過氧化氫酵素的基因多型性與急性心肌梗塞的關聯性

近來許多的研究顯示，血管的發炎反應在急性心肌梗塞的發展中，扮演一個重要的角色。低密度脂蛋白（low-density lipoprotein , LDL）滲透並滯留在動脈內膜，在動脈壁引發發炎反應。被氧化的低密度脂蛋白（oxidised low-density lipoprotein, LDLox）已被報導為增加過氧化物生成的媒介，因這個媒介而產生的活性氧（reactive oxygen species, ROS）會造成斑塊的形成。但這些效應可被超氧化物歧化酶（superoxide dismutases, SOD）及過氧化氫酶（catalase）所防止，超氧化物歧化酶（SOD）可以將過氧化陰離子（superoxide anion）轉為過氧化氫，catalase再將過氧化氫還原成水。本篇研究的主要目的，是去檢測catalase基因多型性跟急性心肌梗塞的發生是否有關聯性。我們完成117個含病患組及對照組的案例，其中28個是有發作過急性心肌梗塞的病人，51個沒有急性心肌梗塞的個體，38個則不具有任何會引起傳統心血管疾病危險因子的人。他們的DNA經過PCR放大及Hinf1的作用後，顯示病患組與對照組之間的-21A/T基因多型性，其頻率分佈是類似的，三者沒有關聯性。由實驗結果我們可以推論：catalase –21A/T基因多型性並不直接影響急性心肌梗塞的發生。

Recently many studies have revealed that vascular inflammation plays an important role in the development of acute myocardial infarction (AMI). The infiltration and retention of low-density lipoprotein （LDL）in the arterial intima initiate an inflammatory response in the artery wall. Oxidised low-density lipoprotein(LDLox) have been reported to mediate enhanced superoxide formation . LDLox-mediated formation of reactive oxygen species （ROS）also causes plaque formation.These effects can be prevented by treatment with superoxide dismutases（SOD）and catalase. The SOD, which convert superoxide anion into hydrogen peroxide, catalase, whereas reduces hydrogen peroxide to water. The aim of the study was to examine whether polymorphism of the catalase gene is associated with the risk of AMI. Therefore, we performed a case-control study from 117patients. The study population comprised of 28 AMI patients,51 healthy individuals without AMI disease history (IIA), and 38 personnel don’t have any conventional cardiovascular disease risk factors (IIB). Catalase gene polymorphism was performed by analyzing Hinf1-digested DNA fragment obtained by polymerase chain reaction (PCR).The –21A/T polymorphism frequency of catalase gene was similar in patients and the controls. No association of –21A/T polymorphism was detected in comparisons with control IIA、control IIB and total control .In conclusion, the catalase gene does not appear to be a susceptibility locus for acute myocardial infarction.