Biochemical and ultrastructural effects of nitrite in rainbow trout: liver hypoxia as the root of the acute toxicity mechanism.
In Salmo gairdneri specimens exposed for 12, 24, 48, and 72 hr to nitrite (450 micrograms NO2-N) the main biochemical parameters of cerebral and hepatic hypoxia were studied. Observations on liver ultrastructure were also made to follow nitrite hepatotoxicity. Furthermore, some physiological alterations in liver mitochondria incubated in a medium containing a nitrite concentration similar to that found in the liver of in vivo exposed trout were studied. Results suggest that tissue hypoxia, due to the nitrite-induced high methemoglobinemia, is too low to be directly responsible for animal death. Nevertheless liver hypoxia is thought to be at the root of nitrite acute toxicity mechanism by producing suitable conditions for toxic potentialities. Thus irreversible and deadly damages arise in liver biochemistry and ultrastructure, particularly at the mitochondrial level.
D000255:Adenosine Triphosphate / Q000032:analysis; D000818:Animals; D001923:Brain Chemistry / Q000187:drug effects; D007773:Lactates / Q000032:analysis; D019344:Lactic Acid; D008099:Liver / Q000032:analysis / Q000187:drug effects* / Q000648:ultrastructure; D008706:Methemoglobin / Q000032:analysis; D008930:Mitochondria, Liver / Q000187:drug effects; D009573:Nitrites / Q000633:toxicity*; D010100:Oxygen; D014337:Trout
D007773:Lactates; D009573:Nitrites; D019344:Lactic Acid; D000255:Adenosine Triphosphate; D008706:Methemoglobin; D010100:Oxygen