Abstract
The stability of hepatic microsomal drug oxidation and its associated electron transport has been studied in rabbits under conditions approximating those existing prior to human autopsy. Aminopyrine N-demethylation, aniline p-hydroxylation. NADPH cytochrome c reductase, NADPH cytochrome P-450 reductase, and the microsomal content of cytochrome P-450 declined appreciably in 2 h when microsomes were prepared from rabbit liver left in situ after death. In livers removed immediately after death and kept on ice these microsomal components remained stable for at least 4.5 h. Evidence of degeneration of human microsomes prepared from liver obtained at autopsy is discussed. The lability of hepatic microsomes from livers left in situ in these experiments or prior to autopsy is most likely secondary to slow cooling of the liver with coincidental autolysis. The possibility that the degeneration observed was due to the rapid growth of bacteria was disproved. These experiments demonstrate that care must be exercised in interpreting data obtained using microsomes from human autopsy material.
Original language | English |
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Pages (from-to) | 29-37 |
Number of pages | 9 |
Journal | Chemico-Biological Interactions |
Volume | 7 |
Issue number | 1 |
DOIs | |
Publication status | Published - Jul 1973 |
Externally published | Yes |
Bibliographical note
Funding Information:i Supported by the Medical Research Council of Canada and by The Canadian Foundation Advancement of Therapeutics.
ASJC Scopus Subject Areas
- Toxicology