Jo Ann Alexander

Studies with mustards. Iv. Effects of nitrogen mustard treatment of deoxyribonuclease and deoxyribonucleic acid upon the enzymic degradation of deoxyribonucleic acid.

Abstract Treatment of either deoxyribonuclease or deoxyribonucleic acid with nitrogen mustard caused a decrease in the rate of enzymic degradation of deoxyribonucleic acid, and the treatment of the nucleic acid caused a greater decrease than treatment of the enzyme. The significance of this finding is discussed.

Identification of 7-(2-hydroxyethyl)guanine as a product of alkylation of calf thymus DNA with Clomesone

Evidence at the molecular level is presented in support of alkylation of O6-guanine moieties of DNA as the mechanism of cytotoxicity of Clomesone to HT-29 cells and consists in the isolation and identification of a product resulting from alkylation of calf thymus DNA with Clomesone, followed by depurination to yield 7-(2-hydroxyethyl)guanine, whose formation is reasonably explained by O6-guanine chloroethylation followed by intramolecular alkylation at N7 of guanine and subsequent hydrolysis to the hydroxyethylguanine.

Induction of sister-chromatid exchanges in L1210 leukemia cells by new antitumor 2-haloethyl(methylsulfonyl) methanesulfonate compounds

The antitumor 2-halo(chloro, bromo, and fluoro)-ethyl(methylsulfonyl) methanesulfonates, ethyl(methylsulfonyl) methanesulfonate, and chlorozotocin, a 2-chloroethylnitrosourea, were evaluated for their potential to induce SCEs in L1210 cells. The results indicate that all the compounds induced approximately 2-fold or greater increases in SCEs in a dose-related manner. 2-Chloroethyl(methylsulfonyl) methanesulfonate, a DNA-interacting agent and a drug selected for clinical trials, exhibited the highest SCE increase in these cells.