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. 2013 Feb 5;14(2):3265-84.
doi: 10.3390/ijms14023265.

Oxidative stress as an underlying contributor in the development of chronic complications in diabetes mellitus

Suziy de M Bandeira  1 , Lucas José S da Fonseca, Glaucevane da S Guedes, Luíza A Rabelo, Marília O F Goulart, Sandra Mary L Vasconcelos
Affiliations

Oxidative stress as an underlying contributor in the development of chronic complications in diabetes mellitus

Suziy de M Bandeira et al. Int J Mol Sci. .

Abstract

The high prevalence of diabetes mellitus and its increasing incidence worldwide, coupled with several complications observed in its carriers, have become a public health issue of great relevance. Chronic hyperglycemia is the main feature of such a disease, being considered the responsible for the establishment of micro and macrovascular complications observed in diabetes. Several efforts have been directed in order to better comprehend the pathophysiological mechanisms involved in the course of this endocrine disease. Recently, numerous authors have suggested that excess generation of highly reactive oxygen and nitrogen species is a key component in the development of complications invoked by hyperglycemia. Overproduction and/or insufficient removal of these reactive species result in vascular dysfunction, damage to cellular proteins, membrane lipids and nucleic acids, leading different research groups to search for biomarkers which would be capable of a proper and accurate measurement of the oxidative stress (OS) in diabetic patients, especially in the presence of chronic complications. In the face of this scenario, the present review briefly addresses the role of hyperglycemia in OS, considering basic mechanisms and their effects in diabetes mellitus, describes some of the more commonly used biomarkers of oxidative/nitrosative damage and includes selected examples of studies which evaluated OS biomarkers in patients with diabetes, pointing to the relevance of such biological components in general oxidative stress status of diabetes mellitus carriers.

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Figures

Figure 1
Figure 1
Schematic overview with some of the inter-related mechanisms involved in the regulation of oxidative balance. Physiologically, a tight control between antioxidants and oxidants is observed. In conditions of oxidative stress, however, an imbalance in favor of reactive oxygen and nitrogen species concentration occurs, leading to endothelial dysfunction, insulin resistance, and to alterations of pancreatic beta-cells. AGEs: advanced glycation end products; BH4: tetrahydrobiopterin; CAT: catalase; eNOS: endothelial nitric oxide synthase; FFA: free fatty acids; GPx: glutathione peroxidase; GR: glutathione reductase; GSH: reduced glutathione; GSSG: oxidized glutathione; H2O2: hydrogen peroxide; •NO: nitric oxide; NOS: nitric oxide synthase; •O2−: superoxide anion radical; •OH: hydroxyl radical; ONOO−: peroxynitrite; RONS: reactive oxygen and nitrogen species; S2: sulfur; SOD: superoxide dismutase; TRX: thioredoxin; TRXP: thioredoxin peroxidase.
Figure 2
Figure 2
Participation of hyperglycemia in triggering the multiple oxidative stress pathways in the course of diabetes. AngII: angiotensin II; eNOS: endothelial nitric oxide synthase; Jac/STAT: janus kinase (Jac)-signal transducer and activator of transcription (STAT); LDL: low density lipoprotein cholesterol; MAPK: mitogen-activated protein kinase; MetS: metabolic syndrome; NF-κb: nuclear transcription factor κb; •NO: nitric oxide; NOS: nitric oxide synthase; •O2−: superoxide anion radical; •OH: hydroxyl radical; ONOO−: peroxynitrite; PCKδ: protein kinase C δ. Adapted from Johansen et al., 2005 [30].
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