Storey K B
Department of Biology, Carleton University, Ottawa, Ontario, Canada.
Comp Biochem Physiol B Biochem Mol Biol. 1996 Jan;113(1):23-35. doi: 10.1016/0305-0491(95)02043-8.
Animal survival during severe hypoxia and/or anoxia is enhanced by a variety of biochemical adaptations including adaptations of fermentative pathways of energy production and, most importantly, the ability to sharply reduce metabolic rate by 5-20 fold and enter a hypometabolic state. The biochemical regulation of metabolic arrest is proving to have common molecular principles that extend across phylogenetic lines and that are conserved in different types of arrested states (not only anaerobiosis but also estivation, hibernation, etc.). Our new studies with anoxia-tolerant vertebrates have identified a variety of regulatory mechanisms involved in both metabolic rate depression and in the aerobic recovery process using as models the freshwater turtle Trachemys scripta elegans and garter snakes Thamnophis sirtalis parietalis. Mechanisms include: 1) post-translational modification of cellular and functional proteins by reversible phosphorylation and changes in protein kinase (PKA, PKC) and/or phosphatase activities to regulate this, 2) reversible enzyme binding associations with subcellular structural elements, 3) differential gene expression and/or mRNA translation producing new mRNA variants and new protein products, 4) changes in protease activity, particularly the multicatalytic proteinase complex, and 5) both constitutive and anoxia-induced modifications to cellular antioxidant systems to deal with oxidative stress during the anoxic-aerobic transition of recovery.
多种生化适应机制可增强动物在严重缺氧和/或无氧环境下的生存能力,这些机制包括能量产生的发酵途径的适应,最重要的是,能够将代谢率急剧降低5至20倍并进入低代谢状态。事实证明,代谢停滞的生化调节具有共同的分子原理,这些原理跨越了系统发育谱系,并且在不同类型的停滞状态(不仅是无氧状态,还包括夏眠、冬眠等)中保守存在。我们对耐缺氧脊椎动物的新研究已经确定了多种参与代谢率降低和有氧恢复过程的调节机制,我们以淡水龟丽纹彩龟和东部袜带蛇为模型进行研究。这些机制包括:1)通过可逆磷酸化对细胞和功能蛋白进行翻译后修饰,并改变蛋白激酶(PKA、PKC)和/或磷酸酶的活性来调节这一过程;2)酶与亚细胞结构元件的可逆结合关联;3)差异基因表达和/或mRNA翻译产生新的mRNA变体和新的蛋白质产物;4)蛋白酶活性的变化,特别是多催化蛋白酶复合体;5)对细胞抗氧化系统的组成性和缺氧诱导性修饰,以应对恢复过程中缺氧-有氧转变期间的氧化应激。