Open AccessInhibition of Intracellular Bleomycin Hydrolase Activity by E‐64 Leads to the Potentiation of the Cytotoxicity of Peplomycin against Chinese Hamster Lung Cells
Author(s) -
Nishimura Chiaki,
Nishimura Toshio,
Tanaka Nobuo,
Yamaguchi Hideyo,
Suzuki Hideo
Publication year - 1989
Publication title -
japanese journal of cancer research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 0910-5050
DOI - 10.1111/j.1349-7006.1989.tb02246.x
Subject(s) - long term potentiation , cytotoxicity , bleomycin , chinese hamster , hamster , intracellular , pharmacology , hydrolase , chemistry , lung , biology , enzyme , in vitro , microbiology and biotechnology , chemotherapy , biochemistry , medicine , receptor
N‐(N‐(L‐3‐ frans ‐carboxyoxiran‐2‐carbonyl)‐L‐leucyl)‐agmatine (E‐64), a thiol protease inhibitor, potentiated the cytotoxicity of peplomycin against the Chinese hamster lung (V79) cell. After the treatment of the cells with E‐64 (50 μg/ml) for 12 h, bleomycin hydrolasc activity of the cells was almost completely inhibited. V79 cells treated with [ 3 H]peplomycin for 24 h in the presence of E‐64 (50 μg/ml) accumulated twice as much [ 3 H]peplomycin and five times less [ 3 H]desamidopeplomycin compared with V79 cells treated in the absence of E‐64. These results suggest that E‐64 increases the sensitivity of V79 cells to peplomycin probably by inhibiting the intracellular bleomycin hydrolasc activity.