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-Tocopherol, but not
-tocopherol, decreases proinflammatory eicosanoids and inflammation damage in rats
Division of Biochemistry and Molecular Biology, University of California, Berkeley; and Children's Hospital Oakland Research Institute, Oakland, California, USA
1Correspondence: CHORI, 5700 Martin Luther King Jr. Way, Oakland, CA 94609-1673, USA. E-mail: bnames{at}uclink4.berkeley.edu
-Tocopherol (
T), the major form of vitamin E in U.S. diets, and its physiological metabolite 2, 7, 8-trimethyl-2-(ß-carboxyethyl)-6-hydroxychroman (
-CEHC), in contrast to
-tocopherol (
T), the primary vitamin E in supplements, inhibit cyclooxygenase-catalyzed synthesis of prostaglandin E2 (PGE2) in activated macrophages and epithelial cells. Here we report that in carrageenan-induced inflammation in male Wistar rats, administration of
T (33 or 100 mg/kg) and
-CEHC (2 mg/pouch), but not
T (33 mg/kg), significantly reduced PGE2 synthesis at the site of inflammation.
T, but not
T, significantly inhibited the formation of leukotriene B4, a potent chemotactic agent synthesized by the 5-lipoxygenase of neutrophils. Although
T had no effect on neutrophil infiltration, it significantly attenuated the partial loss of food consumption caused by inflammation-associated discomfort. Administration of
T led consistently to a significant reduction of inflammation-mediated increase in 8-isoprostane, a biomarker of lipid peroxidation.
T at 100 mg/kg reduced TNF-
(65%;P=0.069), total nitrate/nitrite (40%;P=0.1), and lactate dehydrogenase activity (30%;P=0.067). Collectively,
T inhibits proinflammatory PGE2 and LTB4, decreases TNF-
, and attenuates inflammation-mediated damage. These findings provide strong evidence that
T shows anti-inflammatory activities in vivo that may be important for human disease prevention and therapy.Jiang, Q., Ames, B. N.
-Tocopherol, but not
-tocopherol, decreases proinflammatory eicosanoids and inflammation damage in rats.
Key Words: vitamin E
-tocopherol metabolite prostaglandin E2 leukotriene B4 TNF-alpha
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