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Vitamin E Modulates Inflammatory Responses Induced by Cigarette Smoke (CS) Exposure in alpha ‐Tocopherol Transfer Protein (TTP) Null Mice

CS induced pulmonary inflammatory responses have been reported to be associated with oxidative stress and decreased levels of vitamin E (alpha‐tocopherol, a‐T), possibly due to increased utilization and turnover (AJCN 2005;81:–103). In order to clarify possible vitamin E related modulations of inflammatory responses and oxidative stress we investigated the effects of a‐ and gamma (g)‐T on acute CS in mice with < 10% of normal plasma and lung tissue a‐T levels due to a genetic defect of a‐tocopherol transfer protein (TTP KO). Mice (4 weeks old) were fed a‐ (35 mg/kg diet) or g‐T (1000 mg/kg diet) for 8–10 weeks and exposed to 60 mg/m3 CS, 6 hr/day for 3 days. Endpoints measured included a‐ & g‐T levels, g‐T metabolites (g‐CEHC), inflammatory responses (IL‐1b, MIP‐2, MMP‐9 & COX‐2) and oxidative stress markers (4‐HNE, HO‐1, CuZnSOD & MnSOD). While a‐ & g‐T levels were not changed, g‐CEHC levels were decreased after CS in both WT and TTP KO mice. HO‐1 and MnSOD were upregulated by CS as compared to air exposed WT and TTP KO mice. At basal level, HO‐1, MnSOD and MMP‐9 were increased in TTP KO mice as compared to WT mice. HO‐1, MnSOD, MMP‐9 and IL‐1b were upregulated when high g‐T diet was fed to WT and TTP KO mice either exposed air or CS. The results suggest that TTP KO mice are more susceptible to CS induced pulmonary inflammation and that vitamin E administration modulates these responses.