Parsons M, Morrow J, Stocco D, Kitos P
J Cell Physiol. 1976 Oct;89(2):209-18. doi: 10.1002/jcp.1040890204.
In this study the resistance of a number of lines of Chinese hamster ovary cells to azaguanine is examined. Those which are drug resistant by virtue of a deficiency of hypoxanthine-guanine phosphoribosyltransferase (HPRT) fail to take up any exogenous hypoxanthine or azaguanine. A second class of drug resistant cells which grow in the reverse selective HAT medium and have levels of HPRT in the range of the wild type parent line take up these purines at lower rates than the nonresistant cells and incorporate smaller amounts of them into trichloracetic acidinsoluble constituents. The results suggest that their basis for resistance resides in lowered incorporation of azaguanine into DNA and RNA, possibly due to a mofified HPRT molecule which accepts hypoxanthine, but not azaguanine as a substrate.
在本研究中,检测了多株中国仓鼠卵巢细胞对氮杂鸟嘌呤的抗性。那些因次黄嘌呤 - 鸟嘌呤磷酸核糖转移酶(HPRT)缺乏而具有耐药性的细胞无法摄取任何外源性次黄嘌呤或氮杂鸟嘌呤。第二类耐药细胞在反向选择的HAT培养基中生长,其HPRT水平在野生型亲本系范围内,摄取这些嘌呤的速率低于非耐药细胞,并且将它们掺入三氯乙酸不溶性成分的量较少。结果表明,它们的耐药基础在于氮杂鸟嘌呤掺入DNA和RNA的量降低,这可能是由于修饰的HPRT分子接受次黄嘌呤但不接受氮杂鸟嘌呤作为底物所致。