The effect of vitamin C supplementation on the development of organ pathology in experimental
Trypanosoma brucei infection in rats was investigated. Infection caused significant (
p<0.05) increases in serum alanine and aspartate aminotransferases as well as in blood urea nitrogen and serum creatinine. Infection also caused significant (
p<0.05) hypoproteinemia and hypoalbuminemia as well as decreases in liver and kidney total homogenate proteins. Supplementation of infected rats with vitamin C prevented the disease-induced elevation of serum creatinine and alanine aminotransferase (ALAT) and also significantly ameliorated the decreases in total protein levels in serum, liver, and kidney, as well as the elevated serum aspartate aminotransferase (ASAT). The trypanosome infection caused depletion of the levels of reduced glutathione (GSH) in the blood, liver, and kidney, as well as reduced the plasma level of ascorbic acid. Vitamin supplementation prevented the depletion of these endogenous antioxidants. We concluded that vitamin C supplementation ameliorates oxidative stress, thereby sparing endogenous antioxidant reserves and protecting tissues and organs against
T. brucei-induced damage.
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