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Oxidative Stress in Human Pathology and Aging: Molecular Mechanisms and Perspectives
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 (...
Autores principales: | , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8833991/ https://www.ncbi.nlm.nih.gov/pubmed/35159361 http://dx.doi.org/10.3390/cells11030552 |
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author | Hajam, Younis Ahmad Rani, Raksha Ganie, Shahid Yousuf Sheikh, Tariq Ahmad Javaid, Darakhshan Qadri, Syed Sanober Pramodh, Sreepoorna Alsulimani, Ahmad Alkhanani, Mustfa F. Harakeh, Steve Hussain, Arif Haque, Shafiul Reshi, Mohd Salim |
author_facet | Hajam, Younis Ahmad Rani, Raksha Ganie, Shahid Yousuf Sheikh, Tariq Ahmad Javaid, Darakhshan Qadri, Syed Sanober Pramodh, Sreepoorna Alsulimani, Ahmad Alkhanani, Mustfa F. Harakeh, Steve Hussain, Arif Haque, Shafiul Reshi, Mohd Salim |
author_sort | Hajam, Younis Ahmad |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-8833991 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-88339912022-02-12 Oxidative Stress in Human Pathology and Aging: Molecular Mechanisms and Perspectives Hajam, Younis Ahmad Rani, Raksha Ganie, Shahid Yousuf Sheikh, Tariq Ahmad Javaid, Darakhshan Qadri, Syed Sanober Pramodh, Sreepoorna Alsulimani, Ahmad Alkhanani, Mustfa F. Harakeh, Steve Hussain, Arif Haque, Shafiul Reshi, Mohd Salim Cells Review 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. MDPI 2022-02-05 /pmc/articles/PMC8833991/ /pubmed/35159361 http://dx.doi.org/10.3390/cells11030552 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Hajam, Younis Ahmad Rani, Raksha Ganie, Shahid Yousuf Sheikh, Tariq Ahmad Javaid, Darakhshan Qadri, Syed Sanober Pramodh, Sreepoorna Alsulimani, Ahmad Alkhanani, Mustfa F. Harakeh, Steve Hussain, Arif Haque, Shafiul Reshi, Mohd Salim Oxidative Stress in Human Pathology and Aging: Molecular Mechanisms and Perspectives |
title | Oxidative Stress in Human Pathology and Aging: Molecular Mechanisms and Perspectives |
title_full | Oxidative Stress in Human Pathology and Aging: Molecular Mechanisms and Perspectives |
title_fullStr | Oxidative Stress in Human Pathology and Aging: Molecular Mechanisms and Perspectives |
title_full_unstemmed | Oxidative Stress in Human Pathology and Aging: Molecular Mechanisms and Perspectives |
title_short | Oxidative Stress in Human Pathology and Aging: Molecular Mechanisms and Perspectives |
title_sort | oxidative stress in human pathology and aging: molecular mechanisms and perspectives |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8833991/ https://www.ncbi.nlm.nih.gov/pubmed/35159361 http://dx.doi.org/10.3390/cells11030552 |
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