title: Ascorbic acid deficiency stimulates hepatic expression of inflammatory chemokine, cytokine-induced neutrophil chemoattractant-1, in scurvy-prone ODS rats.
abstract: ODS rat has a hereditary defect in ascorbic acid biosynthesis and is a useful animal model for elucidating the physiological role of ascorbic acid. We previously demonstrated by using ODS rats that ascorbic acid deficiency changes the hepatic gene expression of acute phase proteins, as seen in acute inflammation. In this study, we investigated the effects of ascorbic acid deficiency on the production of inflammatory chemokine, cytokine-induced neutrophil chemoattractant-1 (CINC-1), in ODS rats. Male ODS rats (6 wk of age) were fed a basal diet containing ascorbic acid (300 mg/kg diet) or a diet without ascorbic acid for 14 d. Obvious symptoms of scurvy were not observed in the ascorbic acid-deficient rats. Ascorbic acid deficiency significantly elevated the serum concentration of CINC-1 on d 14. The liver and spleen CINC-1 concentrations in the ascorbic acid-deficient rats were significantly elevated to 600% and 180% of the respective values in the control rats. However, the lung concentration of CINC-1 was not affected by ascorbic acid deficiency. Ascorbic acid deficiency significantly elevated the hepatic mRNA level of CINC-1 (to 480% of the value in the control rats), but not the lung mRNA level. These results demonstrate that ascorbic acid deficiency elevates the serum, liver and spleen concentrations of CINC-1 as seen in acute inflammation, and suggest that ascorbic acid deficiency stimulate the hepatic CINC-1 gene expression.
authors.affiliation: Department of Food & Nutritional Sciences, College of Bioscience and Biotechnology, Chubu University, Aichi, Japan. horiof@isc.chubu.ac.jp
authors.forename: Fumihiko
authors.initials: F
authors.lastname: Horio
authors.forename: Keiichiro
authors.initials: K
authors.lastname: Kiyama
authors.forename: Misato
authors.initials: M
authors.lastname: Kobayashi
authors.forename: Kaori
authors.initials: K
authors.lastname: Kawai
authors.forename: Takanori
authors.initials: T
authors.lastname: Tsuda
mesh_terms: D000818:Animals; D016632:Apolipoprotein A-I / Q000235:genetics; D001057:Apolipoproteins E / Q000235:genetics; D001205:Ascorbic Acid / Q000032:analysis / Q000097:blood; D001206:Ascorbic Acid Deficiency / Q000235:genetics / Q000378:metabolism*; D015152:Blotting, Northern; D001835:Body Weight; D054360:Chemokine CXCL1; D019743:Chemokines, CXC / Q000032:analysis / Q000097:blood / Q000235:genetics*; D015870:Gene Expression; D020022:Genetic Predisposition to Disease; D006242:Haptoglobins / Q000235:genetics; D008099:Liver / Q000737:chemistry / Q000378:metabolism*; D008168:Lung / Q000737:chemistry; D008297:Male; D009929:Organ Size; D012333:RNA, Messenger / Q000032:analysis; D051381:Rats; D011922:Rats, Mutant Strains; D012614:Scurvy / Q000235:genetics*; D013154:Spleen / Q000737:chemistry
chemical_list: D016632:Apolipoprotein A-I; D001057:Apolipoproteins E; D054360:Chemokine CXCL1; D019743:Chemokines, CXC; C513297:Cxcl1 protein, rat; D006242:Haptoglobins; D012333:RNA, Messenger; D001205:Ascorbic Acid