Gas and tar phases of commercially available filter cigarettes were tested for ferritin-iron-releasing effects and polyunsaturated-fatty-acid oxidant capacity in vitro. A vacuum pump-dependent apparatus with Cambridge filters was used to separate gas and tar; the former was directly smoked into reaction mixtures, while the latter was extracted from Cambridge filters in aqueous medium and freshly used at 40 to 80% final concentrations. Both phases induced ferritin iron release, which was not antagonized by superoxide dismutase (SOD). In specific experiments, 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 peroxidation; however, a marked prooxidant effect (inhibited by 20 microM deferoxamine mesylate and significantly decreased by 40 microM vitamin E) was observed only with gas, whereas tar extracts showed antioxidant effects. Accordingly, tar extracts could also antagonize lipid peroxidation driven by non-chelated iron or by peroxyl radicals. In the absence of ferritin, gas-induced lipid peroxidation was very low, and tar extracts were apparently ineffective. Thus, the intrinsic lipoperoxidative capacity of cigarette smoke is low and is due to gas; however, when smoke interacts with ferritin, a marked iron-driven peroxidation becomes manifest essentially with gas, tar components acting as antioxidants. The present data suggest that cigarette-smoke-mediated iron mobilization from ferritin may represent a specific prooxidant mechanism related to cigarette smoking in vivo.

Cigarette smoke, ferritin, and lipid peroxidation

LAPENNA, Domenico;MEZZETTI, Andrea;CIOFANI, Giuliano;CONSOLI, Agostino;MARZIO, Leonardo;CUCCURULLO, Franco
1995-01-01

Abstract

Gas and tar phases of commercially available filter cigarettes were tested for ferritin-iron-releasing effects and polyunsaturated-fatty-acid oxidant capacity in vitro. A vacuum pump-dependent apparatus with Cambridge filters was used to separate gas and tar; the former was directly smoked into reaction mixtures, while the latter was extracted from Cambridge filters in aqueous medium and freshly used at 40 to 80% final concentrations. Both phases induced ferritin iron release, which was not antagonized by superoxide dismutase (SOD). In specific experiments, 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 peroxidation; however, a marked prooxidant effect (inhibited by 20 microM deferoxamine mesylate and significantly decreased by 40 microM vitamin E) was observed only with gas, whereas tar extracts showed antioxidant effects. Accordingly, tar extracts could also antagonize lipid peroxidation driven by non-chelated iron or by peroxyl radicals. In the absence of ferritin, gas-induced lipid peroxidation was very low, and tar extracts were apparently ineffective. Thus, the intrinsic lipoperoxidative capacity of cigarette smoke is low and is due to gas; however, when smoke interacts with ferritin, a marked iron-driven peroxidation becomes manifest essentially with gas, tar components acting as antioxidants. The present data suggest that cigarette-smoke-mediated iron mobilization from ferritin may represent a specific prooxidant mechanism related to cigarette smoking in vivo.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11564/161452
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