• 1 January 1977
    • journal article
    • research article
    • Vol. 68  (2) , 175-182
Abstract
Antitumor activity of 1-(.gamma.-chloropropyl)-2-chloromethylpiperidine hydrobromide (CAP-2) was studied in vivo and in vitro, using various rat ascites hepatoma cell lines. Among 8 ascites hepatoma cell lines, AH-13 was extremely sensitive to in vivo antitumor and in vitro lethal action of the agent, whereas AH-44 was resistant in both cases. The sensitivity of ascites hepatoma cell lines to CAP-2, nitrogen mustard-N-oxide, 4-nitroquinoline-1-oxide and UV ray in vitro was widely different but their relative sensitivities were similar against these agents. for all agents, AH-13 was inactivated rapidly and AH-109A moderately, whereas AH-44 was relatively resistant. These results indicate that the sensitivity of the cells to CAP-2 may be closely related to their repair capability of damaged DNA. Similar experiments using various DNA repair deficient mutants of Escherichia coli B strain demonstrated that the repair deficient mutants were several times more sensitive to CAP-2 than the wild type strain. From these results, it may be concluded that CAP-2 induces DNA lesions repairable by the same repair mechanisms that work on pyrimidine dimers.

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