-like receptor (NLRP3) inflammasome gene expression was upregulated in the spleen and head kidney of CH3HgCl-exposed grass carp. Dietary supplementation with Ph2Se2 ameliorated these CH3HgCl-mediated alterations on purinergic enzymes, and their activities returned to baseline levels (except NTPDase activity for ADP). Based on these results, purinergic signaling in immune organs and lymphocytes can be considered a pathway linked to pro-inflammatory effects during exposure to environmental CH3HgCl concentrations, which may contribute to mortality of the affected fish. Since dietary supplementation with 3 mg Ph2Se2/kg in the feed prevented the CH3HgCl-induced alterations, it can be considered a potential suitable treatment to prevent impaired immune and inflammatory responses caused by Hg.
机译:本研究旨在评估与二苯基(PH2Se2)的膳食补充剂是否会通过对鱼类免疫器官中嘌呤能信号传导的保护作用,通过对甲基汞(CH3HGCL)引发的免疫和炎症反应进行饮食。腺苷三磷酸三磷酸(ATP)和腺苷二磷酸(ADP)中的组织和淋巴细胞核苷酶(NTPDASE)活性在暴露于CH3HCC中的草鲤(Ctenopharyncodon idella)中的头肾和脾脏中下调。同时,上调腺苷脱胺酶(ADA)活性。此外,在CH3HCCL暴露的草鲤的脾脏和头肾上,上调核苷酸结合的寡聚化结构域样受体(NLRP3)炎症组基因表达。用pH2Se2进行膳食补充剂可改善这些CH3HGCL介导的嘌呤能酶的改变,其活性恢复到基线水平(除了ADP的NTPDase活性除外)。基于这些结果,免疫器官和淋巴细胞中的嘌呤能信号传导可以被认为是在暴露于环境CH 3 HCL浓度期间与促炎作用有关的途径,这可能导致受影响鱼的死亡率。由于饲料中的膳食补充剂,以防止CH3HGCL诱导的改变,因此可以认为是预防HG引起的免疫和炎症反应的潜在合适的处理。

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