Effect of exogenous ascorbic acid intake on biosynthesis of ascorbic acid in mice

Tsao, Constance S.; Young, May

doi:10.1016/0024-3205(89)90421-9

Cited by 34 publications

(25 citation statements)

References 15 publications

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“…A direct inhibition of GULO by L-AA is unlikely, since the addition of super physiologic amounts of L-AA to liver homogenates did not alter the rate of L-AA formation in vitro (data not shown). This is in agreement with previous observations with either glucuronolactone (a precursor of gulonolactone) or gulonolactone as substrate (Tsao andYoung 1989, 1990). Tsao and Young (1989) also found a negative correlation between GULO activity and L-AA content in the hepatic portal blood of mice.…”

Section: Discussionsupporting

confidence: 82%

“…The control mechanism for the conversion of gulonolactone to L-AA is stereospecific because large amounts of dietary erythorbic acid, a stereo isomer of AA, could not reduce the rate of L-AA formation when gulonolactone was used as substrate (Tsao and Young 1990). Furthermore, Tsao and Young (1989) suggested that the feedback control mechanism for the enzymatic conversion of glucuronolactone to gulonolactone was not stereospecific.…”

Section: Discussionmentioning

confidence: 99%

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Intragenic deletion in the gene encoding L-gulonolactone oxidase causes vitamin C deficiency in pigs

et al. 2004

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The absence of L-ascorbic acid (L-AA, or AA) synthesis in scurvy-prone organisms, including humans, other primates, guinea pigs, and flying mammals, was traced to the lack of L-gulonolactone oxidase (GULO) activity. GULO is a microsomal enzyme that catalyzes the terminal step in the biosynthesis of L-AA. Clinical cases of scurvy were described in a family of Danish pigs. This trait is controlled by a single autosomal recessive allele designated od (osteogenic disorder). Here we demonstrate that the absence of GULO activity and the associated vitamin C deficiency in od/od pigs is due to the occurrence of a 4.2-kbp deletion in the GULO gene. This deletion includes 77 bp of exon VIII, 398 bp of intron 7 and 3.7 kbp of intron 8, which leads to a frame shift. The mutant protein is truncated to 356 amino acids, but only the first 236 amino acids are identical to the wild-type GULO protein. In addition, the od allele seems to be less expressed in deficient and heterozygous pigs compared with the normal allele in heterozygous and wild-type animals as determined by ribonuclease protection assay. We also developed a DNA-based test for the diagnosis of the deficient allele. However, we failed to identify the mutated allele in other pig populations.

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Section: Discussionsupporting

confidence: 82%

Section: Discussionmentioning

confidence: 99%

Intragenic deletion in the gene encoding L-gulonolactone oxidase causes vitamin C deficiency in pigs

et al. 2004

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“…One of the toxic mechanisms of organotellurium compounds is their ability to generate some oxidizing radicals agents (Chen et al, 2001), but in this study the lipid peroxidation was not increased by the organotellurium compound. Furthermore, Vitamin C, levels, a non-enzymatic antioxidant defense (Tsao and Young, 1989), was not modified by organotellurium treatment. In addition, the sub-chronic treatment did not significantly altered GSH, which plays a central role in the endogenous antioxidant defense (Nogueira et al, 2004).…”

Section: Discussionmentioning

confidence: 86%

A biochemical and toxicological study with diethyl 2-phenyl-2-tellurophenyl vinylphosphonate in a sub-chronic intraperitoneal treatment in mice

et al. 2007

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“…In fact, vitamin A concentration in plasma of the exercised rats was always lower than that of nonexercised rats (from 3.8% to 20.0%). Biosynthesis of vitamin C in rat liver meets its daily needs, yet supplemental amounts given orally can improve antioxidant defences in this animal [Djurašević et al, 2008], and influence blood plasma concentrations of the vitamin [Tsao & Young, 1989]. A study by Banhegyi et al [1997] proved that long-term supplementing mice with vitamin C inhibited its biosynthesis in the liver.…”

Section: Discussionmentioning

confidence: 99%

Antioxidant Vitamins as Oxidative Stress Markers in Rat Plasma After Physical Exercise - a Short Report

Wawrzyniak¹,

Hamułka²,

Drywień³

et al. 2014

Pol. J. Food Nutr. Sci.

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The aim of the study was to verify the hypothesis that β-carotene, vitamin E, vitamin C administered individually or in combination may differently modify their levels in blood plasma being also markers of the oxidative stress. Male Wistar rats were supplemented antioxidants per os (α-tocopherol -2 mg/d, ascorbic acid -12 mg/d, β-carotene -1 mg/d), both individually or in combination of 2 or 3, for 14 days. During experiment, half of the animals in each group (n=8) were subjected to treadmill exercise for 15 min at the speed of 20 m/min, to induce oxidative stress. Vitamins in rat plasma were assessed by the high-performance liquid chromatography (HPLC). Results suggest that vitamin E and C supplemented simultaneously may provide some benefit during physical exercise. The significant influence of administered α-tocopherol acetate and physical exercise on the level of α-tocopherol in the plasma was observed. Thus only the concentration of α-tocopherol in blood may be treated as a marker of oxidative stress.

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Effect of exogenous ascorbic acid intake on biosynthesis of ascorbic acid in mice

Cited by 34 publications

References 15 publications

Intragenic deletion in the gene encoding L-gulonolactone oxidase causes vitamin C deficiency in pigs

Intragenic deletion in the gene encoding L-gulonolactone oxidase causes vitamin C deficiency in pigs

A biochemical and toxicological study with diethyl 2-phenyl-2-tellurophenyl vinylphosphonate in a sub-chronic intraperitoneal treatment in mice

Antioxidant Vitamins as Oxidative Stress Markers in Rat Plasma After Physical Exercise - a Short Report

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