Oxidative stress versus antioxidant defenses in patients with acute myocardial infarction.
Acute myocardial infarction (AMI) is a highly dynamic event, which is associated with increasing production of reactive oxygen species (ROS). The imbalance between ROS production and antioxidant defenses leads to the condition known as oxidative stress. The most widely recognized effect of increasing oxidative stress is the oxidation and damage of macromolecules, membranes, proteins, and DNA. Therefore, in this study we sought to evaluate oxidative stress and antioxidant defenses in patients with AMI. Lipid peroxidation, protein carbonyl levels, and enzymatic and nonenzymatic antioxidants were assessed in samples obtained from 40 AMI patients and 40 control patients. AMI was characterized by clinical, electrocardiographic, and laboratory criteria. The control group was divided into two groups of 20 patients: a control group with healthy patients and a risk group. Our results demonstrated an increase in substances reactive to thiobarbituric acid (TBARS) and carbonyl protein levels in the AMI and risk groups. In addition, a positive correlation was found between TBARS, carbonyl protein levels, and troponin I in AMI patients. Surprisingly, for the enzymatic antioxidant defenses, catalase and superoxide dismutase, we observed an increase in these parameters in the AMI and risk groups when compared with healthy patients. However, a decrease in nonenzymatic antioxidants such as vitamin C and vitamin E was observed in AMI patients when compared with the healthy group and the risk group. The increase in oxidative stress was probably a result of the elevation in ROS production due to the ischemic/reperfusion event that occurs in AMI, in addition to the decrease of nonenzymatic antioxidant defenses.
Departamento de Química, Centro de Ciências Naturais e Exatas, Programa de Pós-Graduação em Bioquímica Toxicológica, Universidade Federal de Santa Maria, Santa Maria, RS, 97105-900, Brazil.
Margarete Dulce
MD
Bagatini
Caroline Curry
CC
Martins
Vanessa
V
Battisti
Diogo
D
Gasparetto
Cintia Saydelles
CS
da Rosa
Roselia Maria
RM
Spanevello
Mushtaq
M
Ahmed
Roberta
R
Schmatz
Maria Rosa Chitolina
MR
Schetinger
Vera Maria
VM
Morsch
D000328:Adult; D000975:Antioxidants / Q000378:metabolism*; D001205:Ascorbic Acid / Q000097:blood; D015415:Biomarkers / Q000097:blood; D001938:Brazil; D016022:Case-Control Studies; D002374:Catalase / Q000097:blood; D005260:Female; D006801:Humans; D015227:Lipid Peroxidation; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000378:metabolism*; D018384:Oxidative Stress; D050050:Protein Carbonylation; D017382:Reactive Oxygen Species / Q000378:metabolism*; D013482:Superoxide Dismutase / Q000097:blood; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D019210:Troponin I / Q000097:blood; D014810:Vitamin E / Q000097:blood
D000975:Antioxidants; D015415:Biomarkers; D017382:Reactive Oxygen Species; D017392:Thiobarbituric Acid Reactive Substances; D019210:Troponin I; D014810:Vitamin E; D002374:Catalase; D013482:Superoxide Dismutase; D001205:Ascorbic Acid