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 Barranco, S. C. Articles by Humphrey, R. M. Search for Related Content PubMed PubMed Citation Articles by Barranco, S. C. Articles by Humphrey, R. M.

Studies on Recovery from Chemically Induced Damage in Mammalian Cells¹

Department of Human Biological Chemistry and Genetics, Division of Cell Biology, The University of Texas Medical Branch, Galveston, Texas 77550 [S. C. B., J. K. N.], and Department of Physics, Section of Cellular Studies, The University of Texas at Houston, M. D. Anderson Hospital and Tumor Institute, Houston, Texas 77025 [R. M. H.]

The survival of plateau-phase or nondividing Chinese hamster ovary cells (in vitro) is reduced to a greater extent by treatments with nitrosourea compounds than are cells treated in the exponential phase of growth. The greatest decrease in the survival fraction occurred following treatments with 1-trans-(2-chloroethyl)-3-(4-methylcyclohexyl)-1-nitrosourea where approximately 128 times more cells were killed in plateau phase than in the dividing state (at the 10 µg/ml-for-1-hr dose). Only 5 times more cells were killed in plateau phase than in exponential growth when cells were treated with 1-(2-chloroethyl)-3-cyclohexyl-1-nitrosourea. Cells treated with either nitrosourea compound failed to recover from potentially lethal damage and sublethal damage. The breakdown products of the nitrosourea compounds are known to inhibit DNA repair and may explain the failure of mammalian cells to recover from sublethal damage and potentially lethal damage induced by these chemicals.

Both dividing and nondividing cells were able to recover from bleomycin-induced potentially lethal damage but not from sublethal damage. The recovery from bleomycin-induced potentially lethal damage by nondividing cells was twice as great as that exhibited by dividing cells; however, potentially lethal damage recovery was sufficiently high for cells in both growth states to conceal the true response to sublethal damage.

¹ Supported by Grant 5 R01 CA15397-02, National Cancer Institute, NIH, USPHS.

Received 9/30/74. Accepted 1/30/75.

This article has been cited by other articles:

				J. Chafouleas, W. Bolton, and A. Means Potentiation of bleomycin lethality by anticalmodulin drugs: a role for calmodulin in DNA repair Science, June 22, 1984; 224(4655): 1346 - 1348. [Abstract] [PDF]