Abstract

Reactive oxygen species (ROS) are well-known for playing a dual role as destructive and constructive species. Indeed, ROS are engaged in many redox-governing activities of the cells for the preservation of cellular homeostasis. However, its overproduction has been reported to result in oxidative stress, which is considered as a deleterious process, and is involved in the damage of cell structures that causes various diseased states. This review provides a concise view on some of the current research published in this topic for an improved understanding of the key roles of ROS in diverse conditions of health and disease. Previous research demonstrated that ROS perform as potential signaling molecules to control several normal physiological functions at the cellular level. Additionally, there is a growing body of evidence supporting the role of ROS in various pathological states. The binary nature of ROS with their profitable and injurious characteristics indicates the complexities of their specific roles at a biological compartment and the difficulties in establishing convenient intervention procedures to treat ROS-related diseases.

Cite this article as: Bardaweel SK, Gul M, Alzweiri M, Ishaqat A, AlSalamat HA, Bashatwah RM. Reactive Oxygen Species: the Dual Role in Physiological and Pathological Conditions of the Human Body. Eurasian J Med 2018; 50(3): 193-201.

Details

Title
Reactive Oxygen Species: the Dual Role in Physiological and Pathological Conditions of the Human Body
Author
Bardaweel, Sanaa K; Gul, Mustafa; Alzweiri, Muhammad; Ishaqat, Aman; ALSalamat, Husam A; Bashatwah, Rasha M
First page
193
Section
Review
Publication year
2018
Publication date
Oct 2018
Publisher
Galenos Publishing House
ISSN
13088734
e-ISSN
13088742
Source type
Scholarly Journal
Language of publication
English
ProQuest document ID
2160142002
Copyright
© 2018. Notwithstanding the ProQuest Terms and conditions, you may use this content in accordance with the associated terms available at http://www.eajm.org/eng/makale/3109/210/Full-Text