| Research Abstract |
As a new function of ascorbic acid (vitamin C), we found that ascorbic acid deficiency caused the stimulation of hepatic expression of acute phase proteins genes in ODS rat unable to synthesize ascorbic acid. Serum concentrations of interleukin-6, an inflammatory cytokine, and CINC-1, an inflammatory chemokine, were elevated in ascorbic acid-deficient ODS rats without growth retardatioon. The hepatic CINC-1 mRNA level was higher in ascorbic acid-deficient ODS rats than that in the control ODS rats. In this study, we hypothesized that ascorbic acid deficiency caused the stimulation of interleikin-6 and CINC-1 genes expression in liver due to influx of endotoxin from the intesitinal lumen to portal vein. However, we could not observe the results supportiong our hypothesis.
We are also maintaining the colony of a novel strain of spontaneously hypertensive rat unable to synthesize ascorbic acid, SHR-od. It has been focused that hypertention accompanies with oxidative stress. In this study, we found that serum and tissue concentrations of ascorbic acid in SHR-od were markedly lower than those in normotensive ODS rats. These low concentrations might be caused by the acceleration of ascorbic acid degradation in SHR-od compared to ODS rats. This result suggests that the requirement of ascorbic acid is increased in hypertensive patients.
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