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Nitric oxide (NO)–induced mitochondrial injury among chicken NO‐generating and target leukocytes
Author(s) -
Sung YenJen,
Dietert Rodney R.
Publication year - 1994
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.56.1.52
Subject(s) - nitric oxide , lipopolysaccharide , biology , mitochondrion , microbiology and biotechnology , macrophage , differential centrifugation , nitrite , cell culture , toxicity , biochemistry , immunology , in vitro , chemistry , endocrinology , ecology , genetics , organic chemistry , nitrate
In an analysis of nitric oxide (NO) production and toxicity, chicken macrophage–generated NO inhibited mitochondrial activity in both NO‐producing macrophages themselves and lymphoid tumor targets. However, differences in targeting of mitochondrial toxicity were observed among these cells. Two chicken macrophage cell lines, HD11 and MQ‐NCSU, produced NO (measured as nitrite) dependent upon concentrations of l‐arginine and bacterial endotoxin (lipopolysaccharide). Mitochondrial activity was negatively correlated with the amount of NO produced. Using a modified MTT assay, NO induced suppression in two mitochondrial complexes. Mitochondrial activity was significantly suppressed among HD11 cells receiving LPS alone (complex I, 63.0 ± 5.5% suppression; complex II, 27.9 ± 5.2%). In contrast, mitochondrial activities in samples receiving LPS plus inhibitor, N G ‐nitro‐l‐arginine methyl ester (NAME; 5 mM) or 2,4‐diamino‐6‐hydroxypyrimidine (DAHP; 5 mM), were not significantly different from control values. When HD11 macrophages were cocultured with lymphoblastoid tumor targets, RECC‐CU60 (T cell) or LSCC‐RP9 (B cell), adding LPS (1 μ g/ml), tumor cell mitochondrial activity was significantly suppressed. In the generator macrophages, complex I was more suppressed than complex II, whereas in lymphoid targets no such difference was observed. These results indicate that NO inhibits complex I and II mitochondrial activity but that differential targeting can occur among chicken leukocyte populations J. Leukoc. Biol . 56: 52–58; 1994.