Survival and adaptation to oxidative stress is important for many organisms, and these occur through the activation of many different signaling pathways. In this report, we showed that Caenorhabditis (C.) elegans G protein–coupled receptor kinases modified the ability of the organism to resist oxidative stress. In acute oxidative stress studies using juglone, loss-of-function grk-2 mutants were more resistant to oxidative stress compared with loss-of-function grk-1 mutants and the wild-type N2 animals. This effect was Ce-AKT-1 dependent, suggesting that Ce-GRK2 adjusted C. elegans oxidative stress resistance through the IGF/insulin-like signaling (IIS) pathway. Treating C. elegans with a GRK2 inhibitor, the selective serotonin reuptake inhibitor paroxetine, resulted in increased acute oxidative stress resistance compared with another selective serotonin reuptake inhibitor, fluoxetine. In chronic oxidative stress studies with paraquat, both grk-1 and grk-2 mutants had longer lifespan compared with the wild-type N2 animals in stress. In summary, this research showed the importance of both GRKs, especially GRK2, in modifying oxidative stress resistance.

氧化应激的生存和适应对许多生物来说很重要，这些通过激活许多不同的信号通路而发生。在这份报告中，我们展示了秀丽隐杆线虫( C. )线虫G 蛋白偶联受体激酶改变了生物体抵抗氧化应激的能力。在使用胡桃的急性氧化应激研究中，与功能丧失的grk-1突变体和野生型 N2 动物相比，功能丧失的grk-2突变体对氧化应激的抵抗力更强。这种效果是CE- AKT-1依赖性，表明铈-GRK2调节秀丽隐杆线虫通过 IGF/胰岛素样信号 (IIS) 通路增强抗氧化应激。与另一种选择性血清素再摄取抑制剂氟西汀相比，用 GRK2 抑制剂（选择性血清素再摄取抑制剂帕罗西汀）治疗线虫导致急性氧化应激抵抗力增加。在使用百草枯的慢性氧化应激研究中，与处于应激状态的野生型 N2 动物相比，grk-1和grk-2突变体的寿命更长。总之，这项研究显示了两种 GRK，尤其是 GRK2，在改变氧化应激抗性方面的重要性。