The use of short-term tests to measure the preventive action of reducing agents on formation and activation of carcinogenic nitroso compounds

Lo, L.W.; Stich, H. F.

doi:10.1016/0027-5107(78)90234-8

Cited by 22 publications

(3 citation statements)

References 30 publications

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“…While its antioxidant properties are well known worldwide, its use as an effective anticancer substance is highly controversial (13). For instance, ascorbic acid has been reported to exhibit anti-carcinogenic and antimutagenic activities (14,15); however, its adverse effects have also been well documented (16,17). …”

Section: Introductionmentioning

confidence: 99%

Effect of ascorbic acid and hydrogen peroxide on mouse neuroblastoma cells

2012

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Ascorbic acid is one of the antioxidant compounds widely used against free radical stress. The present study was undertaken to examine whether ascorbic acid and hydrogen peroxide (H2O2), alone or in combination, could influence cell viability. The murine neuroblastoma cell line, N2a, was used to perform a dose response curve for ascorbic acid. It was observed that ascorbic acid alone at physiological concentrations (0.1–0.4 mM) did not cause any cell death. However, at pharmacological concentrations (1–6 mM), ascorbic acid caused dose-dependent cell death. The lethal concentration at which 50% cells were killed (LC50) was determined to be approximately 3.141 mM ascorbic acid at 24 h. H2O2 up to 300 μM alone did not cause significant cell death. In the combined treatment, when the cells were treated with ascorbic acid at physiological concentrations (0.4 mM) and H2O2 at 400 μM, higher rates of cell death were observed compared to the cell death rates caused by either compound alone. Subsequent experiments revealed that cell death was partly mediated through the loss of total glutathione levels in the cells. These data suggest that the combination of ascorbic acid and H2O2 is disadvantageous for cancer cell survival. Further studies are required to ascertain the physiological significance of these observations.

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Section: Introductionmentioning

confidence: 99%

Effect of ascorbic acid and hydrogen peroxide on mouse neuroblastoma cells

2012

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“…of DNA fragmentation or DNA repair , 1977cLo and Stich, 1978) by carcinogens do not reveal whether these DNA lesions will be actually translated into mutations. On the other hand, the use of mutations of bacteria and yeast as an endpoint could easily lead to an over or under estimation of the actual carcinogenic activity of a compound for man.…”

Section: New Prioritiesmentioning

confidence: 99%

“…A few promising exploratory attempts along this line have already been made. We have successfully applied human cells as subjects and DNA repair synthesis as the endpoint to reveal the preventive action of several reducing agents (Lo and Stich, 1978). Moreover, Salmonella typhirnurileraz treated with carcinogens and reducing agents, anti-oxidants or selenium, readily reveals the antimutagenic effect of these compounds (Rosin and Stich, 1978a,b;Jacobs et al , 1977).…”

Section: New Prioritiesmentioning

confidence: 99%

Invitation Paper: Can Mutation Theories of Carcinogenesis Set Priorities for Carcinogen Testing Programs?

Stich¹,

Acton²

1979

Can. J. Genet. Cytol.

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The recent activity in designing, validating and implementing short-term tests for carcinogens has been spurred by the fairly convincing correlation between the carcinogenicity and mutagenicity of chemicals and by the assumption that mutations are somehow involved in neoplastic transformation. Moreover, it has been tacitly assumed that the mutagenic capacity alone of compounds would induce regulatory agencies to pass rules for their removal from man's environment, and would lead the public to avoid them. The actual response, however, is quite different. Government departments shy away from making any decisions on the basis of in vitro test systems, the public at large is becoming irritated by daily announcements that many of their cherished habits could adversely affect their health, and industries feel threatened and may reduce their search for new beneficial chemicals. The reluctance to accept wholeheartedly the mutagenicity tests for the detection of carcinogens is partly due to the uncertainty about the involvement of mutations in the formation of benign and malignant tumors. Following the initial rapid advances in the detection of environmental chemicals with carcinogenic and mutagenic properties, we seem to have arrived at the cross roads: we must now set new priorities for future research, and must make an unbiased assessment of the actual hazard of a compound to man and the human population.

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