Cells Are Exposed to Reactive Oxygen Species in Oxidative Stress

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The term oxidative stress is often used to imply a condition in which cells are exposed to excessive levels of either molecular oxygen or chemical derivatives of oxygen called reactive oxygen species; (Kojda et al., 1999). This occurs when molecules of oxygen are reduced to various subunits such as water, the production of superoxide anion radical, hydrogen peroxide and hydrogen radicals (Geller, D.A., et al. 1993). On the other hand ROS has different effects on individual blood vessels and also play a very important role on the physiological and pathological aspects of the vessels. The main ROS in blood vessels are superoxides. Super oxides are formed from the remains of reduced oxygen which is catalysed by two enzymes which are NADPH oxidase and xanthine oxidase (Taniyama et al., 2003). Superoxides are able to act on different cells but it can produce ROS by reacting with other substances, for e.g. superoxides can react with Nitric oxide to produce peroxynitrite which is potentially deleterious of ROS (Helmut, 1997). This happens by the use of superoxide dismutase enzyme, by the use of this enzyme a production of stable ROS is formed such as hydrogen peroxide (H2O2) which is then broken down into water (H2O) and oxygen (O2), this occurs in all types of vascular cells (Taniyama et al., 2003)

Figure 1: Formation of free radicals in biological systems (Vet med, 2014)


The major source of reactive oxygen species in both endothelial and vascular smooth muscle cells are membrane bound oxidases, which utilise NADH and NADPH as substrates (Kojda et al., 1999).

Impaired endothelium dependent vasorelaxation:

ROS plays a very important role in the endothelium dysfunction and ...

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... migration and proliferation of smooth muscle cells which are involved in the inflammatory lesions. These aid in further thickening the artery by slow dilation, this is called “remodelling”. Monocyte-derived macrophages and specific subtypes of T lymphocytes are mainly associated with the inflammatory response (Russell, 1997).

Normal endothelium permeability is mediated by nitric oxide. So an unbalance in this would lead to an increase in the endothelial permeability and thus leads to formation of atherosclerosis lesions. At the beginning fatty streaks are made of monocytes consisting of lipids and macrophages along with T-lymphocytes and this combines with the smooth muscle cells in later stages. This leads to a foam cell formation which is stimulated by macrophage stimulating factors, tumour necrosis factors and oxidised low density lipoprotein (Russell, 1997).

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