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J. Biochem, 1984, Vol. 95, No. 6 1775-1782
© 1984 Japanese Biochemical Society

research-article

Mechanism of Phorbol Myristate Acetate-Induced Lymphotoxin Production by a Human T Cell Hybridoma1

Yoshiro KOBAYASHI, Makoto ASADA and Toshiaki OSAWA

Division of Chemical Toxicology and Immunochemistry, Faculty of Pharmaceutical Sciences, The University of Tokyo Hongo, Bunkyo-ku, Tokyo 113

Various hydroxyl radical scavengers markedly inhibited phorbol myristate acetate (PMA)-induced lymphotoxin (LT) production by a human T cell hybridoma, AC5-8. Among those we tested, tetramethylurea (TMU) was the most potent scavenger, and it was revealed that TMU must be added before 2 h have elapsed after PMA addition in order for LT production to be inhibited. In concordance with this fact, soluble NADPH dependent O2– forming enzyme(s) were activated several fold by PMA. PMA also induced DNA strand breaks, a process markedly inhibited by TMU. As expected, ADP-ribosyl transferase (ADPRT), which is well known to require DNA strand breaks for its enzymatic activity, was activated by PMA treatment. In addition, specific inhibitors for ADPRT, namely 3-amino-benzamide and nicotinamide, inhibited PMA-induced LT production. Taken together, these three successive events, activation of soluble NADPH dependent O2– forming enzyme(s), DNA strand breaks and activation of ADPRT, may be required for PMA-induced LT production by AC5-8.

1 This study was supported by research grants from the Ministry of Education, Science and Culture of Japan, the R. Naito Foundation for Medical Research and the Suzuken Memorial Foundation.


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