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Cytokinin alleviates cypermethrin toxicity in Nostoc muscorum by involving nitric oxide: Regulation of exopolysaccharides secretion, PS II photochemistry and reactive oxygen species homeostasis.
Chemosphere ( IF 8.8 ) Pub Date : 2020-06-14 , DOI: 10.1016/j.chemosphere.2020.127356
Santwana Tiwari 1 , Nidhi Verma 1 , Sheo Mohan Prasad 1 , Vijay Pratap Singh 2
Affiliation  

Growth of the most important nitrogen fixing cyanobacterium Nostoc muscorum is reported to be badly affected by the application of insecticides. To overcome their damaging effects, several strategies are being used. Out of these, some works on kinetin (KN, a synthetic cytokinin) has been recognized that it can overcome toxicity of insecticides in cyanobacteria. Besides this, it is now known that every hormone needs certain second messengers such as nitric oxide (NO) for its action. But implication of NO in KN-mediated regulation of insecticide toxicity is yet to be investigated. Hence in the current study, we have investigated the possible involvement of NO in KN-mediated regulation of cypermethrin toxicity in the cyanobacterium Nostoc muscorum. Cypermethrin decreased growth of Nostoc muscorum which was accompanied by decreased pigment contents and altered photosystem II (PS II) photochemistry that resulted in inhibition of photosynthetic process but KN significantly ameliorated cypermethrin toxicity. Cypermethrin induced production of free radicals (in-vivo and in-vitro) and weakened defensive mechanism (enzymatic and non-enzymatic defense system) which was restored by KN. Further, the results revealed that NG-nitro-l-arginine methyl ester (l-NAME, an inhibitor of nitric oxide synthase) worsened the effect of cypermethrin toxicity even in the presence of KN while 2-4-carboxyphenyl-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (c-PTIO, a scavenger of NO) reversed KN-mediated amelioration even in the presence of sodium nitroprusside (SNP, an NO donor), suggesting that endogenous NO is required for mitigation of cypermethrin toxicity. Overall, our results first time show that endogenous NO is essential for KN-mediated mitigation of cypermethrin toxicity in the Nostoc muscorum.



中文翻译:

细胞分裂素通过参与一氧化氮减轻Nostoc粘液中的氯氰菊酯毒性:调节胞外多糖分泌,PS II光化学和活性氧稳态。

据报道,最重要的固氮蓝藻黏菌的生长受到杀虫剂施用的严重影响。为了克服它们的破坏作用,正在使用几种策略。其中,一些关于激动素(KN,一种合成的细胞分裂素)的研究被认为可以克服杀虫剂在蓝细菌中的毒性。除此之外,现在知道每种激素都需要某些第二信使,例如一氧化氮(NO)才能发挥作用。但是,NO在KN介导的杀虫剂毒性调节中的意义尚待研究。因此,在当前的研究中,我们研究了NO可能参与了KN介导的氯氰菊酯对粘菌蓝藻中氯氰菊酯毒性的调节。氯氰菊酯的生长下降伴有色素含量降低和光系统II(PS II)光化学改变的Nostoc muscorum导致光合作用受到抑制,但KN显着改善了氯氰菊酯的毒性。氯氰菊酯诱导自由基的产生(体内体外),并削弱了防御机制(酶和非酶防御系统),该防御机制被KN恢复。此外,结果表明,NG硝基精氨酸甲酯(-NAME,一氧化氮合酶的抑制剂)即使在存在KN的情况下,氯氰菊酯的毒性也会恶化,而2-4-羧基苯基-4,4,5,5-四甲基咪唑啉-1-氧基-3-氧化物(c-PTIO ,即使在存在硝普钠(SNP,NO供体)的情况下,NO的清除剂也可以逆转KN介导的改善,这表明减轻氯氰菊酯毒性需要内源性NO。总体而言,我们的结果首次表明,内源性NO对于KN介导的Nostoc粘液中氯氰菊酯毒性的缓解至关重要

更新日期:2020-07-08
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