Biochemical basis of ozone toxicity

Aerobic organisms by definition require oxygen, and the importance of iron in aerobic respiration has long been recognized, but despite their beneficial roles, these elements can pose a real threat to the organism. During oxygen reduction, reactive species such as O2-. and H2O2 are formed readily. Iron can combine with these species, or with molecular oxygen itself, to generate free radicals which will attack the polyunsaturated fatty acids of membrane lipids. This oxidative deterioration of membrane lipids is known as lipid peroxidation. To protect itself against this form of attack, the organism possesses several types of defense mechanisms. Under normal conditions, these defenses appear to offer adequate protection for cell membranes, but the possibility exists that certain foreign compounds may interfere with or even overwhelm these defenses, and herein could lie a general mechanism of toxicity. This possible cause of toxicity is discussed in relation to other suggested causes.

Lipid peroxidation and mechanisms of toxicity.

Introduction -- Chapter 1 Physical-chemical properties of ozone. natural production of ozone. the toxicology of ozone -- Chapter 2 How ozone is generated and its concentrations measured? -- Chapter 3 Preparation of ozonated water and oil for the topical therapy. ozone as a drinking water disinfectant. ozone disinfection to prevent nosocomial infections.-Chapter 4 How does ozone act? how and why can we avoid ozone toxicity? -- Chapter 5 How is ozone administered? -- Chapter 6 The actual six therapeutic modalities -- Chapter 7 The potential toxicity of ozone. side effects and contraindications of ozone therapy -- Chapter 8 Is ozone really a “wonder drug”? -- Chapter 9 The clinical application of ozone therapy -- Chapter 10 The dilemma between hyperbaric oxygen therapy (hot) and ozone therapy -- Chapter 11 The promising future of ozone therapy in medicine.

OZONE A New Medical Drug

Ozone is one of the most toxic and ubiquitous air pollutants. This review focuses on the toxic effects of ozone in animals and on the similarities and disimilarities between the toxic effects in animals and humans. The molecular basis for the toxicity of ozone is discussed, based on the vigorous oxidizing properties of ozone. Despite the existence of anatomical differences between human, subhuman primate, and dog lungs versus common experimental rodent lungs, the anatomical lesion of ozone inhalation occurs at the functionally equivalent site of the junction between the conducting airway and the respiratory region. Ciliated cells of the upper airways and the type 1 cell of the centriacinar region are most affected. Type 2 cell proliferation is a hallmark of ozone toxicity. A wide variety of biochemical and physiological changes have been noted in several animal species and in humans. Considerable evidence for a free-radical-mediated or lipid peroxide-mediated toxicity is evident, especially in the induction of the glutathione peroxidase system and the protective effects of vitamins C and E. Ozone appears to be a weak mutagen and to produce chromosomal abnormalities. Defects in defense against airborne infection are present in animals, which are more susceptible to airborne infection after ozone exposure. Epidemiological studies, however, fail to detect increased respiratory infections in humans due to ozone. Despite the variety of toxic effects, few qualitative differences between species are apparent; rather, quantitative differences do occur. Ozone may thus be an ideal compound for quantitative extrapolation of toxicity from animals to humans.

Ching K. Chow

Papers

Influence of dietary vitamin E on the red cells of ozone-exposed rats