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Increased Resistance to the Anticellular Effect of Interferon in an Ultraviolet Light-resistant Human Cell Line, UV^r-1

Nobuo Suzuki^1,

¹ Department of Microbiology
³ Department of Pediatrics
and⁴ Department Obstetrics and Gynecology, School of Medicine, Chiba University, Inohana, Chiba 280
² Department Division of Physiology and Pathology, National Institute of Radiological Sciences, Chiba 260
⁵ Department of Neurosurgery, National Tosei Hospital, Shizuoka 411
and⁶ Department Research Institute for Chemodynamics, Chiba University, Chiba 280, Japan

Interferon (, and ) susceptibility was tested in a human cell line, UV^r-1, a u.v. light-resistant variant of RSa cells; the latter have high sensitivity to both u.v. lethality and the cell profileration inhibition (anticellular) effect of human interferon (HuIFN) preparations. UV^r-1 cells were less sensitive than the parental RSa cells to the inhibitory effects of HuIFN preparations, as measured by cell proliferation and the incorporation of [³H]deoxythymidine and [³H]deoxyadenosine into acid-insoluble cellular material. Nevertheless, UV^r-1 cells exposed to HuIFN showed almost the same enhanced levels of antiviral activity and pppA(2'p5'A)_n synthetase activity as similarly treated RSa cells. Further, UV^r-1 cells had much the same binding capacity for ¹²⁵I-labelled HuIFN-A. Thus, it seems likely that the variant has an increased resistance to the anticellular effect but not to the antiviral effect of HuIFN preparations. UV^r-1 cells showed no significant difference from RSa cells in u.v.-induced DNA repair synthesis. However, when a comparison was made between the susceptibility of normal fibroblasts and fibroblasts from patients with Cockayne's syndrome, characterized by an altered u.v. sensitivity but no alteration of DNA repair replication synthesis, the Cockayne's syndrome fibroblasts, CCK-3 and CCK-4, were more susceptible to HuIFN- as judged by cell proliferation and deoxythymidine incorporation tests.

Keywords: interferon (HuIFN), u.v.-resistant variant, DNA repair, anticellular action

Present address: Department of Biochemistry, School of Medicine, Chiba University, Chiba 280, Japan.

Received 12 September 1985; accepted 2 January 1986.