Saturday, December 17, 2011

vitamin C and alcohol induced oxidative stress

Posted by Chantel M. Contributed by US National Library of Medicine National Institutes of Health

In the study of "Impact of massive ascorbic acid supplementation on alcohol induced oxidative stress in guinea pigs" by Suresh MV, Sreeranjit Kumar CV, Lal JJ, Indira M., posted in US National Library of Medicine National Institutes of Health, found that Administration of ascorbic acid also reduced the activity of gamma-glutamyl transpeptidase (GGT), the marker enzyme of alcohol induced toxicity. The vitamin E level, which was reduced by alcohol intake, was raised by the co-administration of AA and alcohol. These studies suggest that a mega dose of AA helps in the prevention of alcohol induced oxidative stress by enhancing the antioxidant capacity and also by reducing the lipid peroxidation products.

vitamin C and cellular energy metabolism.

Posted by Chantel M. Contributed by US National Library of Medicine National Institutes of Health

In the study of "Vitamin C deficiency activates the purine nucleotide cycle in zebrafish" by Kirkwood JS, Lebold KM, Miranda CL, Wright CL, Miller GW, Tanguay RL, Barton CL, Traber MG, Stevens JF., posted in US National Library of Medicine National Institutes of Health, found that irreversibly deaminates AMP to form IMP. We found a 47% increase in AMPD activity in the AA deficient zebrafish, complementary to the 44-fold increase in IMP concentration. These results suggest that vitamin C is crucial for the maintenance of cellular energy metabolism.

Vitamin C and iron-refractory iron deficiency anemia (IRIDA).

Posted by Chantel M. Contributed by US National Library of Medicine National Institutes of Health

In the study of "Responsiveness to oral iron and ascorbic acid in a patient with IRIDA" by Cau M, Galanello R, Giagu N, Melis MA., posted in US National Library of Medicine National Institutes of Health, reported that a female infant homozygous for a loss of function mutation in TMPRSS6 gene, who responded to oral iron therapy when supplemented with ascorbic acid.

Vitamin C and Glaucoma.

Posted by Chantel M. Contributed by US National Library of Medicine National Institutes of Health

In the study of "Association between a SLC23A2 gene variation, plasma vitamin C levels, and risk of glaucoma in a Mediterranean population" by Zanon-Moreno V, Ciancotti-Olivares L, Asencio J, Sanz P, Ortega-Azorin C, Pinazo-Duran MD, Corella D., posted in US National Library of Medicine National Institutes of Health, found that The rs1279683 single-nucleotide polymorphisms (SNPs) in SLC23A2 was significantly associated with lower plasma concentrations of vitamin C and with higher risk of primary open-angle glaucoma (POAG) in the G allele (GG subjects) subjects.

Vitamin C deficiency and chronic ultraviolet-B exposure

Posted by Chantel M. Contributed by US National Library of Medicine National Institutes of Health

In the study of "The effect of vitamin C deficiency and chronic ultraviolet-B exposure on corneal ultrastructure: a preliminary investigation" by Hayes S, Cafaro TA, Boguslawska PJ, Kamma-Lorger CS, Boote C, Harris J, Young R, Hiller J, Terrill N, Meek KM, Serra HM., posted in US National Library of Medicine National Institutes of Health, found that UVB-induced changes in the corneal ultrastructure were most pronounced in animals fed an ascorbic acid-deficient diet. This suggests that ascorbic acid may play a vital role in protecting the corneal stroma from the harmful effects of UVB.

Monday, December 12, 2011

Life-threatening thiamine deficiency in infants

Posted by Chantel M. Contributed by US National Library of Medicine National Institutes of Health

In the study of "Outbreak of life-threatening thiamine deficiency in infants in Israel caused by a defective soy-based formula" by Fattal-Valevski A, Kesler A, Sela BA, Nitzan-Kaluski D, Rotstein M, Mesterman R, Toledano-Alhadef H, Stolovitch C, Hoffmann C, Globus O, Eshel G., posted in US National Library of Medicine National Institutes of Health, indicated that Clinician awareness of the possibility of thiamine deficiency even in well-nourished infants is important for early recognition and prevention of irreversible brain damage. Therapy with large doses of thiamine should be initiated at the earliest suspicion of vitamin depletion, even before laboratory evidence is available and before neurologic or cardiologic symptoms appear.

Thiamine and acid tolerance of Listeria monocytogenes.

Posted by Chantel M. Contributed by US National Library of Medicine National Institutes of Health

In the study of "Thiamine plays a critical role in the acid tolerance of Listeria monocytogenes" by Madeo M, O'Riordan N, Fuchs TM, Utratna M, Karatzas KA, O'Byrne CP., posted in US National Library of Medicine National Institutes of Health, found that Thiamine-depleted cultures failed to produce significant concentrations of acetoin, consistent with the known thiamine dependence of acetolactate synthase, an enzyme required for acetoin synthesis from pyruvate. As acetoin synthesis is a proton-consuming process, we suggest that the acid sensitivity observed in thiamine-depleted cultures may be owing to an inability to produce acetoin.