The effects of oxidative stress on the development of atherosclerosis
Author:
Khosravi Mohsen1, Poursaleh Adeleh1, Ghasempour Ghasem1, Farhad Shaikhnia1, Najafi Mohammad2
Affiliation:
1. Biochemistry Department, Firoozabadi Hospital , Iran University of Medical Sciences , Tehran , Iran 2. Microbial Biotechnology Research Center, Biochemistry Department, Firoozabadi Hospital , Iran University of Medical Sciences , Tehran , Iran
Abstract
Abstract
Atherosclerosis is a cardiovascular disease (CVD) known widely world wide. Several hypothesizes are suggested to be involved in the narrowing of arteries during process of atherogenesis. The oxidative modification hypothesis is related to oxidative and anti-oxidative imbalance and is the most investigated. The aim of this study was to review the role of oxidative stress in atherosclerosis. Furthermore, it describes the roles of oxidative/anti-oxidative enzymes and compounds in the macromolecular and lipoprotein modifications and in triggering inflammatory events. The reactive oxygen (ROS) and reactive nitrogen species (RNS) are the most important endogenous sources produced by non-enzymatic and enzymatic [myeloperoxidase (MPO), nicotinamide adenine dinucleotide phosphate (NADH) oxidase and lipoxygenase (LO)] reactions that may be balanced with anti-oxidative compounds [glutathione (GSH), polyphenols and vitamins] and enzymes [glutathione peroxidase (Gpx), peroxiredoxins (Prdx), superoxide dismutase (SOD) and paraoxonase (PON)]. However, the oxidative and anti-oxidative imbalance causes the involvement of cellular proliferation and migration signaling pathways and macrophage polarization leads to the formation of atherogenic plaques. On the other hand, the immune occurrences and the changes in extra cellular matrix remodeling can develop atherosclerosis process.
Publisher
Walter de Gruyter GmbH
Subject
Clinical Biochemistry,Molecular Biology,Biochemistry
Reference227 articles.
1. AC’t Hoen, P., Van der Lans, C.A., Van Eck, M., Bijsterbosch, M.K., Van Berkel, T.J., and Twisk, J. (2003). Aorta of ApoE-deficient mice responds to atherogenic stimuli by a prelesional increase and subsequent decrease in the expression of antioxidant enzymes. Circ. Res. 93, 262–269. 2. Agrawal, R., Muangman, S., Layne, M., Melo, L., Perrella, M., Lee, R., Zhang, L., Lopez-Ilasaca, M., and Dzau, V. (2004). Pre-emptive gene therapy using recombinant adeno-associated virus delivery of extracellular superoxide dismutase protects heart against ischemic reperfusion injury, improves ventricular function and prolongs survival. Gene Ther. 11, 962–969. 3. Ahn, J., Gammon, M.D., Santella, R.M., Gaudet, M.M., Britton, J.A., Teitelbaum, S.L., Terry, M.B., Nowell, S., Davis, W., Garza, C., et al. (2005). Associations between breast cancer risk and the catalase genotype, fruit and vegetable consumption, and supplement use. Am. J. Epidemiol. 162, 943–952. 4. Allentoff, A.J., Bolton, J.L., Wilks, A., Thompson, J.A., and Ortiz de Montellano, P.R. (1992). Heterolytic versus homolytic peroxide bond cleave by sperm whale myoglobin and myoglobin mutants. J. Am. Chem. Soc. 114, 9744–9749. 5. Antman, E.M. and Braunwald, E. (1997). Acute myocardial infarction. In: Heart Disease, a Textbook of Cardiovascular Disease, Vol. II, 5th ed., E. Braunwald, ed. (Philadelphia: W.B. Saunders Company), pp. 1184–1288.
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