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Regulation of manganese superoxide dismutase and other antioxidant genes in
normal and leukemic hematopoietic cells and their relationship to
cytotoxicity by tumor necrosis factor
M Kizaki, A Sakashita, A Karmakar, CW Lin and HP Koeffler
Department of Medicine, Keio University, Tokyo, Japan.
Myeloid cells are a major source of superoxide and other oxygen
metabolites. As a protective mechanism, cells express antioxidant enzymes
including manganese superoxide dismutase (Mn-SOD), copper-zinc SOD
(Cu/Zn-SOD), and glutathione peroxidase (GSX-PX). Even though hematopoietic
cells are a major source of oxidants, little is known of their expression
of antioxidants. We found that seven myeloid leukemic cell lines blocked at
different stages of differentiation constitutively expressed Mn-SOD,
Cu/Zn-SOD, and GSX-PX RNAs. Level of Mn-SOD activities paralleled levels of
Mn-SOD RNA. Terminal differentiation of native HL-60 cells to either
granulocytes or macrophages did not alter levels of Mn-SOD RNA but markedly
decreased cell division. Myeloid leukemic lines sensitive to cytotoxic
effects of tumor necrosis factor (TNF) as well as normal peripheral blood
lymphocytes and monocytes, dramatically increased their levels of Mn- SOD
RNA in the presence of TNF. In contrast, Cu/Zn-SOD and GSX-PX RNA levels
did not increase in these same cells. TNF-resistant leukemic lines had
higher constitutive levels of Mn-SOD RNA and activity; and these levels did
not change in the presence of TNF. Antisense but not random
oligonucleotides to Mn-SOD markedly increased the sensitivity to the
inhibitory effects of TNF for both the native HL-60 (TNF-sensitive) and
K562 (TNF-resistant) cell lines. Further studies showed that the antisense
oligonucleotides entered the cells and resulted in decreased levels of
Mn-SOD RNA. The data suggest that Mn-SOD may provide protection against
cytotoxicity of TNF in hematopoietic cells.
Volume 82,
Issue 4,
pp. 1142-1150,
08/15/1993
Copyright © 1993 by The American Society of Hematology
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