%0 Journal Article
%T Amfizemli Hastalarda ¦Á1-Proteinaz  nhibit r¨¹ Aktivitesi ve Fenotiplerinin Belirlenmesi
%A £¿zden Tacal
%A Nilg¨¹n S¨¹mer
%A L¨¹tfi £¿£¿pl¨¹
%J T¨¹rk Biyokimya Dergisi
%D 2006
%I Turkish Biochemical Society
%X In our study, functionally active ¦Á1-proteinase inhibitor (¦Á1-PI) levels and phenotypeswere determined in sera of patients with emphysema and in that of healthy subjects. Patients were classified according to their smoking habits: Group I consistedof 7 nonsmoking (or limited history of smoking) patients. Group II consisted of heavily smoking 14 patients. Four patients having intermediate smoking habits were considered independently (Group III). Two of these patients were siblings with a history of familial emphysema. The Control group consisted of 28 healthy nonsmokingsubjects. Active serum ¦Á1-PI levels were assayed spectrophotometrically, by determining the extent of trypsin inhibition. ¦Á1-PI phenotypes were determined by isoelectric focusing on polyacrylamide gels. Once the serum ¦Á1-PI levels have been compared, the differences between Group I and Group II and the Control group were statistically insignificant (p >0.05). Isoelectric focusing results showed that all but 4 patients had the M1M1 or M1M2 phenotype. (The siblings in the Group III had the ZZ phenotype and 2 patients in Group II had undefined phenotypes). Considering these results, we concluded that, with the exception the siblings expressingthe ZZ variant, the development of emphysema in our patients was caused by an increase in elastase load rather than a deficiency in antielastase capacity. The increase in elastase load was most likely due to biological and chemical oxidants in the lungs
%K Emphysema
%K ¦Á1-proteinase inhibitor
%K phenotypes
%K cigarette smoking
%K isoelectric focusing.
%U http://www.turkjbiochem.com/2006/169.pdf