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Bleomycin (BLM) is clinically useful in the treatment of humansquamouscell carcinomas, testicular carcinoma, and malignant lymphoma. The antibiotic is less effective for adenocarcinoma and sarcomas. The less effectiveness of BLMmay be due to lowered BLMsensitivity of tumor cells. The determinant of BLMsensitivity is thought to be drug uptake, BLMhydrolase activity, enzymes involved in DNA breakdown and enzymes for DNA repair1*^. Therefore, to elucidate the mechanisms of cellular resistance to BLMis important in the treatment of neoplasms. Miyaki et aLz) reported that BLM-resistant rat ascites hepatoma cells show higher BLM hydrolase activity than BLMsensitive hepatoma cells. Akiyamaand Kuwano4) isolated BLM-resistant mutants of Chinese hamster ovary (CHO) cell lines, whose resistance is due to higher BLMhydrolase activity. We obtained BLM-resistant mutant cell lines of murine lymphoma L51 78Y, which showed similar level of BLM-inactivating activity as the parental cells5). Changes of membrane-associated enzymeactivities in the resistant cells have been observed6), which supports the hypothesis that the resistance is attributed to decreased uptake or retention of BLMin the resistant cells by alteration of plasma membrane. For the purpose of elucidating mechanisms of BLMresistance, we studied BLMuptake in the sensitive and resistant cells using [3H]peplomycin (PEP), an antibiotic of BLM group, which contains 3((5)-l-phenylethyl)aminopropyl amino group7). The results are presented in this publication. PEP and [3H]PEP (phenyl-m-3H, 250 /*Ci/mg)8)

Cellular uptake and efflux of peplomycin in sensitive and bleomycin-resistant subline of mouse lymphoblastoma L5178Y cells.