Inhibitory effect of vitamin E on proinflammatory cytokines-and endotoxin-induced nitric oxide release in alveolar macrophages

Dietary lycopene supplementation suppresses Th2 responses and lung eosinophilia in a mouse model of allergic asthma

“…A negative association has been reported between intakes of vitamin E-rich foods and serum IgE and atopy [28]. Additionally, vitamin E has been shown to promote a Th1 phenotype in mice [29] and reduce lipopolysaccharide (LPS)-induced nitric oxide (NO) release from rat alveolar macrophages [30]. The potential benefit of β-carotene in a model of allergic inflammation is less clear.…”

The effects of erdosteine, N-acetylcysteine, and vitamin E on nicotine-induced apoptosis of pulmonary cells

“…NAC modulated the production and release of cytokines during the local inflammatory response and protected lung tissue from oxygen radicals generated during phagocytosis, thereby attenuating the cigarette smoke-induced hyperplastic and metaplastic changes of lung epithelial cells (Balansky et al, 1999). Vitamin E, which decreases the level of TNF-␣ in human monocytes, modulated TNF-␣ activities and further decreased DNA fragmentation (Khanduja et al, 2005). Antioxidants reduced the rate of pulmonary epithelial cell apoptosis and inhibited the increase in local TNF-␣ levels caused by nicotine.…”

Antioxidant Vitamins and Their Use in Preventing Cardiovascular Disease

“…Scavenger receptors, such as CD36, known to be important for oxidized LDL uptake by macrophages, are down regulated by vitamin E [40,41]. Finally, vitamin E inhibits the activity of inducible NOS (iNOS) and NADPH oxidase, thereby inhibiting the macrophage respiratory burst [42,43]. …”