Biochemistry, Department of

 

ORCID IDs

0000-0001-7421-5424

Date of this Version

2018

Citation

Oxidative Medicine and Cellular Longevity Volume 2018, Article ID 5730395, 9 pages

Comments

Copyright © 2018 Samia Boukhenouna et al.

Open access

https://doi.org/10.1155/2018/5730395

Abstract

Chronic obstructive pulmonary disease (COPD) includes chronic bronchitis and emphysema. Environmental exposure, primarily cigarette smoking, can cause high oxidative stress and is the main factor of COPD development. Cigarette smoke also contributes to the imbalance of oxidant/antioxidant due to exogenous reactive oxygen species (ROS). Moreover, endogenously released ROS during the inflammatory process and mitochondrial dysfunction may contribute to this disease progression. ROS and reactive nitrogen species (RNS) can oxidize different biomolecules such as DNA, proteins, and lipids leading to epithelial cell injury and death. Various detoxifying enzymes and antioxidant defense systems can be involved in ROS removal. In this review, we summarize the main findings regarding the biological role of ROS, which may contribute to COPD development, and cytoprotective mechanisms against this disease progression.

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