Vitamin E Suppresses the Induction of Reactive Oxygen Species Release by Lipopolysaccharide, Interleukin-1β and Tumor Necrosis Factor-α in Rat Alveolar Macrophages

• Published in: Journal of Nutritional Science and Vitaminology 1999, Vol.45(6), pp.675-686
• Main Authors: PATHANIA, Vandana, SYAL, Nidhi, PATHAK, Chander Mohan, KHANDUJA, Krishan Lal
• Format: Article
• Language: English
• Subjects: alveolar macrophages; Biological and medical sciences; Fundamental and applied biological sciences. Psychology; Fundamental immunology; Immunobiology; interleukin-1β; lipopolysaccharide; Modulation of the immune response (stimulation, suppression); tumor necrosis factor-α; vitamin E
• ISSN: 0301-4800; 1881-7742
• DOI: 10.3177/jnsv.45.675

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-α-tocopheryl acetate, α-TA) supplementation for 10d on the activation state of rat alveolar macrophages induced by lipopolysaccharide (LPS), interleukin (IL)-1β or tumor necrosis factor (TNF)-α on the basis of their ability to produce reactive oxygen species (ROS), such as superoxide (O-2) and H2O2. LPS treatment (1 and 10μg/mL) caused 2.44 and 2.54-fold increases in O-2, and 2.1 and 2.3-fold increases in H2O2, respectively, from alveolar macrophages (AMs) in the diet group fed 50mg α-TA/kg. However, this enhancement was not observed for the AMs of the diet groups fed 250 or 1, 250mg α-TA /kg. Similar results were obtained on treating the AMs with proinflammatory cytokines IL-1β or TNF-α. 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, 250mg α-TA/kg diet) supplementation. It may therefore, be concluded that high α-TA supplementation in the diet modulates the activation of AMs in rats.