HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Sugiyama, M. Articles by Ogura, R. Search for Related Content PubMed PubMed Citation Articles by Sugiyama, M. Articles by Ogura, R. Social Bookmarking                      What's this?

J. Biol. Chem., Vol. 266, Issue 6, 3383-3386, 02, 1991

Effect of ascorbic acid on DNA damage, cytotoxicity, glutathione reductase, and formation of paramagnetic chromium in Chinese hamster V- 79 cells treated with sodium chromate(VI)

M Sugiyama, K Tsuzuki and R Ogura
Department of Medical Biochemistry, Kurume University School of Medicine, Japan.

The effect of pretreatment with ascorbic acid (vitamin C) on chromate- induced DNA damage, cytotoxicity, and enzyme inhibition as well as on the cellular reduction of chromium(VI) was investigated using Chinese hamster V-79 cells. Cellular pretreatment with nontoxic levels of 1 mM ascorbic acid for 24 h prior to exposure resulted in a significant increase (1.7-fold) in cellular levels of this vitamin. Alkaline elution assays demonstrated that this pretreatment decreased cellular levels of Na2CrO4-induced alkali-labile sites while the numbers of DNA- protein crosslinks produced by chromate increased. In colony-forming assays, pretreatment with ascorbic acid enhanced the cytotoxicity of chromate. However, the inhibition of glutathione reductase attributed to Na2CrO4 was attenuated by this pretreatment. Under the same experimental condition, the uptake of chromate in pretreated cells was found to increase. ESR studies revealed that cellular pretreatment with ascorbic acid reduced the level of chromium(V) intermediate and increased the level of chromium(III) complex, indicating that cellular reduction of chromium(VI) to chromium(III) was accelerated by this vitamin. These results suggest that ascorbic acid decreases chromate- induced alkali-labile sites and chromium inhibition of glutathione reductase, but it enhances DNA-protein cross-links and cytotoxicity caused by this metal through its ability to directly reduce chromium(VI).
CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

This article has been cited by other articles:

				S.-M. Chuang, G.-Y. Liou, and J.-L. Yang Activation of JNK, p38 and ERK mitogen-activated protein kinases by chromium(VI) is mediated through oxidative stress but does not affect cytotoxicity Carcinogenesis, August 1, 2000; 21(8): 1491 - 1500. [Abstract] [Full Text] [PDF]

				D. L. Carlisle, D. E. Pritchard, J. Singh, B. M. Owens, L. J. Blankenship, J. M. Orenstein, and S. R. Patierno Apoptosis and P53 Induction in Human Lung Fibroblasts Exposed to Chromium (VI): Effect of Ascorbate and Tocopherol Toxicol. Sci., May 1, 2000; 55(1): 60 - 68. [Abstract] [Full Text] [PDF]

				J.-M. P. Yuann, K. J. Liu, J. W. Hamilton, and K. E. Wetterhahn In vivo effects of ascorbate and glutathione on the uptake of chromium, formation of chromium(V), chromium–DNA binding and 8-hydroxy-2'-deoxyguanosine in liver and kidney of Osteogenic Disorder Shionogi rats following treatment with chromium(VI) Carcinogenesis, July 1, 1999; 20(7): 1267 - 1275. [Abstract] [Full Text] [PDF]