Catalase expression in delayed and premature aging mouse models
Catalase expression in delayed and premature aging mouse models
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DOI：
10.1016/s0531-5565(00)00079-6
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发表时间：
2000-03-01
影响因子：
3.9
通讯作者：
Rakoczy, SG
中科院分区：
文献类型：
--
作者：
Brown-Borg, HM;Rakoczy, SG
人们认为，随着衰老而发生的生理衰退部分是由于正常代谢过程中产生的活性氧簇（ROS）产生的氧化损伤累积造成的。两种衰老的遗传小鼠模型，艾姆斯侏儒和生长激素（GH）转基因小鼠，表明激素水平可能在抗氧化防御和衰老中发挥作用。为了探索这种可能性，过氧化氢酶（CAT），一种参与消除ROS的酶，在长寿侏儒和短命转基因小鼠中进行了评估。与年龄匹配的野生型小鼠相比，3、6、13-15和24月龄侏儒小鼠肝脏中的过氧化氢酶活性和/或蛋白质显著升高。相比之下，当与野生型小鼠相比时，在3个月和10至12个月大的GH转基因小鼠中分别观察到CAT蛋白减少50%和38%（P < 0.05）。与野生型小鼠相比，老年侏儒小鼠的肾脏表现出显著增加的CAT活性（22%），蛋白质（16%）和mRNA表达（59%）。相反，GH转基因小鼠的肾脏显示CAT活性降低。这项研究的结果表明，激素状态调节抗氧化机制和CAT是重要的整体防御能力，相对于寿命在减速（侏儒）和加速（转基因）的哺乳动物模型老化。(C)2000 Elsevier Science Inc. All rights reserved.
The physiological decline that occurs with aging is thought to result, in part, from accumulation of oxidative damage produced by reactive oxygen species (ROS) generated during normal metabolism. Two genetic mouse models of aging, the Ames dwarf and growth hormone (GH) transgenic, suggest that hormone levels may play a role in antioxidative defense and aging. To explore this possibility, catalase (CAT), an enzyme involved in elimination of ROS, was evaluated in long-lived dwarf and short-lived transgenic mice. Catalase activity and/or protein was significantly elevated in livers from dwarf mice at 3, 6, 13-15, and 24 months of age when compared to age-matched wild type mice. In contrast, a 50 and 38% reduction (P < 0.05) in CAT protein was observed in 3 and 10 to 12 month old GH transgenics respectively, when compared to wild type mice. Kidneys from old dwarf mice exhibited significantly increased CAT activity (22%), protein (16%) and mRNA expression (59%) compared to wild type mice. Conversely, kidneys from GH transgenic mice showed reductions in CAT activity. The results of this study suggest that hormonal status modulates antioxidative mechanisms and that CAT is important in overall defense capacity with respect to lifespan in both decelerated (dwarf) and accelerated (transgenic) mammalian models of aging. (C) 2000 Elsevier Science Inc. All rights reserved.