CIGARETTE-SMOKE, FERRITIN, AND LIPID-PEROXIDATION

Gas and tar phases of commercially available filter cigarettes were te sted for ferritin-iron-releasing effects and polyunsaturated-fatty-aci d oxidant capacity in vitro A vacuum pump-dependent apparatus with Cam bridge filters was used to separate gas and tar; the former was direct ly smoked into reaction mixtures, while the latter was extracted from Cambridge filters in aqueous medium and freshly used at 40 to 80% fina l concentrations. Both phases induced ferritin iron release, which was not antagonized by superoxide dismutase (SOD). In specific experiment s, we have also shown that gas and tar extracts could cross an organic (i.e., chloroform)-phospholipid layer before mobilizing ferritin iron . Once delocalized from ferritin, iron could trigger lipid peroxidatio n; however, a marked prooxidant effect (inhibited by 20 mu M deferoxam ine mesylate and significantly decreased by 40 mu M vitamin E) was obs erved only with gas, whereas tar extracts showed antioxidant effects. Accordingly, tar extracts could also antagonize lipid peroxidation dri ven by non-chelated iron or by peroxyl radicals. in the absence of fer ritin, gas-induced lipid peroxidation was very low, and tar extracts w ere apparently ineffective. Thus, the intrinsic lipoperoxidative capac ity of cigarette smoke is low and is due to gas; however, when smoke i nteracts with ferritin, a marked iron-driven peroxidation becomes mani fest essentially with gas, tar components acting as antioxidants. The present data suggest that cigarette-smoke-mediated iron mobilization f rom ferritin may represent a specific prooxidant mechanism related to cigarette smoking in vivo.