Biochemical Changes Induced by Emphysema in Children

Abstract

In the lung, the pathogenesis of emphysema (Em) is complicated and involves several endogenous factors: protease-antiprotease imbalance, α1-antitrypsin deficiency, oxidative stress (OS), and ion imbalance. It is our contention that an increase in the free Fe level in combination with a significant decrease of SOD activity that we detected is disadvantageous for patients with lung pathology, particularly in cases with complicated Em. GP and SOD activity decrease in patients with Em. The Zn/Cu ratio also decreases during Em, whereas the Zn in/Cu ratio is increased, when compared with patients without Em. We discovered the activation of HNE (not distinctively expressed, but obviously, prolonged over time), and have assumed an increase in cathepsin G activity (according to antiG activation). A moderate rise in the MMP-7 level can indicate an inactivation of the remodeling processes in these patients, and a part of the compensatory mechanisms. This assumption is confirmed by the MMP-7 correlation links found in cases of Em, with anti-NE and anti-G activity (r=+0.67 and r=+0.64, correspondingly) that the use of antioxidants alone has little effect, as these drugs cannot neutralize the main chain of free-radical reactions, namely Fe2+. Most likely, iron chelators will need to be included in lung pathology treatment, particularly in children to prevent an intensification of OS, underlying the development of multiple organ deficiency.

Keywords

• emphysema
• human neutrophilic elastase
• matrix metalloproteinases
• free ions
• erythrocyte
• glutathione peroxidase
• superoxide dismutase.