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Nitrogen oxide‐induced autoprotection in isolated rat hepatocytes
Author(s) -
Kim Young-Myeong,
Bergonia Hector,
Lancaster Jack R.
Publication year - 1995
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(95)01115-u
Subject(s) - cycloheximide , nitric oxide , chemistry , in vivo , nitric oxide synthase , snap , downregulation and upregulation , thioacetamide , biochemistry , heme , heme oxygenase , reactive oxygen species , toxicity , paraquat , glutathione , pharmacology , biology , protein biosynthesis , enzyme , computer graphics (images) , microbiology and biotechnology , organic chemistry , computer science , gene
Pretreatment of rat hepatocytes with low‐dose nitrogen oxide (addition of SNAP in vitro or induction of nitric oxide synthase in vitro or in vivo) imparts resistance to killing and decrease in aconitase and mitochondrial electron transfer from a second exposure to a higher dose of SNAP. Induction of this resistance is prevented by cycloheximide, indicating upregulation of protective protein(s). Ferritin levels are increased as are nonheme iron‐NO EPR signals. Tin‐protoporphyrin (SnPP) prevents protection, suggesting involvement of hsp32 (heme oxygenase) and/or guanylyl cyclase (GC). Cross‐resistance to H 2 O 2 killing is also observed, which is also prevented by cycloheximide and SnPP. Thus, hepatocytes possess inducible protective mechanisms against nitrogen oxide and reactive oxygen toxicity.