Abstract
Oxygen and ozone both have been found to enhance or to inhibit the development of tumors in mouse lung. As a general rule, preexposure to the oxidant, before administration of a carcinogen, or exposure to high levels for a comparatively short time immediately following carcinogen administration favors development of tumors. On the other hand, prolonged exposure begun after a certain time following carcinogen exposure inhibits tumor development. The paradoxical effects of the two oxidants depend on experimental design; results can be tentatively explained in terms of oxidant-induced cell proliferation or by oxidant-mediated cytotoxicity. Besides being capable of modifying chemically induced lung tumorigenesis, ozone and oxygen also appear to induce tumors in mouse lung on their own. The conclusions drawn from the study of mouse lung tumors have recently been reinforced in experiments with hamsters, where hyperoxia has clear tumor-modulating effects.