کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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2910388 | 1174623 | 2008 | 5 صفحه PDF | دانلود رایگان |

SummaryBackgroundHyperglycemia causes tissue injury leading to vascular damage through generation of free radicals and their effect on endothelium in diabetics. The present study has been designed to evaluate the oxidant stress by measuring malondialdehyde, antioxidant status and nitric oxide synthase activity in diabetic foot ulcer.Materials and methodsThirty-two diabetic patients with peripheral vascular disease [PVD] and foot ulcer, fifteen diabetic patients without evidence of significant diabetic neuropathy or peripheral vascular disease and fifteen healthy control subjects were included in this study. Blood samples were taken for estimation of malondialdehyde, Vitamin E and superoxide dismutase [SOD] enzyme. Immunocytochemical staining of full thickness skin biopsies for NADPH diaphorase was carried out which is colocalised with nitric oxide synthase.ResultsSerum malondialdehyde level was significantly higher in the patients with PVD as compared with the diabetic controls [1.164 ± 0.371 vs. 0.710 ± 0.277 nmol/mL] and non-diabetic controls. Superoxide dismutase and tocopherol [Vitamin E] levels were significantly lower in patients with PVD than in diabetics without PVD.Immunocytochemical studyThe tissue section obtained from 10 diabetic wound stained for NADPH diaphorase activity show intense staining while the control sections of the skin biopsy from diabetic patients without PVD did not show staining of the tissue.ConclusionDiabetic wounds have high level of NO synthase activity favoring heightened NO production. Increased free radicals generation [evidenced by increased malondialdehyde and superoxide dismutase level] and reduced level of antioxidants [Vitamin E] or endothelial resistance to NO might be contributory to ineffectiveness of NO on microcirculation. No such study has been done earlier to show a complex abnormality of oxidative stress in diabetic foot lesions.
Journal: Diabetes & Metabolic Syndrome: Clinical Research & Reviews - Volume 2, Issue 2, June 2008, Pages 109–113