Reference List

Notes: Seven UV-sensitive clones were isolated from the mouse cell lines, FM3A and L5178Y, rsing Leaderberg style replica plating. UV-sensitive clones were found at a frequency of 1 in 886 clones of FM3A and of 6 in L5178Y, after treatment with N-methyl-N'-nitrosofuanidine, but no UV-sensitive clones were obtained in the untreated controls. The Do values of freshly isolated clones were 10 to21 ergs/mm2 (mainly 10 to13 ergs/mm2), while the original FM3A and L5178Y lines had Do values of 32 ergs/mm2. The UV-sensitive clones were found to be rather stable for a period ranging lose their UV-sensitivity, in terms of increase in Do values or n values. More stable UV-sensitive subclones could be isolated froom these populations by cloning using the replica plating method.
Reference ID: 1574

Notes: Murine leukemic lymphoblasts L5178Y-R(LY-R) undergo conversion into their L5178Y-S(LY-S) variant as result of prolonged (5 months to 4 years) cultivation in vitro. LY-R cells are highly tumorigenic in DBA/2 mice; resistant to X-ray (Do (mean lethal dose (recipuocal of the slope of the linear portion of dosesurvival curve))=0.91 grays); and sensitive to ultraviolet radiation (Do=0.7J/sq m), short (up to 60 min) heat (43C) treatment, and certain potential cancer durgs. LY-S cells are practically nontumorigenc in DBA/2 mice ;sensitive to X-ray (Do=0.56 grays); and resistant to ultraviolet radiation (Do=5.5 J/sq m), ahort heat treatment, and the durgs.
Reference ID: 1468

Notes: Althouth several types of procedures are able to synchronize the growth of cultured mammalian cells, none has been applied successfully to the mouse lymphoma cell line (L5178Y).This led us to search for a new method of synchronization and to develop the present method of successive treatment with excess thymidine and coleemid. Exponentially growing cells were subjected to excess thymidine to arrest (or retared) cell growth just before and/or at S stage. After several hours of thymidine treatment, most G2, M and G1 stage cells entered and remained in the S period which occupies 7.3 hr of hte total generation time of 10.8 hr. To compress the cell population into an even narrower region of the life cycle, the excess thymidine was removed and colemid was added to arrest mitotic cells in metaphase. The removal of colcemid, then, allowed the cells progress through the life cycle in a partially synchronized fashion.
Reference ID: 1978

Notes: Cultures of radioresistant (LY-R) and radiosensitive (LY-S) strains of L5178Y mouse lymphoma cells were exposed continuously to X-rays delivered at dose rates ranging from 0.003 to 0.025 Gy/h for up to 35 days. Populations of both strains proliferated actively during the exposure, but the growth rates were reduced in a dose rate-dependent manner. The reduction of growth rate occurred for strain LY-S earlier during the exposure and at lower dose rates than for strain LY-R. The survival (as measured by colony forming ability) of strain LY-R was affected only slightly at all dose rates applied. For strain LY-S, a decrease in the surviving fraction was observed in the initial part of the exposure. This decrease was followed by a plateau and eventually by an increase, in some cases to values close to the control level. The increase in the surviving fraction indicated that the radioresistance of the exposed LY-S cells had increased. This pattern was particularly clear for dose rates greater than 0.014 Gy/h. The pre-irradiated cells exhibited radioresistance when exposed to acute X-radiation after termination of the chronic exposure. The increase in radiation resistance was stable for at least 70 days after termination of the protracted exposure. These results show that mutagenic and/or selective phenomena leading to an increase in radiation resistance of mammalian cells can be caused by protracted exposures to X-rays at dose rates permitting active proliferation
Reference ID: 2500