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Purinergic signalling as a potential pathway for trichlorfon induced-inflammation and impairment of the immune response using freshwater silver catfish

机译:用淡水银鲶鱼称为Trichlorfon诱导炎症和免疫应答损伤的嘌呤能信号传导

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Adenosine triphosphate (ATP) and adenosine (Ado) are the main molecules of the purinergic signalling involved in toxicological mechanisms induced by pesticides. These molecules participate in the regulation of immune and inflammatory responses due to their interaction with purinereceptors in the extracellular medium. In the literature, the ATP and Ado are related with pro-inflammatory and immunomodulatory effects, respectively. Thus, the aim of this study was to evaluate whether the purinergic signalling can be considered a potential target for trichlorfon-induced inflammation and impairment of the immune response. Seric and splenic triphosphate diphosphohydrolase (NTPDase) activities using ATP as substrate were reduced at 22 mg/L after 48 h of exposure compared to the control group, while NTPDase activity using ADP as substrate was lower only in the serum of silver catfish at the same period. On the other hand, seric and splenic adenosine deaminase (ADA) activities and metabolites of nitric oxide (NOx) levels were increased at 22 mg/L after 48 h of exposure compared to the control group. The enzymatic activity of the purinergic signalling did not return to control levels after 48 h of recovery period in trichlorfon-free water. Based on these evidences, we concluded that trichlorfon interferes with the purinergic signalling, causing impairment of the immune and inflammatory responses by reducing ATP hydrolyses, possible leading to its accumulation in the extracellular environment. In addition, there is an increase in Ado desamination and possible reduction of it in the extracellular medium, leading to a self-sustained pro-inflammatory deleterious cycle. In summary, the purinergic signalling can be considered a potential target for trichlorfon-induced inflammation and impairment of the immune response in freshwater silver catfish at exposure to 22 mg/L.
机译:腺苷三磷酸(ATP)和腺苷(ADO)是杀虫剂诱导的毒理学机制涉及的嘌呤能信号传导的主要分子。这些分子由于它们与细胞外培养基中的嘌呤受体的相互作用而参与免疫和炎症反应的调节。在文献中,ATP和ADO分别与促炎和免疫调节效果有关。因此,本研究的目的是评估嘌呤能信号传导是否可以被认为是Trichlorfon诱导的炎症和免疫应答损伤的潜在目标。与对照组48小时后,使用ATP作为底物的SeriC和脾三磷酸二磷酸二磷酸二磷酸二磷酶(NTPDase)活性在22mg / L下降,而使用ADP作为底物的NTPDase活性仅在银鲶鱼的血清中较低时期。另一方面,与对照组相比,在48小时后,丝状和脾腺苷脱胺酶(ADA)活酶(ADA)活性和一氧化氮(NOx)水平的含量(NOx)水平升高。纯化信号传导的酶活性在无氯氟烃水中的回收期48小时后没有恢复到对照水平。基于这些证据,我们得出结论,Trichlorfon干扰了嘌呤能信号传导,通过减少ATP水解产生免疫和炎症反应的损害,可能导致其在细胞外环境中的积累。此外,在细胞外培养基中,ADO脱析和可能还原它的增加,导致自我持续的促炎性有害循环。总之,嘌呤能信号传导可以被认为是Trichlorfon诱导的炎症的潜在目标,并且在暴露于22 mg / L时在淡水银鲶中的免疫应答的损伤。

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