• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

氧化应激与人类疾病和衰老:分子机制与展望。

Oxidative Stress in Human Pathology and Aging: Molecular Mechanisms and Perspectives.

机构信息

Department of Biosciences, Division Zoology, Career Point University, Hamirpur 176041, India.

Toxicology and Pharmocology Laboratory, Department of Zoology, School of Biosciences and Biotechnology, Baba Ghulam Shah Badshah University, Rajouri 185234, India.

出版信息

Cells. 2022 Feb 5;11(3):552. doi: 10.3390/cells11030552.

DOI:10.3390/cells11030552
PMID:35159361
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8833991/
Abstract

Reactive oxygen and nitrogen species (RONS) are generated through various endogenous and exogenous processes; however, they are neutralized by enzymatic and non-enzymatic antioxidants. An imbalance between the generation and neutralization of oxidants results in the progression to oxidative stress (OS), which in turn gives rise to various diseases, disorders and aging. The characteristics of aging include the progressive loss of function in tissues and organs. The theory of aging explains that age-related functional losses are due to accumulation of reactive oxygen species (ROS), their subsequent damages and tissue deformities. Moreover, the diseases and disorders caused by OS include cardiovascular diseases [CVDs], chronic obstructive pulmonary disease, chronic kidney disease, neurodegenerative diseases and cancer. OS, induced by ROS, is neutralized by different enzymatic and non-enzymatic antioxidants and prevents cells, tissues and organs from damage. However, prolonged OS decreases the content of antioxidant status of cells by reducing the activities of reductants and antioxidative enzymes and gives rise to different pathological conditions. Therefore, the aim of the present review is to discuss the mechanism of ROS-induced OS signaling and their age-associated complications mediated through their toxic manifestations in order to devise effective preventive and curative natural therapeutic remedies.

摘要

活性氧和氮物种(RONS)通过各种内源性和外源性过程产生;然而,它们被酶和非酶抗氧化剂中和。氧化剂的产生和中和之间的失衡导致氧化应激(OS)的发展,进而导致各种疾病、障碍和衰老。衰老的特征包括组织和器官功能的逐渐丧失。衰老理论解释说,与年龄相关的功能丧失是由于活性氧(ROS)的积累,以及它们随后的损伤和组织畸形。此外,由 OS 引起的疾病和障碍包括心血管疾病[CVDs]、慢性阻塞性肺疾病、慢性肾脏病、神经退行性疾病和癌症。ROS 诱导的 OS 由不同的酶和非酶抗氧化剂中和,防止细胞、组织和器官受损。然而,长期的 OS 通过降低还原剂和抗氧化酶的活性来降低细胞抗氧化状态的含量,从而导致不同的病理状况。因此,本综述的目的是讨论 ROS 诱导的 OS 信号转导及其与年龄相关的并发症的机制,这些并发症通过其在毒性表现中介导,以设计有效的预防和治疗性天然治疗方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1342/8833991/32d957bf6c17/cells-11-00552-g011.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1342/8833991/bc24cbd3d787/cells-11-00552-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1342/8833991/89b81c5fefc6/cells-11-00552-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1342/8833991/d2ac3dd2ad9e/cells-11-00552-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1342/8833991/a76f122322c4/cells-11-00552-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1342/8833991/db4bc286eaf5/cells-11-00552-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1342/8833991/27bf4687aa80/cells-11-00552-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1342/8833991/d795a48acd27/cells-11-00552-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1342/8833991/20ef6e62a2de/cells-11-00552-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1342/8833991/f629513affad/cells-11-00552-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1342/8833991/8bdf5b0e657f/cells-11-00552-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1342/8833991/32d957bf6c17/cells-11-00552-g011.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1342/8833991/bc24cbd3d787/cells-11-00552-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1342/8833991/89b81c5fefc6/cells-11-00552-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1342/8833991/d2ac3dd2ad9e/cells-11-00552-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1342/8833991/a76f122322c4/cells-11-00552-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1342/8833991/db4bc286eaf5/cells-11-00552-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1342/8833991/27bf4687aa80/cells-11-00552-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1342/8833991/d795a48acd27/cells-11-00552-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1342/8833991/20ef6e62a2de/cells-11-00552-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1342/8833991/f629513affad/cells-11-00552-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1342/8833991/8bdf5b0e657f/cells-11-00552-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1342/8833991/32d957bf6c17/cells-11-00552-g011.jpg

相似文献

1
Oxidative Stress in Human Pathology and Aging: Molecular Mechanisms and Perspectives.氧化应激与人类疾病和衰老:分子机制与展望。
Cells. 2022 Feb 5;11(3):552. doi: 10.3390/cells11030552.
2
Oxidative stress, aging, and diseases.氧化应激、衰老和疾病。
Clin Interv Aging. 2018 Apr 26;13:757-772. doi: 10.2147/CIA.S158513. eCollection 2018.
3
Oxidative and antioxidative mechanisms in oral cancer and precancer: a review.口腔癌和癌前病变中的氧化和抗氧化机制:综述。
Oral Oncol. 2014 Jan;50(1):10-8. doi: 10.1016/j.oraloncology.2013.09.011. Epub 2013 Oct 11.
4
Mitochondria induce oxidative stress, generation of reactive oxygen species and redox state unbalance of the eye lens leading to human cataract formation: disruption of redox lens organization by phospholipid hydroperoxides as a common basis for cataract disease.线粒体诱导氧化应激,产生活性氧和眼睛晶状体的氧化还原状态失衡,导致人类白内障形成:磷脂氢过氧化物破坏晶状体的氧化还原组织,作为白内障疾病的共同基础。
Cell Biochem Funct. 2011 Apr;29(3):183-206. doi: 10.1002/cbf.1737. Epub 2011 Mar 7.
5
Oxidative stress and protein aggregation during biological aging.生物衰老过程中的氧化应激与蛋白质聚集
Exp Gerontol. 2001 Sep;36(9):1539-50. doi: 10.1016/s0531-5565(01)00139-5.
6
Oxidative Stress in Ageing and Chronic Degenerative Pathologies: Molecular Mechanisms Involved in Counteracting Oxidative Stress and Chronic Inflammation.氧化应激与衰老和慢性退行性病变:对抗氧化应激和慢性炎症的分子机制
Int J Mol Sci. 2022 Jun 30;23(13):7273. doi: 10.3390/ijms23137273.
7
An integrated view of oxidative stress in aging: basic mechanisms, functional effects, and pathological considerations.衰老过程中氧化应激的综合观点:基本机制、功能影响及病理考量
Am J Physiol Regul Integr Comp Physiol. 2007 Jan;292(1):R18-36. doi: 10.1152/ajpregu.00327.2006. Epub 2006 Aug 17.
8
Impacts of oxidants and antioxidants on the emergence and progression of Alzheimer's disease.氧化剂和抗氧化剂对阿尔茨海默病的发生和发展的影响。
Neurochem Int. 2022 Feb;153:105268. doi: 10.1016/j.neuint.2021.105268. Epub 2021 Dec 23.
9
Antioxidant responses to oxidant-mediated lung diseases.抗氧化剂对氧化介导的肺部疾病的反应。
Am J Physiol Lung Cell Mol Physiol. 2002 Aug;283(2):L246-55. doi: 10.1152/ajplung.00491.2001.
10
The role of antioxidants and antioxidant-related enzymes in protective responses to environmentally induced oxidative stress.抗氧化剂和抗氧化相关酶在环境诱导的氧化应激保护反应中的作用。
Mutat Res. 2009 Mar 31;674(1-2):137-47. doi: 10.1016/j.mrgentox.2008.09.015. Epub 2008 Oct 8.

引用本文的文献

1
Arsenic-induced nephrotoxicity: Mechanisms, biomarkers, and preventive strategies for global health.砷诱导的肾毒性:全球健康的机制、生物标志物及预防策略
Vet World. 2025 Jul;18(7):2136-2157. doi: 10.14202/vetworld.2025.2136-2157. Epub 2025 Jul 30.
2
[ Granules enhance synaptic plasticity in aging rats by regulating the BDNF/TrkB signaling pathway].颗粒通过调节脑源性神经营养因子/酪氨酸激酶受体B信号通路增强衰老大鼠的突触可塑性
Nan Fang Yi Ke Da Xue Xue Bao. 2025 Aug 20;45(8):1589-1598. doi: 10.12122/j.issn.1673-4254.2025.08.03.
3
Role of cellular senescence in hepatic diseases (Review).

本文引用的文献

1
Coadministration of Melatonin and Insulin Improves Diabetes-Induced Impairment of Rat Kidney Function.褪黑素和胰岛素联合给药可改善糖尿病引起的大鼠肾功能损害。
Neuroendocrinology. 2022;112(8):807-822. doi: 10.1159/000520280. Epub 2021 Oct 21.
2
Mitochondrial-derived compartments facilitate cellular adaptation to amino acid stress.线粒体衍生隔室促进细胞适应氨基酸应激。
Mol Cell. 2021 Sep 16;81(18):3786-3802.e13. doi: 10.1016/j.molcel.2021.08.021.
3
What Is the Metabolic Amplification of Insulin Secretion and Is It (Still) Relevant?
细胞衰老在肝脏疾病中的作用(综述)
Int J Mol Med. 2025 Nov;56(5). doi: 10.3892/ijmm.2025.5623. Epub 2025 Sep 5.
4
Dendritic spine degeneration is associated with age-related decline in recognition and spatial memory in male mice.树突棘退化与雄性小鼠与年龄相关的认知和空间记忆衰退有关。
Brain Struct Funct. 2025 Aug 28;230(7):142. doi: 10.1007/s00429-025-03002-7.
5
Skin Aging and Carotenoids: A Systematic Review of Their Multifaceted Protective Mechanisms.皮肤老化与类胡萝卜素:对其多方面保护机制的系统综述
Nutrients. 2025 Aug 9;17(16):2596. doi: 10.3390/nu17162596.
6
Carbon Dots for Nucleic Acid-Based Diagnostics and Therapeutics: Focus on Oxidative DNA Damage.用于基于核酸的诊断与治疗的碳点:聚焦于氧化性DNA损伤
Int J Mol Sci. 2025 Aug 21;26(16):8077. doi: 10.3390/ijms26168077.
7
Systematic Characterization of Antioxidant Shielding Capacity Against Oxidative Stress of Aerial Part Extracts of .对……地上部分提取物抗氧化应激的抗氧化屏蔽能力的系统表征
Antioxidants (Basel). 2025 Jul 30;14(8):935. doi: 10.3390/antiox14080935.
8
A Systematic Review of Genetic Variants in Glutathione S-Transferase Genes and Their Dual Role in SARS-CoV-2 Pathogenesis: From Acute Respiratory Complications to Long COVID.谷胱甘肽S-转移酶基因中的遗传变异及其在SARS-CoV-2发病机制中的双重作用:从急性呼吸并发症到长期新冠的系统综述
Antioxidants (Basel). 2025 Jul 25;14(8):912. doi: 10.3390/antiox14080912.
9
Genetic Variants in Antioxidant Genes Modulate the Relationships Among Obesity-Related Oxidative Stress Markers in Mexican Children.抗氧化基因中的遗传变异调节墨西哥儿童肥胖相关氧化应激标志物之间的关系。
Antioxidants (Basel). 2025 Jul 22;14(8):896. doi: 10.3390/antiox14080896.
10
Benefits of Maternal Choline Supplementation on Aged Basal Forebrain Cholinergic Neurons (BFCNs) in a Mouse Model of Down Syndrome and Alzheimer's Disease.孕期补充胆碱对唐氏综合征和阿尔茨海默病小鼠模型中老年基底前脑胆碱能神经元(BFCNs)的益处。
Biomolecules. 2025 Aug 5;15(8):1131. doi: 10.3390/biom15081131.
什么是胰岛素分泌的代谢放大作用,它(现在)仍然相关吗?
Metabolites. 2021 Jun 2;11(6):355. doi: 10.3390/metabo11060355.
4
DHODH and cancer: promising prospects to be explored.二氢乳清酸脱氢酶与癌症:有待探索的广阔前景
Cancer Metab. 2021 May 10;9(1):22. doi: 10.1186/s40170-021-00250-z.
5
Parkinson's disease: Alterations in iron and redox biology as a key to unlock therapeutic strategies.帕金森病:铁和氧化还原生物学的改变作为解锁治疗策略的关键。
Redox Biol. 2021 May;41:101896. doi: 10.1016/j.redox.2021.101896. Epub 2021 Feb 14.
6
Mitochondrial Dysfunction in Parkinson's Disease: Focus on Mitochondrial DNA.帕金森病中的线粒体功能障碍:聚焦于线粒体DNA
Biomedicines. 2020 Dec 10;8(12):591. doi: 10.3390/biomedicines8120591.
7
Mitochondria-Associated Endoplasmic Reticulum Membranes in the Pathogenesis of Type 2 Diabetes Mellitus.线粒体相关内质网膜在2型糖尿病发病机制中的作用
Front Cell Dev Biol. 2020 Oct 20;8:571554. doi: 10.3389/fcell.2020.571554. eCollection 2020.
8
ER-mitochondria contacts promote mitochondrial-derived compartment biogenesis.内质网-线粒体接触促进线粒体衍生区室的发生。
J Cell Biol. 2020 Dec 7;219(12). doi: 10.1083/jcb.202002144.
9
Acetaminophen-induced renal toxicity: preventive effect of silver nanoparticles.对乙酰氨基酚诱导的肾毒性:银纳米颗粒的预防作用
Toxicol Res (Camb). 2020 Jun 17;9(4):406-412. doi: 10.1093/toxres/tfaa040. eCollection 2020 Jul.
10
A Study of the Relationship Between Uric Acid and Substantia Nigra Brain Connectivity in Patients With REM Sleep Behavior Disorder and Parkinson's Disease.快速眼动睡眠行为障碍与帕金森病患者尿酸与黑质脑连接性之间关系的研究
Front Neurol. 2020 Aug 5;11:815. doi: 10.3389/fneur.2020.00815. eCollection 2020.