Ranjan Plant Physiology and Biochemistry Laboratory, Department of Botany, University of Allahabad, Prayagraj, 211002, India.
Ranjan Plant Physiology and Biochemistry Laboratory, Department of Botany, University of Allahabad, Prayagraj, 211002, India.
Chemosphere. 2020 Nov;259:127356. doi: 10.1016/j.chemosphere.2020.127356. Epub 2020 Jun 14.
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.
据报道，应用杀虫剂会严重影响最重要的固氮蓝藻 Nostoc muscorum 的生长。为了克服它们的破坏性影响，正在使用几种策略。其中一些关于激动素 (KN，一种合成细胞分裂素) 的工作已被认识到，它可以克服杀虫剂对蓝藻的毒性。除此之外，现在已知每种激素都需要某些第二信使，如一氧化氮 (NO) 来发挥作用。但是，NO 在 KN 介导的杀虫剂毒性调节中的作用仍有待研究。因此，在当前的研究中，我们研究了 NO 在 KN 介导的 Nostoc muscorum 中环丙甲氧基菊酯毒性调节中的可能作用。拟除虫菊酯降低了 Nostoc muscorum 的生长，同时伴随着色素含量的降低和光系统 II (PS II) 光合作用的改变，导致光合作用过程受到抑制，但 KN 显著改善了拟除虫菊酯的毒性。拟除虫菊酯诱导自由基的产生（体内和体外），削弱了防御机制（酶和非酶防御系统），而 KN 则恢复了这些机制。此外，结果表明，NG-硝基-L-精氨酸甲酯（l-NAME，一氧化氮合酶抑制剂）即使在 KN 存在的情况下也会加重拟除虫菊酯毒性的影响，而 2-4-羧基苯基-4,4,5,5-四甲基恶唑啉-1-氧-3-氧化物（c-PTIO，NO 清除剂）即使在硝普钠（SNP，NO 供体）存在的情况下，也逆转了 KN 介导的改善作用，表明内源性 NO 是减轻拟除虫菊酯毒性所必需的。总的来说，我们的研究结果首次表明，内源性 NO 是 KN 介导的 Nostoc muscorum 中环丙甲氧基菊酯毒性缓解所必需的。
