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Hamster fibrosarcoma cells were synchronized by mitotic selection and exposed to varying concentrations of 1-beta-D-arabinofuranosylcytosine (ara-C) for 2 hr in mid-S phase. There was a direct relationship between DNA synthesis inhibition and cytotoxicity produced by ara-C once DNA synthesis was decreased by over 85%. The noncytotoxic concentration of 10(-5) M ara-C produced little chromatid breakage; but extensive chromatid breakage and chromosomal rearrangement were seen in cells treated with the cytotoxic concentration of 10(-3) M ara-C, thus supporting earlier observations that chromatid breakage is highly correlated with cytotoxicity. Predominantly small DNA was synthesized when cells were treated with both 10(-5) and 10(-3) M ara-C, and this DNA could be completely chased into high-molecular-weight DNA after addition of deoxycytidine. Both concentrations of ara-C also inhibited, to different degrees, the joining of intermediate-size DNA fragments into larger DNA; thus neither parameter appeared directly related to the ara-C-produced cytotoxicity.
P A Jones, and
M S Baker, and
W F Benedict
February 1975,
Journal of the National Cancer Institute,
P A Jones, and
M S Baker, and
W F Benedict
November 1970,
Cancer research,
P A Jones, and
M S Baker, and
W F Benedict
March 1968,
Molecular pharmacology,
P A Jones, and
M S Baker, and
W F Benedict
August 1976,
Biochemistry,
P A Jones, and
M S Baker, and
W F Benedict
May 1975,
Biomedicine / [publiee pour l'A.A.I.C.I.G.],
P A Jones, and
M S Baker, and
W F Benedict
January 1976,
Medical and pediatric oncology,
P A Jones, and
M S Baker, and
W F Benedict
October 1979,
Cancer research,
P A Jones, and
M S Baker, and
W F Benedict
March 1968,
Molecular pharmacology,
P A Jones, and
M S Baker, and
W F Benedict
January 1988,
Medical oncology and tumor pharmacotherapy,
P A Jones, and
M S Baker, and
W F Benedict
November 1970,
Cancer research,
