In the lungs, deficiency of alpha-1antitrypsin can lead to the development of emphysema. Emphysema involves destruction of the lung’s air sacs (alveoli), where oxygen from the air is exchanged for carbon dioxide in the blood. Alpha 1–antitrypsin is a protein produced by the liver and that circulates in the blood. Among other functions, the protein protects the lungs so they can function properly. In people with the disorder, the liver produces too little or no alpha 1 -antitrypsin. Without enough alpha-1 antitrypsin, neutrophil elastase is free to destroy air sac tissue. 60 emphysema patients were included in the study. 100 healthy non-smokers’ were served as controls. Their baseline clinical examination, Alpha 1- antitrysin (AAT), malondialdehyde (MDA) and vitamin E were measured. The mean levels of Alpha 1 antitrysin and vitamin E in the patients at baseline were lower (P< 0.001) than the controls. The malondialdehyde were high (P<0.001) in the emphysema patients compared to controls. We found decreased levels of Alpha 1- antitrysin and vitamin E and increased levels of malondialdehyde (MDA). Thus the present study confirmed the existence of oxidative stress and altered levels of alpha 1- antitrypsin in emphysema patients.
Keywords: Emphysema, α-1-antitrypsin, Vitamin E, Oxidative stress, ROS, Malondialdehyde