Malondialdehyde (MDA) is a product of free-radical reaction with lipids and has been implicated in a variety of pathological processes including inflammation and carcinogenesis. In order to document the toxic reactions related to the pathogenic mechanisms of mineral fibers, asbestos and other mineral dusts were examined for their potency to produce lipid peroxidation using the thiobarbital method for MDA measurement. Human peripheral blood-derived neutrophils (PMN), guinea pig peritoneal macrophages, and guinea pig alveolar lavage cells produced MDA when treated with crocidolite asbestos. Of the various mineral dusts tested, only crocidolite showed a significant increase of MDA production. The amount of MDA produced by PMN treated with crocidolite increased with milling the fiber and with the incubation time. Both superoxide dismutase (SOD) and catalase were examined for their ability to inhibit MDA formation. At concentrations of up to 50 μg/106Cells, SOD did not inhibit the MDA formation in macrophages. However, catalase at the same concentration inhibited MDA formation in macrophages completely. A possible mechanism of MDA formation and its relationship with superoxide production are discussed
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