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Blood, Vol. 96 No. 1 (July 1), 2000:
pp. 307-313
Oxidative stress interferes with cancer chemotherapy: inhibition
of lymphoma cell apoptosis and phagocytosis
Emily Shacter,
Joy A. Williams,
Roger M. Hinson,
Sema Sentürker, and
Yang-ja Lee
From the Laboratory of Immunology, Division of Therapeutic Proteins,
Center for Biologics Evaluation and Research, Food and Drug
Administration, Bethesda, MD.
Many antineoplastic drugs kill tumor cells by inducing apoptosis.
This highly controlled mechanism of cell death is thought to be
physiologically advantageous because apoptotic cells are removed by
phagocytosis before they lose their permeability barrier, thus
preventing induction of an inflammatory response to the dying cells. In
contrast, necrotic cells lyse and release their contents into the
extracellular space, thus inducing inflammation. In this report, we
examine the effects of oxidative stress on chemotherapy-induced cell
killing. We find that H2O2 inhibits the ability
of 4 different chemotherapy drugs (VP-16, doxorubicin, cisplatin, and
AraC) to induce apoptosis in human Burkitt lymphoma cells.
H2O2 shifts the form of cell death from
apoptosis to pyknosis/necrosis, which occurs after a significant delay
compared with chemotherapy-induced apoptosis. It can also lower the
degree of cell killing by these drugs. These effects of
H2O2 can be prevented by the antioxidant agents
Desferal, Tempol, and dimethylsulfoxide. Phagocytosis by monocyte-derived macrophages of VP-16-treated lymphoma cells is also
inhibited by H2O2. Cells killed with
H2O2 (with or without VP-16) do ultimately
undergo phagocytosis, but this occurs only after they have lost their
permeability barrier. Thus, membrane-intact apoptotic cells are
recognized and phagocytosed by monocyte-derived macrophages, but
membrane-intact pyknotic/necrotic cells are not. The results
suggest that chemotherapy-induced apoptosis and phagocytosis of cancer
cells may be enhanced by including certain antioxidant agents in the
treatment protocol.
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