Glycolaldehyde induces oxidative stress in the heart: a clue to diabetic cardiomyopathy?
Cardiovascular complications account for 80% of the mortality related to diabetes mellitus. Hyperglycemia is believed to be the major culprit of angiopathy and cardiomyopathy. High glucose levels and oxidative stress cause elevation of Advanced Glycation End-products that are known to contribute to diabetic complications and correlate with many diseases. However, there are few reports describing the effects of glycating agents other than glucose. Here, we aimed to evaluate the effects of glycolaldehyde (GA) on oxidative stress parameters in the heart of Wistar rats. Male Wistar rats received a single injection of GA (10, 50 or 100 mg/Kg) and were sacrificed 6, 12 or 24 h after injection. As indexes of oxidative stress, we quantified protein carbonylation, lipid peroxidation and total reduced thiols. The activities of superoxide dismutase, catalase and glyoxalase I were assayed. Also, the content of N (ɛ)-(carboxymethyl)lysine (CML) was quantified. Glycolaldehyde induced an imbalance in the redox status, with increased protein carbonylation and lipoperoxidation. Catalase and glyoxalase I had a decrease in their activities. Despite the oxidative stress, we observed no increase in CML content. These results suggest that short-chain aldehydes such as GA might have a significant role in the development of diabetic cardiomyopathy.
Lorenzi
Rodrigo
R
Centro de Estudos em Estresse Oxidativo, Universidade Federal do Rio Grande do Sul, Porto Alegre, Rio Grande do Sul, Brazil. lorenzi_rodrigo@yahoo.com.br
Andrades
Michael Everton
ME
Bortolin
Rafael Calixto
RC
Nagai
Ryoji
R
Dal-Pizzol
Felipe
F
Moreira
José Cláudio Fonseca
JC
D000079:Acetaldehyde / Q000008:administration & dosage / Q000031:analogs & derivatives* / Q000378:metabolism; D000818:Animals; D009202:Cardiomyopathies / Q000209:etiology / Q000378:metabolism*; D002374:Catalase / Q000378:metabolism; D048909:Diabetes Complications / Q000209:etiology / Q000378:metabolism*; D007275:Injections, Intravenous; D007791:Lactoylglutathione Lyase / Q000378:metabolism; D015227:Lipid Peroxidation; D008239:Lysine / Q000031:analogs & derivatives / Q000378:metabolism; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D010084:Oxidation-Reduction; D018384:Oxidative Stress; D050050:Protein Carbonylation; D051381:Rats; D017208:Rats, Wistar; D013438:Sulfhydryl Compounds / Q000378:metabolism; D013482:Superoxide Dismutase / Q000378:metabolism; D013997:Time Factors
D013438:Sulfhydryl Compounds; C048496:N(6)-carboxymethyllysine; D002374:Catalase; D013482:Superoxide Dismutase; D007791:Lactoylglutathione Lyase; D000079:Acetaldehyde; D008239:Lysine; C010972:glycolaldehyde