Abstract
Experimental evidences suggest that hyperglycaemia-induced overproduction of reactive oxygen species and subsequent damage to proteins, lipids and DNA may play a key role in the development of distal symmetric polyneuropathy (DSPN)—the most common complication of diabetes mellitus. The study population consisted of 51 individuals aged 52–82 years classified into 3 groups: 16 patients diagnosed with type 2 diabetes mellitus (T2DM) with DSPN, 16 T2DM patients without DSPN and 19 control subjects without diabetes and neuropathy. The study was conducted to determine the activity of antioxidant enzymes: catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPX) and total antioxidant status (TAS) in the examined groups. An alkaline comet assay was used to determine the extent of DNA damage of oxidized purines as glicosylo-formamidoglicosylase (Fpg) sites, and oxidized pyrimidines as endonuclease III (Nth) sites. A significant decrease of SOD (P < 0.05), GPX (P < 0.05) and nonsignificant decrease of CAT (P > 0.05), and TAS status (P > 0.05) were seen in T2DM patients with neuropathy compared to T2DM patients as well as controls. T2DM patients with or without neuropathy revealed significantly lower (P < 0.05) plasma concentration of nitrous oxide compared to the control subjects. Endogenous level of oxidative DNA damage in T2DM patients with DSPN was significantly higher compared both to the controls and T2DM patients without DSPN (P < 0.001). Moreover, lymphocytes isolated from T2DM patients with DSPN were more susceptible to oxidative DNA lesions induced by hydrogen peroxide than from T2DM patients without DSPN (P < 0.001). Our results confirm hypothesis that oxidative stress may play a substantial role in the development and progression of diabetic distal symmetric polyneuropathy.
Highlights
IntroductionDiabetic neuropathies are the most common, and at the same time the least recognized and understood long-term complication of diabetes, occurring both in type 1 and type 2 diabetic patients [1,2,3,4,5,6,7]
Diabetic neuropathies are the most common, and at the same time the least recognized and understood long-term complication of diabetes, occurring both in type 1 and type 2 diabetic patients [1,2,3,4,5,6,7].It is estimated, that neuropathy may be present in up to 10 % of patients at diagnosis of type 2 diabetes mellitus (T2DM) and affects up to 50 % of patients with long term diabetes
The study population consisted of 51 individuals aged 52–82 years classified into 3 groups: 16 patients diagnosed with type 2 diabetes mellitus (T2DM) with distal symmetric polyneuropathy (DSPN), 16 T2DM patients without DSPN and 19 control subjects without diabetes and neuropathy
Summary
Diabetic neuropathies are the most common, and at the same time the least recognized and understood long-term complication of diabetes, occurring both in type 1 and type 2 diabetic patients [1,2,3,4,5,6,7] It is estimated, that neuropathy may be present in up to 10 % of patients at diagnosis of type 2 diabetes mellitus (T2DM) and affects up to 50 % of patients with long term diabetes. The diagnosis of DSPN is typically made in patients with poor glycemic control and its prevalence increases with age and duration of diabetes. This form of neuropathy is often accompanied by autonomic neuropathy [10]. DSPN is the main cause of serious chronic complications of diabetes including foot ulceration, Mol Biol Rep (2012) 39:8669–8678
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