Abstract

ABSTRACTMyocardial infarction (MI) is the most important reasons of mortality and morbidity in developed countries. It is detected that about half of the deaths, no matter what reason, in the USA is sourced from MI. In recent years, the number of scientific studies have increased on some genetic risk factors responsible from the formation of MI. One of the most popular of these is the one searching for the relations between the I/D polymorphism in the ACE gene and MI. Nowadays there are various studies showing that the free radicals are responsible from the ischemic myocardial wounds. Especially the hydroxy radical is shown to cause some differences in the myocard. In the pathogenesis of ischemic tissue defect, the free radicals are put forward to be effective, malondialdehyde (MDA) which is a subproduct of oxidation, is a value measurable by the TBA method. MDA, one of the compounds formed as a result of peroxidation of membrane phospholipids, is accepted as an indicator of LP. In this study, it is assumed that ACE I/D gene polymorphism is a useful indicator in the detection of the risk of cardiovascular disease, the better control of the people in high risk group and the optimal cure to start at an earlier stage. By the help of these studies the risk factors of genetic origin, using the genetic indicators and new risk factors, and supporting the information by some easily performed biochemical experiments would supply great easiness in diagnosis and cure and save life. The scope of this study is to compare the distribution of gene polymorphism between people suffered from MI and healthy people and to search the relation between ACE gene polymorphism and MDA, the marker of lipid perokxidation (LP) formed as a result of MI. Two groups were covered in our study, one consisting of 104 people of various ages previously suffered from MI and the other consisting of 100 healthy people. Using the blood samples taken from these two groups, data for the following variables was obtained: DNA isolation, PCR, agarose gel electrophoresis and MDA as the marker of blood lipid peroxidation.

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