PMID- 22718504 OWN - NLM STAT- MEDLINE DCOM- 20121214 LR - 20211021 IS - 1573-4978 (Electronic) IS - 0301-4851 (Print) IS - 0301-4851 (Linking) VI - 39 IP - 9 DP - 2012 Sep TI - Evaluation of oxidative stress markers in pathogenesis of diabetic neuropathy. PG - 8669-78 LID - 10.1007/s11033-012-1722-9 [doi] AB - 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. FAU - Kasznicki, Jacek AU - Kasznicki J AD - Department of Internal Medicine, Diabetology and Clinical Pharmacology, Medical University of Lodz, ul. Parzeczewska 35, 95-100 Zgierz, Poland. jacek.kasznicki@umed.lodz.pl FAU - Kosmalski, Marcin AU - Kosmalski M FAU - Sliwinska, Agnieszka AU - Sliwinska A FAU - Mrowicka, Malgorzata AU - Mrowicka M FAU - Stanczyk, Malgorzata AU - Stanczyk M FAU - Majsterek, Ireneusz AU - Majsterek I FAU - Drzewoski, Jozef AU - Drzewoski J LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20120621 PL - Netherlands TA - Mol Biol Rep JT - Molecular biology reports JID - 0403234 RN - 0 (Antioxidants) RN - 0 (Biomarkers) RN - EC 1.15.1.1 (Superoxide Dismutase) SB - IM MH - Aged MH - Aged, 80 and over MH - Antioxidants/metabolism MH - *Biomarkers MH - DNA Damage MH - Diabetic Neuropathies/*genetics/*metabolism MH - Female MH - Humans MH - Male MH - Middle Aged MH - *Oxidative Stress MH - Superoxide Dismutase/metabolism PMC - PMC3404273 EDAT- 2012/06/22 06:00 MHDA- 2012/12/15 06:00 PMCR- 2012/06/21 CRDT- 2012/06/22 06:00 PHST- 2012/02/02 00:00 [received] PHST- 2012/06/06 00:00 [accepted] PHST- 2012/06/22 06:00 [entrez] PHST- 2012/06/22 06:00 [pubmed] PHST- 2012/12/15 06:00 [medline] PHST- 2012/06/21 00:00 [pmc-release] AID - 1722 [pii] AID - 10.1007/s11033-012-1722-9 [doi] PST - ppublish SO - Mol Biol Rep. 2012 Sep;39(9):8669-78. doi: 10.1007/s11033-012-1722-9. Epub 2012 Jun 21.