| ironjustice@aol.com 2006-03-22, 3:40 pm |
| [The role of oxidative stress in the pathogenesis of pulmonary
emphysema]
Vucevic D, Radosavljevic T, Zunic S, Dordevic-Denic G, Pesic BC,
Radak D
Med Pregl. 2005 Sep-Oct ; 58(9-10): 472-7
OXIDATIVE PULMONARY DAMAGE: The pathogenesis of pulmonary emphysema is
incompletely understood. Nearly 90% of all patients with chronic
obstructive pulmonary diseases are smokers. Cigarette smoke is a rich
source of oxidants. Oxidative stress increases oxidant generation,
which cannot be neutralized with antioxidant defense mechanisms.
Lipids, proteins and deoxyribonucleic acid are components of the cell
that are most sensitive to oxidative damage. Oxygen radicals can modify
amino acid side chains, form protein aggregates, cleave peptide bonds,
and make proteins more susceptible to proteolytic degradation. It has
been shown that neutrophils have a principal effector role in pulmonary
tissue damage. Neutrophil elastase can damage air spaces by degrading
elastin, and a variety of extracellular membrane proteins,
proteoglycans, and glycoproteins. Neutrophil elastase can also
stimulate inflammation by increasing interleukin-8 synthesis.
Additionally, neutrophil elastase can activate or inactivate inhibitors
of neutrophil collagenase, and secretory leukoprotease proteinase
inhibitor. Apart from neutrophils, oxidative stress causes activation
of other phagocytes and severe inflammatory response ensues. LIPID
PEROXILATION AND PULMONARY EMPHYSEMA: Except protein oxidation and
lipid peroxidation, oxidants may disturb signal transmission in the
cells, as well as normal cell membrane function and function of
organelles. Modified structure of deoxyribonucleic acid may cause
mutations, which in absence of repairation enzyme activity lead to cell
injury. IRON AND OXIDATIVE STRESS: Iron metabolism is also important in
the development of pulmonary emphysema due to its role in production of
some oxidants.
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