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Fig. 1. Plasma concentration profiles of EM A ; , DLZ B ; , and VER C ; in the experiment of bolus injection of DLZ, VER, and EM. EM, DLZ, and VER were administered through the femoral vein at doses of 10, 5, and 5 mg kg, respectively. Each point represents the mean S.D. n 4. Johannes Reuchlin wrote two books on Cabala. The first, De verbo mirifico 1494 ; , speaks of the "wonderworking word, " YHShVH, the miraculous name of Jesus derived from the tetragrammaton of the Old Testament: YHVH, with the letter shin added in its midst. On this, refer to Wilhelm Schmidt-Biggemann's "History and Prehistory of the Cabala of JHSVH, " in Hebrew to Latin, Latin to Hebrew: The Mirroring of Two Cultures in the Age of Humanism [BERLIN STUDIES IN JUDAISM, 1], edited by Giulio Busi Berlin: Institut fr Judaistik, Freie Universitt Berlin Torino: Nino Aragno Editore, 2006 ; . The second, De arte cabalistica 1516 ; , is a broader, more informed excursion into various kabbalistic concerns. It appeared in English translation in 1983 Abaris Books, Inc. this translation was reprinted with a new introduction by Moshe Idel in 1993 Lincoln: Bison Books, University of Nebraska Press ; as On the Art of the Kabbalah. A discussion of Reuchlin's writings, especially De verbo mirifico, constitutes the fourth chapter of The Most Ancient Testimony: Sixteenth-Century Christian-Hebraica in the Age of Renaissance Nostalgia, by Jerome Friedman Athens: Ohio University Press, 1983 ; . On Reuchlin Bis 2-chloroethyl ; sulfde-resistan t L-Cells 10 ; . In the present study, the presumed target, DNA, was alkylated to a similar extent in all cell strains immediately after the treatment. Cell size does not appear therefore to be a significant factor in explaining the relative resistance of these cells. The smaller average size .of the resistant cells in this and the previous study 10 ; may be a result of their slower growth rate, if it is accepted that all of these cells attain a similar maximum size just prior to cell division. Our results also exclude a decreased permeability of the cells for bis 2-chloroethyl ; sulfide as a cause of their resistance. In contrast, the nitrogen mustard-resistant'cell lines derived by Rutman et al. 13 ; and Goldenberg 5 ; clearly owed their resistance to a lessened permeability to the drug. [See also Refs. 7 and 19, in which the authors utilized the cells derived by Rutman et al. 13 ; .] It was anticipated that our substrains would exhibit cross-resistance to the alkylating agents MMS and DMM as well as to UV and X-radiation because all of these agents are thought to exert their toxic effect by damaging DNA. Cross-resistance was seen clearly only for substrains L H3 and L H4 towards DMM. The increased sensitivity of L H17 cells towards DMM and X-rays was unexpected. Sinclair 14 ; and Suit 16 ; have described, respectively, the properties of Chinese hamster and mouse mammary tumor cells that survived a large dose of ionizing radiation. The Chinese hamster cells, in common with our resistant substrain cells, were smaller and had a longer doubling time than the parental strain, but their radiosensitivity was increased. A similar finding was reported for the mammary tumor. All of these divergent results point up the complex nature of acquired resistance to alkylating agents and radiation and suggest that there are numerous mechanisms in mammalian cells that can lead to the resistant state, not all of which are common when the comparison is made between different alkylating agents, ionizing radiation, and UV radiation. The most promising difference between L-cells and the resistant substrains that can be used to provide an explanation of the resistance to bis 2-chloroethyl ; sulfide was the ability of the latter to excise alkylation products at a rate 2 to 3 times faster than the former. This finding is undoubtedly insufficient to account completely for the resistance, but it may reflect an increased overall ability of the resistant cells to "repair" damaged DNA. Rutman et al. 13 ; and Connors and Double 4 ; have described tumor cells that remained viable after degrees of DNA alkylation that were lethal to the parental cells from which they were derived, and although the mechanism was not clear it appeared likely that the resistant cells had an enhanced mechanism for repairing alkylated DNA. Finally this study confirms the previous findings with L-cells 11 ; that bis 2-chloroethyl ; sulfide cross-links the DNA molecule in mammalian cells and that the cross-links can be removed rapidly. REFERENCES.

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