Vitamin E suppresses the induction of reactive oxygen species release by lipopolysaccharide, interleukin-1beta and tumor necrosis factor-alpha in rat alveolar macrophages.

Over the last decade, although investigations have suggested that vitamin E affects the immune response, not much is known about its affect on the alveolar macrophage functions. In the present study, we have investigated the effect of high vitamin E (DL-alpha-tocopheryl acetate, alpha-TA) supplementation for 10 d on the activation state of rat alveolar macrophages induced by lipopolysaccharide (LPS), interleukin (IL)-1beta or tumor necrosis factor (TNF)-alpha on the basis of their ability to produce reactive oxygen species (ROS), such as superoxide (O2-*) and H2O2. LPS treatment (1 and 10 microg/mL) caused 2.44 and 2.54-fold increases in O2-*, and 2.1 and 2.3-fold increases in H2O2, respectively, from alveolar macrophages (AMs) in the diet group fed 50 mg alpha-TA/kg. However, this enhancement was not observed for the AMs of the diet groups fed 250 or 1,250 mg alpha-TA/kg. Similar results were obtained on treating the AMs with proinflammatory cytokines IL-1beta or TNF-alpha. The observed suppression in ROS release in response to various stimulants may be due to the direct and/or indirect effect of high vitamin E (250 and 1,250 mg alpha-TA/kg diet) supplementation. It may therefore, be concluded that high alpha-TA supplementation in the diet modulates the activation of AMs in rats.