Biosynthesis of L-Ascorbic Acid: Missing Steps in Animals incapable of synthesizing the Vitamin

Chatterjee, I. B.; Kar, Nirmal C.; Ghosh, Nilabja; Guha, B. C.

doi:10.1038/192163a0

Cited by 41 publications

(19 citation statements)

References 6 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…All animal treatment procedures met the NIH guidelines [20] and Institutional Animal Ethics committee guidelines. The guinea pig was used as a model animal, because, like humans, guinea pigs cannot synthesize ascorbic acid [21,22]. The guinea pigs were fed an ascorbate-free diet for 7 days to minimize the ascorbate level of plasma and tissues [15].…”

Section: Methodsmentioning

confidence: 99%

Black tea prevents cigarette smoke-induced apoptosis and lung damage

et al. 2007

View full text Add to dashboard Cite

BackgroundCigarette smoking is a major cause of lung damage. One prominent deleterious effect of cigarette smoke is oxidative stress. Oxidative stress may lead to apoptosis and lung injury. Since black tea has antioxidant property, we examined the preventive effect of black tea on cigarette smoke-induced oxidative damage, apoptosis and lung injury in a guinea pig model.MethodsGuinea pigs were subjected to cigarette smoke exposure from five cigarettes (two puffs/cigarette) per guinea pig/day for seven days and given water or black tea to drink. Sham control guinea pigs were exposed to air instead of cigarette smoke. Lung damage, as evidenced by inflammation and increased air space, was assessed by histology and morphometric analysis. Protein oxidation was measured through oxyblot analysis of dinitrophenylhydrazone derivatives of the protein carbonyls of the oxidized proteins. Apoptosis was evidenced by the fragmentation of DNA using TUNEL assay, activation of caspase 3, phosphorylation of p53 as well as over-expression of Bax by immunoblot analyses.ResultsCigarette smoke exposure to a guinea pig model caused lung damage. It appeared that oxidative stress was the initial event, which was followed by inflammation, apoptosis and lung injury. All these pathophysiological events were prevented when the cigarette smoke-exposed guinea pigs were given black tea infusion as the drink instead of water.ConclusionCigarette smoke exposure to a guinea pig model causes oxidative damage, inflammation, apoptosis and lung injury that are prevented by supplementation of black tea.

show abstract

Section: Methodsmentioning

confidence: 99%

Black tea prevents cigarette smoke-induced apoptosis and lung damage

et al. 2007

View full text Add to dashboard Cite

show abstract

“…in some fishes [5], in some passeriform birds [7], in some bats [8], in guinea pigs [10] and in primates of the suborder Haplorrhini (e.g. monkeys, apes and humans) [7], [9]–[10]. All of these species lack activity of L-Gulonolactone oxidase (GULO) in their livers (or kidneys) to catalyze the last step of the Vc synthesis pathway so that they need to compensate by obtaining Vc from their food [8]–[10].…”

Section: Introductionmentioning

confidence: 99%

Recent Loss of Vitamin C Biosynthesis Ability in Bats

et al. 2011

View full text Add to dashboard Cite

The traditional assumption that bats cannot synthesize vitamin C (Vc) has been challenged recently. We have previously shown that two Old World bat species (Rousettus leschenaultii and Hipposideros armiger) have functional L-gulonolactone oxidase (GULO), an enzyme that catalyzes the last step of Vc biosynthesis de novo. Given the uncertainties surrounding when and how bats lost GULO function, exploration of gene evolutionary patterns is needed. We therefore sequenced GULO genes from 16 bat species in 5 families, aiming to establish their evolutionary histories. In five cases we identified pseudogenes for the first time, including two cases in the genus Pteropus (P. pumilus and P. conspicillatus) and three in family Hipposideridae (Coelops frithi, Hipposideros speoris, and H. bicolor). Evolutionary analysis shows that the Pteropus clade has the highest ω ratio and has been subjected to relaxed selection for less than 3 million years. Purifying selection acting on the pseudogenized GULO genes of roundleaf bats (family Hipposideridae) suggests they have lost the ability to synthesize Vc recently. Limited mutations in the reconstructed GULO sequence of the ancestor of all bats contrasts with the many mutations in the ancestral sequence of recently emerged Pteropus bats. We identified at least five mutational steps that were then related to clade origination times. Together, our results suggest that bats lost the ability to biosynthesize vitamin C recently by exhibiting stepwise mutation patterns during GULO evolution that can ultimately lead to pseudogenization.

show abstract

“…9,10) However, AA synthesis was identified mainly in the livers of most mammalian species including mice and rats. 11) AA is believed to undergo subsequent transport to the ovaries, where cellular uptake occurs through an energy-dependent process. 12) In this study, to ascertain the reason for ovarian SMP30/GNL expression, we examined SMP30/GNL, Cyp19a1 and Gulo expressions and AA levels in the mouse ovaries during gestation by using wild-type and SMP30/GNL knockout mice.…”

Section: )mentioning

confidence: 99%

“…11) If SMP30/ GNL participates in an AA synthetic process in the ovaries of mice, Gulo, which catalyzes the last step of AA production, must also be expressed in the ovary. Accordingly, mRNA expression of Gulo was examined by RT-PCR.…”

Section: Smp30/gnl Mrna Expression In the Mouse Ovarymentioning

confidence: 99%

Senescence Marker Protein-30/Gluconolactonase Expression in the Mouse Ovary during Gestation

Kagami

Kondo

Handa

et al. 2013

Biological & Pharmaceutical Bulletin

View full text Add to dashboard Cite

Senescence marker protein-30 (SMP30) was first described as a physiologic entity that decreases in the rat liver and kidney with aging. Previously, we established that SMP30 is the lactone-hydrolyzing enzyme gluconolactonase (GNL), which is involved in ascorbic acid (AA) biosynthesis. In the present study, we found SMP30/GNL mRNA expressed in the mouse ovary. To ascertain the reason for ovarian SMP30/GNL expression, we examined mice during gestation. SMP30/GNL mRNA expression was evident at the start of gestation, increased for the next eight days then decreased rapidly. Moreover, L-gulono-γ-lactone oxidase (Gulo) mRNA, which catalyzes the last step of AA, was found in the ovaries of these mice. The variations of these genes' expression showed an inverse pattern to that of Cyp19a1 (aromatase) mRNA expression. Therefore, the SMP30/GNL and Gulo mRNA expression might be regulated by estrogen levels in the ovary. Since the presence of both SMP30/GNL and Gulo mRNAs could indicate that AA synthesis occurs in the ovary, we quantified AA levels in mouse ovaries during gestation. However, no correlation was found between changes of AA content and SMP30/GNL or Gulo mRNAs expression at this site. Moreover, we compared the changes of AA content during gestation between wild-type and SMP30/GNL knockout mice, which cannot synthesize AA, and found no significant differences between them. These results indicated that, although AA synthesis might occur in the ovaries, the amount of AA which is synthesized in ovaries must be quite low and insufficient to influence the AA content in ovary.Key words ascorbic acid; senescence marker protein-30; gluconolactonase; ovary; estrogen After the discovery of senescence marker protein-30 (SMP30) as a protein that decreases with aging in the liver, kidney, and lung, 1,2) SMP30 transcripts were detected in not only the liver, kidney, and lungs of mice but also in their brain and testes, as established by reverse transcription-polymerase chain reaction (RT-PCR) analysis.3) In humans, SMP30 in parenchymal cells of the liver, proximal tubular cells of the kidney, acinal and ductal cells of the pancreas, and fasciculate cells of the adrenal cortex was seen by immunohistochemical staining.2) To clarify the relationship between decreases of SMP30 and organ disorders associated with aging, we established SMP30 knockout mice. 4) These knockout mice are viable and fertile but lower in body weight and shorter in life span than their wild-type counterparts.5) Throughout our experiments in vitro and in vivo, the livers from SMP30 knockout mice were far more susceptible to TNF-α-and Fasmediated apoptosis than those from the wild-type. 4)

show abstract

Biosynthesis of L-Ascorbic Acid: Missing Steps in Animals incapable of synthesizing the Vitamin

Cited by 41 publications

References 6 publications

Black tea prevents cigarette smoke-induced apoptosis and lung damage

Black tea prevents cigarette smoke-induced apoptosis and lung damage

Recent Loss of Vitamin C Biosynthesis Ability in Bats

Senescence Marker Protein-30/Gluconolactonase Expression in the Mouse Ovary during Gestation

Contact Info

Product

Resources

About