The analysis of inflammation-like response caused by ascorbic acid deficiency in ODS rats unable to synthesize ascorbic acid.

作为抗坏血酸（维生素C）的新功能，我们发现抗坏血酸缺乏可刺激不能合成抗坏血酸的ODS大鼠肝脏急性期蛋白基因的表达。在抗坏血酸缺乏的ODS大鼠中，血清白细胞介素-6（一种炎症细胞因子）和cinc1（一种炎症趋化因子）的浓度升高，但没有生长迟缓。抗坏血酸缺乏的ODS大鼠肝脏cinc1 mRNA水平高于对照组。在这项研究中，我们假设抗坏血酸缺乏引起肝脏中白细胞介素-6和cinc1基因表达的刺激，这是由于内毒素从肠腔流入门静脉所致。然而，我们无法观察到支持我们假设的结果。我们也在维持一种不能合成抗坏血酸的新型自发性高血压大鼠的菌落。人们一直关注的是，高血压伴随着氧化应激。在本研究中，我们发现SHR-od大鼠的血清和组织抗坏血酸浓度明显低于正常ODS大鼠。这些低浓度可能是由于与ODS大鼠相比，SHR-od大鼠的抗坏血酸降解加速所致。这一结果提示高血压患者对抗坏血酸的需要量增加。

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.