The need for a mammalian test system for mutagens: Action of some reducing agents

Stich, H. F.; Wei, Lan; Lam, Peter

doi:10.1016/s0304-3835(78)80039-1

Cited by 74 publications

(10 citation statements)

References 10 publications

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“…In the studies of Stich et al (1978), MacRae and Stich (1979) as well as in the present one, GSH was applied in Eagle's MEM, whereas 0nfelt and Klasterska (1983,1984) and, probably, Speit et al (1980) used Hank's solution. Our observation that the genotoxic effects of GSH were abolished by application in Hank's may explain the striking discrepancies between the different studies.…”

Section: Discussionmentioning

confidence: 84%

“…Their genotoxic properties have also been demonstrated. With respect to GSH, Stich et al (1978) reported the induction of unscheduled DNA synthesis and clastogenicity in the presence of Cu 2+ ions in human fibroblasts and CHO cells at 10 -2 or 10 -3 moles/1 GSH, respectively, after a 3 h exposure. At higher concentrations both activities declined.…”

Section: Discussionmentioning

confidence: 99%

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Exogenous glutathione induces sister chromatid exchanges, clastogenicity and endoreduplication in V79-E Chinese hamster cells

Trust

Bach

1985

Cell Biol Toxicol

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Glutathione (GSH) dissolved in Eagle's MEM and added to cultures of V79-E cells in concentrations between 2.5 X 10(-4) and 10(-3) moles/l for 1 h induces a dose-dependent cell cycle delay, sister chromatid exchanges and clastogenic damage. 7-8% of the metaphases showed endoreduplication at a recovery phase of 25 and 30 h after treatment with 10(-3) moles/l GSH. Higher concentrations were lethal. The highest tolerated dose corresponds to the intracellular GSH level in V79-E cells. In the same range of concentrations, glutathione disulfide was inactive. Endoreduplication induction by GSH is G2-phase specific and endoreduplication metaphases show a reduced occurrence of single SCEs when extrapolated to the diploid complement. The adverse effects of GSH are independent of the presence of serum in the culture fluid but completely abolished when the treatment is performed in Hank's solution instead of MEM. The mechanism of genotoxicity of exogenous GSH is discussed but, at present, no pertinent explanation can be given.

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Section: Discussionmentioning

confidence: 84%

Section: Discussionmentioning

confidence: 99%

Exogenous glutathione induces sister chromatid exchanges, clastogenicity and endoreduplication in V79-E Chinese hamster cells

Trust

Bach

1985

Cell Biol Toxicol

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“…Stich et al (1978) and MacRae and Stich (1979) reported a "unique dose-response" of thiols (cysteine, cysteamine, GSH) in clastogenicity, unscheduled DNA synthesis and SCE assays in CHO cells with one or two maxima and a decline of genotoxicity at higher concentrations. Recently, we performed a pilot experiment with GSH, the GSH-mimicking drug 2-mercaptopropionylglycine, and cysteine.…”

Section: Thustmentioning

confidence: 99%

The mechanism of cytogenetic genotoxicity of exogenous glutathione in V-79 cells in vitro?implication of hydrogen peroxide and general traits of oxidative chromosome damage

Thust

1988

Cell Biol Toxicol

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The mechanism of cytogenetic genotoxicity (clastogenicity, induction, cell cycle delay) of 10(-3) M glutathione in V79-E cells, as described by Thust and Bach (1985), was studied in detail by using different treatment conditions. It was found that 1-cystine is the essential cofactor in the incubation system. Catalase, but not superoxide dismutase, abolished the genotoxic effect, and the iron chelator desferoxamine, as well as the hydroxyl radical scavenger mannitol, diminished the activity. It is suggested that glutathione, in combination with V79-E cells and cystine, forms a hydrogen peroxide-generating system which provokes the adverse effects. Glutathione as well as 1-cysteine and 2-mercaptopropionylglycine, which were checked for comparison, show a "paradoxic genotoxicity," i.e., at 10(-2) M the effects return almost to the level of controls. Concentration dependence and other criteria of cytogenetic genotoxicity observed with glutathione show obvious similarities to those of other oxidatively acting agents and reveal striking differences to the cytogenetic effects of "typical" genotoxins.

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“…Thus, oxidative stress appears to be involved in the process of mutagenesis, carcinogenesis, and aging [1]. Evidence has been obtained that free radicals are mutagenic and can induce base changes, single-strand breaks and apurinic/apyrimidinic sites [3][4][5], possibly leading to the onset of chromosome aberrations (CA) [6].…”

Section: Introductionmentioning

confidence: 99%

Comparative study of the effects of vitamin c and bleomycin on smokers' and non-smokers' lymphocytes in clastogenicity assays

Cecchi

Takahashi

1999

Teratog. Carcinog. Mutagen.

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Free radicals are products of metabolic reactions and of external factors that can injure different biological molecules. However, different antioxidant agents can prevent the action of these reactive species and the damage they cause. Vitamin C (VC) is an important micronutrient found in the diet, which presents defense mechanisms against the free radicals that challenge the cells of the organism. The objective of the present study was to investigate the effect of VC as a modulator of the damage induced in DNA by bleomycin (BLM) in lymphocytes from smokers and non‐smokers. The difference in response to the mutagenic potential of BLM between smokers and non‐smokers was also investigated. Peripheral blood lymphocyte cultures were treated simultaneously with BLM (20 μg/ml) and/or VC (100, 200, and 400 μg/ml) in the G2 phase of the cell cycle. The results obtained did not demonstrate a statistically significant difference in the response to the antitumor agent BLM between smokers and non‐smokers. The data also showed that VC had no significant modulating effect on the frequency of chromosome aberrations induced by BLM in the cells of smokers and non‐smokers under the experimental conditions used. Teratogenesis Carcinog. Mutagen. 19:43–51, 1999. © 1999 Wiley‐Liss, Inc.

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The need for a mammalian test system for mutagens: Action of some reducing agents

Cited by 74 publications

References 10 publications

Exogenous glutathione induces sister chromatid exchanges, clastogenicity and endoreduplication in V79-E Chinese hamster cells

Exogenous glutathione induces sister chromatid exchanges, clastogenicity and endoreduplication in V79-E Chinese hamster cells

The mechanism of cytogenetic genotoxicity of exogenous glutathione in V-79 cells in vitro?implication of hydrogen peroxide and general traits of oxidative chromosome damage

Comparative study of the effects of vitamin c and bleomycin on smokers' and non-smokers' lymphocytes in clastogenicity assays

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