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Phorbol myristate acetate induced neutrophil autotoxicity
Author(s) -
Tsan MinFu
Publication year - 1980
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.1041050215
Subject(s) - phorbol , superoxide dismutase , catalase , chemistry , trypan blue , myeloperoxidase , microbiology and biotechnology , tetradecanoylphorbol acetate , chronic granulomatous disease , reactive oxygen species , biochemistry , granulocyte , neutrophile , superoxide , biology , immunology , enzyme , in vitro , inflammation , protein kinase c
The viability of neutrophils in the condition under which they kill neoplastic cells was studied. In the presence of phorbol myristate acetate (PMA) the 51 Cr‐release by human neutrophils was markedly stimulated. The PMA‐induced 51 Cr‐release by neutrophils correlated well with the number of nonviable neutrophils as determined by the uptake of trypan blue. Phorbol myristate acetate had no effect on the 51 Cr‐release by lymphocytes, LPC‐1 myeloma cells, ovarian ascites tumor cells, or neutrophils from a patient with chronic granulomatous disease. This suggests that the effect of PMA is not due to its nonspecific toxic effect; instead, it is dependent on the reactive oxygen species produced by the normal neutrophils. Catalase, cytochrome C, histidine, and methionine inhibited the PMA‐induced 51 Cr‐release by human neutrophils, whereas superoxide dismutase, myeloperoxidase inhibitors, and some hydroxyl radical scavengers or singlet oxygen quenchers had no effect. The clumping of neutrophils induced by PMA was also important in the PMA‐induced 51 Cr‐release by human neutrophils.