ABSTRACT
I. Introduction 426
II. Reactive Oxygen Species 427
A. Sources of ROS in the Lung 429
III. Antioxidant Defense Mechanisms 430
A. Antioxidant Enzymes in the Lung 431
Superoxide Dismutases 431
Catalase 431
Glutathione Peroxidase and Glutathione Reductase 432
B. Nonenzymatic Antioxidants 432
Vitamin C and Vitamin E 432
Glutathione 432
Uric Acid 432
IV. Biophysical and Biochemical Alterations of the Surfactant
System by ROS 433
A. Effects of ROS on Pulmonary Surfactant 433
Biochemical Modifications of Surfactant by ROS 434
B. Effects of Oxidation on the Interfacial Properties of
Pulmonary Surfactant 436
C. Pathological Processes Involving ROS in the Lung 438
Hyperoxia 439
Adult Respiratory Distress Syndrome 439
Asthma 440
COPD and Emphysema 441
Damage of Surfactant by Cigarette Smoke 441
V. Summary 441
References 442
I. Introduction
The toxicity of oxygen originates from its property to dismutate into oxygen
radicals known as reactive oxygen species (ROS). These radicals can react
with biomolecules, thus changing and inactivating these molecules. ROS are pro-
duced continuously in the body as byproducts of normal aerobic respiration and
other biochemical processes. However, when an organ or tissue is placed under
oxidative stress, ROS production can overwhelm the body’s endogenous anti-
oxidant defense systems and lead to tissue damage. The lung is the first to
encounter inspired oxygen. Its cells are exposed to higher oxygen concentrations
than cells in other organs, and owing to its large surface area, the lung is a
primary target of oxidant injury.
