Study on the Relationship between Manganese Superoxide Dismutase Gene Variants and the Levels of Blood Lipid and Homocysteine / 现代检验医学杂志
Journal of Modern Laboratory Medicine
;
(4): 12-15, 2016.
Artículo
en Chino
| WPRIM
| ID: wpr-493704
ABSTRACT
Objective To investigate the relationship between manganese superoxide dismutase (Mn-SOD)9 Ala/Val genetic polymorphisms and the levels of blood lipid and homocysteine (HCY).Methods The genotypes of Mn-SOD 9 Ala/Val ge-netic polymorphisms were identified by sequencing method,the serum activities of T-SOD and Mn-SOD were detected by colorimetric method,the serum level of HCY was detected by enzymatic method,and the serum levels of cholesterol (TC), triglyceride (TG),high density lipoprotein cholesterol (HDL-C)and low density lipoprotein cholesterol (LDL-C)were de-tected by end-point method in 137 patients with coronary heart disease (CHD)and 85 controls.Results Compared with the control group,the VV genotype and V allele of Mn-SOD 9 Ala/Val genetic polymorphisms in the CHD group were higher, while the serum activities of T-SOD and Mn-SOD in the CHD group was significantly lower.The serum activities of T-SOD and Mn-SOD of the Mn-SOD 9 VV genotype was significantly lower than the Mn-SOD 9 AA genotype.Compared with the Mn-SOD 9 AA genotype,the serum levels of TC,TG,LDL-C and HCY of the Mn-SOD 9 VV genotype were significantly higher,while the serum level of HDL-C was significantly lower.The serum activity of Mn-SOD was negativelycorrelated with the serum levels of TC,TG,LDL-C and HCY and positively correlated with the serum level of HDL-C.Conclusion The antioxidative ability in patients with CHD was decreased.Mn-SOD 9 Ala/Val genetic polymorphisms led to lipid metab-olism disorders by affecting the Mn-SOD activity,promoting the development of CHD.HCY resulted in increased oxidative substances by self-oxidation and inhibition of the Mn-SOD activity,increasing the risk of CHD.
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Índice:
WPRIM (Pacífico Occidental)
Idioma:
Chino
Revista:
Journal of Modern Laboratory Medicine
Año:
2016
Tipo del documento:
Artículo
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