Pereira M D, Herdeiro R S, Fernandes P N, Eleutherio E C A, Panek A D
Departamento de Bioquímica, Instituto de Química, UFRJ, 21949-900 Rio de Janeiro, Brazil.
Biochim Biophys Acta. 2003 Mar 17;1620(1-3):245-51. doi: 10.1016/s0304-4165(03)00003-5.
Eukaryotic cells have developed mechanisms to rapidly respond towards the environment by changing the expression of a series of genes. There is increasing evidence that reactive oxygen species (ROS), besides causing damage, may also fulfill an important role as second messengers involved in signal transduction. Recently, we have demonstrated that deletion of SOD1 is beneficial for the acquisition of tolerance towards heat and ethanol stresses. The present report demonstrates that a sod1 mutant was the only one capable of acquiring tolerance against a subsequent stress produced by menadione, although this mutant strain had exhibited high sensitivity to oxidative stress. By measuring the level of intracellular oxidation, lipid peroxidation as well as glutathione metabolism, we have shown that in the SOD1-deleted strain, an unbalance occurs in the cell redox status. These results indicated that the capacity of acquiring tolerance to oxidative stress is related to a signal given by one or all of the above factors.
真核细胞已发展出通过改变一系列基因的表达来快速响应环境的机制。越来越多的证据表明,活性氧(ROS)除了会造成损伤外,还可能作为参与信号转导的第二信使发挥重要作用。最近,我们已经证明,超氧化物歧化酶1(SOD1)的缺失有利于获得对热应激和乙醇应激的耐受性。本报告表明,sod1突变体是唯一能够获得对甲萘醌产生的后续应激的耐受性的突变体,尽管该突变菌株对氧化应激表现出高敏感性。通过测量细胞内氧化水平、脂质过氧化以及谷胱甘肽代谢,我们发现,在缺失SOD1的菌株中,细胞氧化还原状态出现失衡。这些结果表明,获得氧化应激耐受性的能力与上述一种或所有因素发出的信号有关。