In vivo antimutagenic effect of ascorbic acid against mutagenicity of the common antiamebic drug diiodohydroxyquinoline

Ghaskadbi, Surendra; Vaidya, V. G.

doi:10.1016/0165-1218(89)90137-7

Cited by 34 publications

(11 citation statements)

References 14 publications

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“…These results corroborate the work of Lemos et al (2005) who showed no genotoxic effects of vitamin A (3.0 mg/mL) or vitamin C (880.5 mg/mL) by the comet assay in CHO cells. The results presented here for fluoxetine treatment via gavage are in line with an earlier reported study showing that vitamin C, administered orally at doses of 100, 200, 400 and 800 mg/kg b.w., did not increase the frequency of chromosome aberrations in bone marrow cells of rats (Ghaskadbi and Vaidya, 1989). The negative results for the MI were similar to those obtained by Nefic (2001), who observed that vitamin C (10 and 100 μg/mL) did not alter the MI of human peripheral lymphocytes treated in vitro.…”

Section: Discussionsupporting

confidence: 75%

Cytotoxicity and mutagenicity of fluoxetine hydrochloride (Prozac), with or without vitamins A and C, in plant and animal model systems

Düsman¹,

Almeida²,

Mariucci³

et al. 2014

Genet. Mol. Res.

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ABSTRACT. Fluoxetine, commonly known as Prozac, is the first representative of the so-called new generation of antidepressants that promise efficacy, with few side effects, against deep depression, nervous bulimia, and anxiety. As there is a growing number of people suffering from anxiety and depression; consequently, the use of fluoxetine is also increasing. Verifying absence of drug effects such as cytotoxicity or mutagenicity is of great importance. Certain vitamins, such as vitamin A (retinol, retinoids) and vitamin C (ascorbic acid) protect and are extremely active against mutagens. We evaluated the cytotoxic and mutagenic activity of fluoxetine, with and without concomitant administration of vitamin A or C, in Allium cepa meristem cells and Wistar rat bone marrow cells. The A. cepa meristem cells Cytotoxicity and mutagenicity of fluoxetine showed fluoxetine cytotoxicity; concomitant treatment with vitamin A or C proved non-protective. Treatment of Wistar rats with fluoxetine intraperitoneally or via gavage did not affect cell division or cause clastogenic effects. Vitamin A and C did not affect the cytotoxicity or mutagenicity of fluoxetine in the rat cells.

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Section: Discussionsupporting

confidence: 75%

Cytotoxicity and mutagenicity of fluoxetine hydrochloride (Prozac), with or without vitamins A and C, in plant and animal model systems

Düsman¹,

Almeida²,

Mariucci³

et al. 2014

Genet. Mol. Res.

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“…Vitamin C (L ascorbic acid) is an excellent antioxidant which can react with and scavenge out many of these free radicals and oxidative products (Shamberger 1984), and thereby protects cells against the genotoxicity of various oxidants (Machlin and Bendich 1987). Fortunately, this vitamin has no genotoxicity of its own (Ghaskadbi andVaidya 1989, Bose and, and is rightly believed to act as a bioantimutagen (kada 1984, Shamberger 1984, Gebhart et al 1985. In most of the previous studies (Hoda andSinha 1991a, b, Hoda et al 1991), the pesticide induced genotoxicity got significantly minimised by the human therapeutic dose of vitamin C (10 mg/kg bw/day), but it (vitamin C) never brought the damage-frequency down to the con trol level.…”

mentioning

confidence: 99%

Dose-Dependent Minimisation of Cytogenetic Toxicity of Endosulfan(an Organochlorine Pesticide) by Vitamin C.

Khan

Sinha

1992

CYTOLOGIA

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“…It forms DNA adducts in rat and human hepatocytes in vitro [34][35][36] and also induces micronuclei in rat liver cells in vivo [20]. Antioxidants are known to reduce mutagenic potential of various mutagens in in vivo studies [37,38]. The identification and characterization of various active principles can help frame important strategies to reduce the risk of cancer in human beings [39].…”

Section: Discussionmentioning

confidence: 98%

Antigenotoxic effect of nordihydroguaiaretic acid against chlormadinone acetate-induced genotoxicity in mice bone-marrow cells

et al. 2007

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Nordihydroguaiaretic acid (NDGA), a phenolic lignan, was tested for its antigenotoxic potential against chlormadinone acetate (CMA)-induced genotoxic damage in mice bone-marrow cells. Doses of about 22.50 mg/kg body weight of CMA were given along with 1, 5 and 10 mg/kg body weight of NDGA intraperitoneally. The treatment resulted in the reduction of sister chromatid exchanges and chromosomal aberrations induced by CMA, suggesting an antigenotoxic potential of NDGA. Earlier studies show that CMA generates reactive oxygen species, responsible for genotoxic damage. The free radical-scavenging property of NDGA is responsible for the reduction of genotoxic damage induced by CMA in mice bone-marrow cells.

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In vivo antimutagenic effect of ascorbic acid against mutagenicity of the common antiamebic drug diiodohydroxyquinoline

Cited by 34 publications

References 14 publications

Cytotoxicity and mutagenicity of fluoxetine hydrochloride (Prozac), with or without vitamins A and C, in plant and animal model systems

Cytotoxicity and mutagenicity of fluoxetine hydrochloride (Prozac), with or without vitamins A and C, in plant and animal model systems

Dose-Dependent Minimisation of Cytogenetic Toxicity of Endosulfan(an Organochlorine Pesticide) by Vitamin C.

Antigenotoxic effect of nordihydroguaiaretic acid against chlormadinone acetate-induced genotoxicity in mice bone-marrow cells

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