2010
DOI: 10.1016/j.bbrc.2010.08.052
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The ascorbic acid paradox

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Cited by 28 publications
(26 citation statements)
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References 40 publications
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“…We found that 30 mg/ml of vitamin C had a better effect on the proliferation of ADSCs than 60 and 90 mg/ml of vitamin C. The ADSCs treated with 30 mg/ml of vitamin C have demonstrated the best cell proliferation activity, which was similar to previous reports about the concentration-dependent effect of vitamin C on cell proliferation. [18][19][20] In addition, our findings also indicated that cell cycle progression was promoted, and the decreased percentage of G 1 phase was obviously observed after incubation with 30 mg/ml of vitamin C for 24 and 48 h, and meanwhile, the increased percentage of the cells at S and G 2 /M phase was also observed. To further investigate the mechanism by which vitamin C increased cell proliferation and promoted cell cycle progression, we detected the cell cycle-associated proteins including cyclin E1, p53, p21, and CDK2.…”
Section: Discussionsupporting
confidence: 61%
“…We found that 30 mg/ml of vitamin C had a better effect on the proliferation of ADSCs than 60 and 90 mg/ml of vitamin C. The ADSCs treated with 30 mg/ml of vitamin C have demonstrated the best cell proliferation activity, which was similar to previous reports about the concentration-dependent effect of vitamin C on cell proliferation. [18][19][20] In addition, our findings also indicated that cell cycle progression was promoted, and the decreased percentage of G 1 phase was obviously observed after incubation with 30 mg/ml of vitamin C for 24 and 48 h, and meanwhile, the increased percentage of the cells at S and G 2 /M phase was also observed. To further investigate the mechanism by which vitamin C increased cell proliferation and promoted cell cycle progression, we detected the cell cycle-associated proteins including cyclin E1, p53, p21, and CDK2.…”
Section: Discussionsupporting
confidence: 61%
“…Inactivation of peroxisomal catalase has been linked to a shorter life span in Caenorhabditis elegans and S. cerevisiae (Petriv and Rachubinski, 2004), yet mice completely deficient in the enzyme develop normally and are apparently healthy (Ho et al , 2004). Catalase inactivation with 3-AT is progeric in human cells (Wood et al , 2006) yet it elicits a hormetic, life span–extending phenotype in S. cerevisiae (Mesquita et al , 2010).…”
Section: Discussionmentioning
confidence: 99%
“…Conversely, the protocol used here (repeated treatment with a low dose) reduced tyrosine hydroxylase staining in the substantia nigra and striatum, and part of the alterations induced by the treatment were not recovered after 30 days of treatment withdrawal [8]. Second, it has been shown that reserpine treatment increases brain oxidative stress and this alteration is accompanied by behavioral deficits [10,22,23]. In addition, in a previous study [9] the repeated treatment with a low dose of reserpine induced an increase in striatal level of lipid peroxidation, which occurred concomitantly to the motor impairment.…”
Section: Discussionmentioning
confidence: 99%