Peroxisomes are highly dynamic intracellular organelles involved in a variety of metabolic functions essential for the metabolism of long-chain fatty acids, d-amino acids, and many polyamines. A byproduct of peroxisomal metabolism is the generation, and subsequent detoxification, of reactive oxygen and nitrogen species, particularly hydrogen peroxide (H₂O₂). Because of its relatively low reactivity (as a mild oxidant), H₂O₂ has a comparatively long intracellular half-life and a high diffusion rate, all of which makes H₂O₂ an efficient signaling molecule. Peroxisomes also have intricate connections to mitochondria, and both organelles appear to play important roles in regulating redox signaling pathways. Peroxisomal proteins are also subject to oxidative modification and inactivation by the reactive oxygen and nitrogen species they generate, but the peroxisomal LonP2 protease can selectively remove such oxidatively damaged proteins, thus prolonging the useful lifespan of the organelle. Peroxisomal homeostasis must adapt to the metabolic state of the cell, by a combination of peroxisome proliferation, the removal of excess or badly damaged organelles by autophagy (pexophagy), as well as by processes of peroxisome inheritance and motility. More recently the tumor suppressors ataxia telangiectasia mutate (ATM) and tuberous sclerosis complex (TSC), which regulate mTORC1 signaling, have been found to regulate pexophagy in response to variable levels of certain reactive oxygen and nitrogen species. It is now clear that any significant loss of peroxisome homeostasis can have devastating physiological consequences. Peroxisome dysregulation has been implicated in several metabolic diseases, and increasing evidence highlights the important role of diminished peroxisomal functions in aging processes.

中文翻译：

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过氧化物酶体中稳态和蛋白稳态的氧化还原调节

过氧化物酶体是高度动态的细胞内细胞器，参与长链脂肪酸，d-氨基酸和许多多胺代谢所必需的各种代谢功能。过氧化物酶体代谢的副产物是活性氧和氮物种，特别是过氧化氢（H ₂ O ₂）的产生和随后的排毒。由于H ₂ O _2的反应性较低（作为弱氧化剂），因此具有较长的细胞内半衰期和较高的扩散速率，所有这些都使H ₂ O ₂一个有效的信号分子。过氧化物酶体与线粒体也有复杂的联系，两个细胞器似乎在调节氧化还原信号通路中都起着重要作用。过氧化物酶体蛋白还受到它们产生的反应性氧和氮物种的氧化修饰和失活，但是过氧化物酶体LonP2蛋白酶可以选择性地去除这种氧化损伤的蛋白，从而延长了细胞器的使用寿命。过氧化物酶体稳态必须通过过氧化物酶体增殖，通过自噬（pexophagy）去除过量或严重受损的细胞器以及过氧化物酶体遗传和运动的过程来适应细胞的代谢状态。最近，抑癌性共济失调毛细血管扩张症（ATM）和结节性硬化症（TSC），已经发现，调节mTORC1信号转导的蛋白可调节exexophagy，以响应某些活性氧和氮物质的可变水平。现在清楚的是，过氧化物酶体内平衡的任何重大损失都可能带来毁灭性的生理后果。过氧化物酶体失调与多种代谢性疾病有关，越来越多的证据凸显了过氧化物酶体功能减弱在衰老过程中的重要作用。