EFFECT OF KEROSENE AND ITS SOOT ON THE CHRYSOTILE-MEDIATED TOXICITY TO THE RAT ALVEOLAR MACROPHAGES

In order to examine the pulmonary toxicity of kerosene oil and its com bustion product (soot) in asbestos-exposed rats, various biochemical a nd chemical parameters were assayed. Treatment of rats with a single i ntratracheal dose of chrysotile asbestos (5 mg) and kerosene (50 mu l) or its soot (5 mg) in combination led to an increased number of pulmo nary alveolar macrophages (PAM), elevated levels of hydrogen peroxide, and thiobarbituric acid-reacting substances, alterations in the activ ities of primary (glutathione peroxidase and catalase) and secondary ( glutathione reductase and glucose-g-phosphate dehydrogenase) endogenou s antioxidant enzymes, and depletion in the levels of glutathione in P ARI compared to the chrysotile, kerosene, or soot alone, These changes may indicate the generation of oxidative stress in the macrophages. T he resulting oxidative stress may be subsequently critical in collapsi ng the cellular membrane, which may change the cell membrane permeabil ity and may also damage the phagolysosomal membrane, thereby releasing the membrane bound enzymes as indicated by an increased leakage of in tracellular acid phosphatase and lactate dehydrogenase. The injury to macrophages may trigger events that lead to lung fibrosis and/or malig nancies in the exposed animals, This study may be helpful in understan ding the etiology of certain clinical and pathological disorders in th e population exposed simultaneously to both asbestos and kerosene or i ts combustion products. (C) 1997 Academic Press.