| Recent studies have shown that the renin-angiotensin system (RAS) correlates with diseases of respiratory system, such as chronic obstructive pulmonary disease (COPD) and pulmonary heart disease. Angiotensin-converting enzyme (ACE) is a key enzyme in RAS, which plays an important role in the RAS and bradykinin system and affects a variety of physiological function in human body. As circulating ACE mainly originates from the pulmonary capillary endothelial cells, it has been hoped to diagnose lung diseases by measuring ACE levels, but reports about ACE levels in lung diseases are varied. Recent interests considered the ACE gene as a candidate sensitive gene to research relative diseases. The ACE gene contains a polymorphism based on the presence (insertion [1]) or absence (deletion [D]) in three genotypes (DD and II homozygotes and ID heterozygotes). The polymorphism of ACE is significantly correlated withserum ACE (sACE). The sACE levels in DD individuals have been found to be the highest of those in the ACE three genotypes, while in II individuals is the lowest and ID individuals is in between. The aim of this work was to investigate the relationship of polymorphism of ACE gene with COPD and pulmonary heart disease.Method: ⑴ 30 healthy subjects, 30 patients with COPD, 30 patients with pulmonary heart disease were studied. ⑵ DNA of white blood cells was abstracted followed by instruction of the reagent box drawing DNA of white blood cells from small dose of whole blood. ⑶ ACE genotypes (DD, ID, II genotypes respectively) were determined in all subjects by polymerase chain reaction (PCR). Meanwhile, sACE levels was determined in all subjects by ultraviolet spectrophotometry. Result: ⑴ sACE level in DD individuals had been found to be the highest of those in ACE three genotypes, while in II individuals was the lowest and in II individuals in between. The sACE levels were (565.02±128.79), (516.30±117.01) and (439.13±105.18)(/L, respectively for genotypes DD,ID and II. ⑵ The levels of sACE in patients with COPD or pulmonary heart disease were significantly higher than in healthy subjects (P<0.01). ⑶ The percentage of I/D allele in patients with COPD and pulmonary heart disease was significantly differed form healthy subjects(x2=6.599, P=0.01). ⑷ The odds ratio of patients (COPD and pulmonary heart disease) with D allele and those with I allele was both 2.6. Conclusion: ⑴ There was a close relation between the sACE levels and ACE genotypes of DD, ID and II. ⑵ The high expression of ACE is due to D allele. (3)The results suggested that D allele of ACE might be a risk factor for COPD and pulmonary heart disease.
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