Gamma-tocopherol (gammaT) complements
alpha-tocopherol (alphaT) by trapping reactive
nitrogen oxides to form a stable adduct, 5-nitro-gammaT [Christen et al., PNAS 94:3217-3222; 1997]. This observation led to the current investigation in which we studied the effects of gammaT supplementation on plasma and tissue
vitamin C,
vitamin E, and
protein nitration before and after
zymosan-induced acute
peritonitis. Male Fischer 344 rats were fed for 4 weeks with either a normal chow diet with basal 32 mg alphaT/kg, or the same diet supplemented with approximately 90 mg d-gammaT/kg. Supplementation resulted in significantly higher levels of gammaT in plasma, liver, and kidney of control animals without affecting alphaT, total alphaT+gammaT or
vitamin C.
Intraperitoneal injection of
zymosan caused a marked increase in
3-nitrotyrosine and a profound decline in
vitamin C in all tissues examined. Supplementation with gammaT significantly inhibited
protein nitration and ascorbate oxidation in the kidney, as indicated by the 29% and 56% reduction of kidney
3-nitrotyrosine and dehydroascorbate, respectively. Supplementation significantly attenuated
inflammation-induced loss of
vitamin C in the plasma (38%) and kidney (20%).
Zymosan-treated animals had significantly higher plasma and tissue gammaT than nontreated pair-fed controls, and the elevation of gammaT was strongly accentuated by the supplementation. In contrast, alphaT did not significantly change in response to
zymosan treatment. In untreated control animals, gammaT supplementation lowered basal levels of
3-nitrotyrosine in the kidney and buffered the
starvation-induced changes in
vitamin C in all tissues examined. Our study provides the first in vivo evidence that in rats with high basal amounts of alphaT, a moderate gammaT supplementation attenuates
inflammation-mediated damage, and spares
vitamin C during
starvation-induced stress without affecting alphaT.