Abstract

Rats pretreated with cod liver oil (CLO) were exposed either to ultraviolet light (UVL) irradiation or to carbon tetrachloride (CCU) and/or trichloroethylene (TCE) treatments, and the amount of exhaled ethane was measured as an index of in vivo lipid peroxidation. The method of ethane collection had been modified relative to existing techniques. UVL irradiation increased ethane production with a lag period of 18–24 hr. In contrast to UVL, CCU and TCE increased the exhalation of ethane without latency, irrespective of CLO pretreatment. The effects of CCU and TCE showed no synergism or additivity. Our data are consistent with the established lipid peroxidation-increasing effect of chlorinated hydrocarbons, and more importantly, they demonstrate for the first time an increase in ethane production due to UVL. The considerable lag period between the irradiation and the ethane production argues against a direct lipid peroxidation-increasing effect of UVL in the skin. It is suggested that the changes are related to leukocyte infiltration of the inflamed skin surface, and that the increased lipid peroxidation results from free radical liberation during phagocytosis. A potential role of slowly released arachidonic acid from the irradiated cells is also considered.

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