Antimutagenic and promutagenic activity of ascorbic acid during oxidative stress

Bijur, Gautam N.; Ariza, Maria E.; Hitchcock, Charles L.; Williams, Marshall V.

doi:10.1002/(sici)1098-2280(1997)30:3<339::aid-em13>3.0.co;2-e

Cited by 58 publications

(36 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In contradiction to our results, ascorbic acid was shown to protect from As 2 O 3 -induced toxicity [63]. However, evidence exists that ascorbic acid, widely praised as an antioxidant [64], can act as an oxidizing agent in the presence of ROS-inducing substances [65,66]. Recently, promising results of a phase I/II combined trial of As 2 O 3 and ascorbic acid were presented [47,[67][68][69].…”

Section: Discussioncontrasting

confidence: 57%

Antimony-trioxide- and arsenic-trioxide-induced apoptosis in myelogenic and lymphatic cell lines, recruitment of caspases, and loss of mitochondrial membrane potential are enhanced by modulators of the cellular glutathione redox system

et al. 2009

View full text Add to dashboard Cite

Antimony-trioxide-and arsenic-trioxide-induced apoptosis in myelogenic and lymphatic cell lines, recruitment of caspases, and loss of mitochondrial membrane potential are enhanced by modulators of the cellular glutathione redox system. Annals of Hematology, Springer Verlag, 2009, 88 (11) (BSO). Other modulators of the cellular redox system showed this effect to a lower extent and enhancement was not consistent for the different cell lines tested. Caspase inhibitors protected cell lines from Sb 2 O 3 -and As 2 O 3 -induced apoptosis. When BSO was added, the inhibitors lost their protective ability. The ability of modulators of the cellular redox system in clinically applicable concentrations to enhance the apoptotic effects of the two oxides in a synergistic way may be helpful to reduce their toxicity by optimizing their dose.

show abstract

Section: Discussioncontrasting

confidence: 57%

Antimony-trioxide- and arsenic-trioxide-induced apoptosis in myelogenic and lymphatic cell lines, recruitment of caspases, and loss of mitochondrial membrane potential are enhanced by modulators of the cellular glutathione redox system

et al. 2009

View full text Add to dashboard Cite

show abstract

“…On the contrary, co-treatment experiments by Kaya et al, (2002) indicate that different concentrations of AA (25, 75 and 250 mM) did not show any antigenotoxic effect on the genotoxicity of 4-nitroquinoline 1-oxide (4-NQO) and Kaya et al (2002) found that when co-treatments experiments with cobalt chloride (CoCl 2 ) were carried out, instead of reducing the genotoxicity of CoCl 2 AA acts as a co-mutagen by inducing a significant increase in the frequency of mutant clones over the values obtained with CoCl 2 alone. Bijur et al (1997) showed that in Chinese hamster ovary cell line AS52 there is a temporal relationship between the anti-and prooxidant activities of a physiologically relevant concentration of AA and oxidative stress. Treatment of cells with AA prior to treatment of the cells with a radical generating system (RGS) results in a statistically significant inhibition of the cytotoxicity and mutagenicity.…”

Section: Discussionmentioning

confidence: 99%

“…However, administration of large amounts of AA to biological systems has lead to genotoxic effects in several different test systems (Shamberger, 1984) because AA has both antioxidant and prooxidant activities (Bijur et al, 1997).…”

Section: Introductionmentioning

confidence: 99%

Modulatory effects of the antioxidant ascorbic acid on the direct genotoxicity of doxorubicin in somatic cells of Drosophila melanogaster

2007

View full text Add to dashboard Cite

In this study two different crosses involving the wing cell markers mwh and flr 3 (standard (ST) cross and high bioactivation (HB) cross, the latter being characterized by a high constitutive level of cytochrome P450 which leads to an increased sensitivity to a number of promutagens and procarcinogens) were used to investigate the modulatory effects of ascorbic acid (AA) combined with the antitumor agent doxorubicin (DXR) in Drosophila melanogaster. We observed that the two different concentrations of AA (50 or 100 mM) had no effect on spots frequencies, while DXR treatments (0.2 or 0.4 mM) gave positive results for all types of spots, when compared to negative control. For marker-heterozygous (MH) flies, a protective effect was observed with the lower concentration of AA (50 mM) that was able to statistically decrease the frequency of spots induced by DXR (0.2 mM), while an enhanced frequency of spots induced by DXR was observed with the higher concentration of AA (100 mM), when compared to DXR treatment (p < 0.05). These results suggest that AA may interfere with free radicals generated by DXR and with other possible reactive metabolites. The efficiency of AA in protecting the somatic cells of D. melanogaster against mutation and recombination induced by DXR is dependent on the dose used and the protection is directly related to the activity of cytochrome P450 enzymes.

show abstract

“…Ascorbic acid and mushroom lectin promotes the expression of SOD 2 gene significantly (p < 0.001). However, evidence indicates that ascorbic acid can also act as an oxidizing agent, particularly in the presence of compound that increases the production of ROS [25]. Mushroom lectin has a potential role to upregulate the mRNA expression of SOD 2 gene because it has ameliorative potentials owing to its antioxidant and trace element contents.…”

Section: Discussionmentioning

confidence: 99%

Sodium Arsenite-Induced Alteration in Hepatocyte Function of Rat with Special Emphasis on Superoxide Dismutase Expression Pathway and its Prevention by Mushroom Lectin

Bera¹,

Rana²,

Bhattacharya³

et al. 2011

Basic &Amp; Clinical Pharmacology &Amp; Toxicology

View full text Add to dashboard Cite

This study was accomplished to exemplify the possible protective role of ascorbic acid and mushroom lectin against arsenic-induced cytotoxicity and impairment of superoxide dismutase (SOD) production pathway in hepatocytes of rat. Hepatocytes were isolated from rat and treated with sodium arsenite (AS), arsenic plus ascorbic acid (AS + AA) and arsenic plus mushroom lectin (AS + ML). A placebo control was also included. Arsenic treatment resulted in the depletion of cell proliferation, phagocytic activity (nitro blue tetrazolium index) and superoxide dismutase (SOD) activity, relative mRNA expression of superoxide dismutase 2 (SOD 2 ) and enhanced production of nitric oxide (NO). Ascorbic acid, a standard antioxidant, could normalize cellular perturbation and SOD production pathway relating to gene expression, whereas partially purified Pleurotus florida lectin (PFL), an edible mushroom containing protein complex, maintained cellular activity and prevented stress by normalizing phagocytic (NBT index) and SOD activities vis-à-vis relative gene expression. It could further defend NO production of hepatocytes. Mushroom lectin strongly prevented sodium arsenite-induced damage of SOD production pathway in hepatocytes, and its effect was also comparable to a standard antioxidant, i.e. ascorbic acid.

show abstract

Antimutagenic and promutagenic activity of ascorbic acid during oxidative stress

Cited by 58 publications

References 19 publications

Antimony-trioxide- and arsenic-trioxide-induced apoptosis in myelogenic and lymphatic cell lines, recruitment of caspases, and loss of mitochondrial membrane potential are enhanced by modulators of the cellular glutathione redox system

Antimony-trioxide- and arsenic-trioxide-induced apoptosis in myelogenic and lymphatic cell lines, recruitment of caspases, and loss of mitochondrial membrane potential are enhanced by modulators of the cellular glutathione redox system

Modulatory effects of the antioxidant ascorbic acid on the direct genotoxicity of doxorubicin in somatic cells of Drosophila melanogaster

Sodium Arsenite-Induced Alteration in Hepatocyte Function of Rat with Special Emphasis on Superoxide Dismutase Expression Pathway and its Prevention by Mushroom Lectin

Contact Info

Product

Resources

About