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Ascorbic Acid Deficiency

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Fumihiko Horio – One of the best experts on this subject based on the ideXlab platform.

  • Ascorbic Acid Deficiency decreases hepatic cytochrome p 450 especially cyp2b1 2b2 and simultaneously induces heme oxygenase 1 gene expression in scurvy prone ods rats
    Bioscience Biotechnology and Biochemistry, 2014
    Co-Authors: Misato Kobayashi, Yukiko Hoshinaga, Natsuko Miura, Yuki Tokuda, Shigeru Shigeoka, Atsushi Murai, Fumihiko Horio

    Abstract:

    The mechanisms underlying the decrease in hepatic cytochrome P-450 (CYP) content in Ascorbic Acid Deficiency was investigated in scurvy-prone ODS rats. First, male ODS rats were fed a diet containing sufficient Ascorbic Acid (control) or a diet without Ascorbic Acid (deficient) for 18 days, with or without the intraperitoneal injection of phenobarbital. Ascorbic Acid Deficiency decreased hepatic microsomal total CYP content, CYP2B1/2B2 protein, and mitochondrial cytochrome oxidase (COX) complex IV subunit I protein, and simultaneously increased heme oxygenase-1 protein in microsomes and mitochondria. Next, heme oxygenase-1 inducers, that is lipopolysaccharide and hemin, were administered to phenobaribital-treated ODS rats fed sufficient Ascorbic Acid. The administration of these inducers decreased hepatic microsomal total CYP content, CYP2B1/2B2 protein, and mitochondrial COX complex IV subunit I protein. These results suggested that the stimulation of hepatic heme oxygenase-1 expression by Ascorbic Acid

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  • Ascorbic Acid Deficiency decreases hepatic cytochrome P-450, especially CYP2B1/2B2, and simultaneously induces heme oxygenase-1 gene expression in scurvy-prone ODS rats
    Bioscience biotechnology and biochemistry, 2014
    Co-Authors: Misato Kobayashi, Yukiko Hoshinaga, Natsuko Miura, Yuki Tokuda, Shigeru Shigeoka, Atsushi Murai, Fumihiko Horio

    Abstract:

    The mechanisms underlying the decrease in hepatic cytochrome P-450 (CYP) content in Ascorbic Acid Deficiency was investigated in scurvy-prone ODS rats. First, male ODS rats were fed a diet containing sufficient Ascorbic Acid (control) or a diet without Ascorbic Acid (deficient) for 18 days, with or without the intraperitoneal injection of phenobarbital. Ascorbic Acid Deficiency decreased hepatic microsomal total CYP content, CYP2B1/2B2 protein, and mitochondrial cytochrome oxidase (COX) complex IV subunit I protein, and simultaneously increased heme oxygenase-1 protein in microsomes and mitochondria. Next, heme oxygenase-1 inducers, that is lipopolysaccharide and hemin, were administered to phenobaribital-treated ODS rats fed sufficient Ascorbic Acid. The administration of these inducers decreased hepatic microsomal total CYP content, CYP2B1/2B2 protein, and mitochondrial COX complex IV subunit I protein. These results suggested that the stimulation of hepatic heme oxygenase-1 expression by Ascorbic Acid

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  • Ascorbic Acid Deficiency stimulates hepatic expression of inflammatory chemokine, cytokine-induced neutrophil chemoattractant-1, in scurvy-prone ODS rats.
    Journal of nutritional science and vitaminology, 2006
    Co-Authors: Fumihiko Horio, Keiichiro Kiyama, Misato Kobayashi, Kaori Kawai, Takanori Tsuda

    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.

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Yoshiji Ohta – One of the best experts on this subject based on the ideXlab platform.

  • Short-term Ascorbic Acid Deficiency induced oxidative stress in the retinas of young guinea pigs
    Journal of Biomedical Science, 2004
    Co-Authors: Yoshiji Ohta, Takashi Yamasaki, Takafumi Niwa, Taku Okubo, Masayuki Horiguchi

    Abstract:

    We examined whether short-term Ascorbic Acid Deficiency induces oxidative stress in the retinas of young guinea pigs. Four-week-old guinea pigs were given a scorbutic diet (20 g/animal/day) with and without adequate Ascorbic Acid (400 mg/animal/day) in drinking water for 3 weeks. The serum concentrations of the reduced form of Ascorbic Acid and the oxidized form of Ascorbic Acid in the deficient group were 14.1 and 4.1%, respectively, of those in the adequate group. The retinal contents of the reduced form of Ascorbic Acid and the oxidized form of Ascorbic Acid in the deficient group were 6.4 and 27.3%, respectively, of those in the adequate group. The retinal content of thiobarbituric Acid-reactive substances, an index of lipid peroxidation, was 1.9-fold higher in the deficient group than in the adequate group. Retinal reduced glutathione and vitamin E contents in the deficient group were 70.1 and 69.4%, respectively, of those in the adequate group. This Ascorbic Acid Deficiency did not affect serum thiobarbituric Acid-reactive substances and reduced glutathione concentrations but increased serum vitamin E concentration. These results indicate that short-term Ascorbic Acid Deficiency induces oxidative stress in the retinas of young guinea pigs without disrupting systemic antioxidant status.

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  • Short-term Ascorbic Acid Deficiency does not impair antioxidant status in lens of guinea pigs.
    Journal of nutritional science and vitaminology, 2004
    Co-Authors: Yoshiji Ohta, Takafumi Niwa, Takashi Yamasaki

    Abstract:

    We examined whether short-term Ascorbic Acid Deficiency impairs antioxidant status in the lens of guinea pigs. Male guinea pigs aged 4 wk were given a scorbutic diet (20 g/animal per day) with and without Ascorbic Acid (400 mg/animal per day) in drinking water for 3 wk. The Ascorbic Acid-deficient group showed no lens opacity. The Ascorbic Acid-deficient group had 14% of serum Ascorbic Acid concentration, 6% of aqueous humor Ascorbic Acid concentration, and 18% of lens Ascorbic Acid content in the Ascorbic Acid-adequate group. There were no differences in the contents of lens reduced glutathione and thiobarbituric Acid reactive substances, an index of lipid peroxidation, between the Ascorbic Acid-deficient and adequate groups, while the deficient group had higher lens vitamin E content than the adequate group. The Ascorbic Acid-deficient group had higher serum vitamin E concentration than the Ascorbic Acid adequate group, while there were no differences in the concentrations of serum reduced glutathione and tiobarbituric Acid reactive substances between the deficient and adequate groups. These results indicate that short-term Ascorbic Acid Deficiency does not impair antioxidant status in the lens of guinea pigs despite induction of severe Ascorbic Acid depletion in the tissue, which may result in no cataract formation.

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  • Prolonged marginal Ascorbic Acid Deficiency induces oxidative stress in retina of guinea pigs.
    International journal for vitamin and nutrition research. Internationale Zeitschrift fur Vitamin- und Ernahrungsforschung. Journal international de vi, 2002
    Co-Authors: Yoshiji Ohta, Takashi Yamasaki, Takafumi Niwa, Taku Okubo, Masayuki Horiguchi

    Abstract:

    We examined whether prolonged marginal Ascorbic Acid Deficiency induces oxidative stress in the retina of guinea pigs. Male guinea pigs aged four weeks were given a scorbutic diet (20 g/animal per day) with either marginally deficient Ascorbic Acid (0.5 mg/animal per day) or adequate Ascorbic Acid (1 g/animal per day) in drinking water for three and six months. The retinal contents of the reduced form of Ascorbic Acid in the deficient group at three and six months were 68.1 and 43.5%, respectively, of that in the corresponding adequate group. The retinal contents of the oxidized form of Ascorbic Acid in the deficient group at three and six months were 1.9- and 2.7-fold, respectively, higher than that in the corresponding adequate group. The content of retinal thiobarbituric Acid reactive substances (TBARS), an index of lipid peroxidation, in the deficient group was 2.5-fold higher than that in the adequate group at six months. The retinal contents of reduced glutathione (GSH) in the deficient group at three and six months were 84.8 and 66.7%, respectively, of that in the corresponding adequate group. The deficient group had 37.5% of retinal vitamin E content of the adequate group at six months. The deficient group had higher serum vitamin E concentration than the adequate group in both experimental periods. There were no differences in serum TBARS and GSH concentrations between the groups at both periods. These results indicate that prolonged marginal Ascorbic Acid Deficiency induces oxidative stress in the retina of guinea pigs without systemic oxidative stress.

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Masayuki Horiguchi – One of the best experts on this subject based on the ideXlab platform.

  • Short-term Ascorbic Acid Deficiency induced oxidative stress in the retinas of young guinea pigs
    Journal of Biomedical Science, 2004
    Co-Authors: Yoshiji Ohta, Takashi Yamasaki, Takafumi Niwa, Taku Okubo, Masayuki Horiguchi

    Abstract:

    We examined whether short-term Ascorbic Acid Deficiency induces oxidative stress in the retinas of young guinea pigs. Four-week-old guinea pigs were given a scorbutic diet (20 g/animal/day) with and without adequate Ascorbic Acid (400 mg/animal/day) in drinking water for 3 weeks. The serum concentrations of the reduced form of Ascorbic Acid and the oxidized form of Ascorbic Acid in the deficient group were 14.1 and 4.1%, respectively, of those in the adequate group. The retinal contents of the reduced form of Ascorbic Acid and the oxidized form of Ascorbic Acid in the deficient group were 6.4 and 27.3%, respectively, of those in the adequate group. The retinal content of thiobarbituric Acid-reactive substances, an index of lipid peroxidation, was 1.9-fold higher in the deficient group than in the adequate group. Retinal reduced glutathione and vitamin E contents in the deficient group were 70.1 and 69.4%, respectively, of those in the adequate group. This Ascorbic Acid Deficiency did not affect serum thiobarbituric Acid-reactive substances and reduced glutathione concentrations but increased serum vitamin E concentration. These results indicate that short-term Ascorbic Acid Deficiency induces oxidative stress in the retinas of young guinea pigs without disrupting systemic antioxidant status.

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  • Prolonged marginal Ascorbic Acid Deficiency induces oxidative stress in retina of guinea pigs.
    International journal for vitamin and nutrition research. Internationale Zeitschrift fur Vitamin- und Ernahrungsforschung. Journal international de vi, 2002
    Co-Authors: Yoshiji Ohta, Takashi Yamasaki, Takafumi Niwa, Taku Okubo, Masayuki Horiguchi

    Abstract:

    We examined whether prolonged marginal Ascorbic Acid Deficiency induces oxidative stress in the retina of guinea pigs. Male guinea pigs aged four weeks were given a scorbutic diet (20 g/animal per day) with either marginally deficient Ascorbic Acid (0.5 mg/animal per day) or adequate Ascorbic Acid (1 g/animal per day) in drinking water for three and six months. The retinal contents of the reduced form of Ascorbic Acid in the deficient group at three and six months were 68.1 and 43.5%, respectively, of that in the corresponding adequate group. The retinal contents of the oxidized form of Ascorbic Acid in the deficient group at three and six months were 1.9- and 2.7-fold, respectively, higher than that in the corresponding adequate group. The content of retinal thiobarbituric Acid reactive substances (TBARS), an index of lipid peroxidation, in the deficient group was 2.5-fold higher than that in the adequate group at six months. The retinal contents of reduced glutathione (GSH) in the deficient group at three and six months were 84.8 and 66.7%, respectively, of that in the corresponding adequate group. The deficient group had 37.5% of retinal vitamin E content of the adequate group at six months. The deficient group had higher serum vitamin E concentration than the adequate group in both experimental periods. There were no differences in serum TBARS and GSH concentrations between the groups at both periods. These results indicate that prolonged marginal Ascorbic Acid Deficiency induces oxidative stress in the retina of guinea pigs without systemic oxidative stress.

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