scholarly journals Precocious development of cytochrome P-450 in neonatal rat liver after glucocorticoid treatment

1979 ◽  
Vol 182 (1) ◽  
pp. 233-235 ◽  
Author(s):  
J E A Leakey ◽  
J R Fouts

Intraperitoneal injection of neonatal rats with glucocorticoid hormones causes precocious development of hepatic cytochrome P-450. Glucagon injection fails to stimulate this cytochrome P-450 development. Adult liver cytochrome P-450 is less responsive to glucocorticoid stimulation than is that of neonatal rat liver. Adrenalectomy of prematurely delivered neonatal animals prevents the early postnatal development of cytochrome P-450. Glucocorticoids failed to increase cytochrome P-450 concentrations in foetal rat liver. These findings imply that, although glucocorticoids are mandatory regulatory factors controlling cytochrome P-450 development, they are not themselves the ‘trigger’ initiating onset of that development.

Abstracts ◽  
1978 ◽  
pp. 289
Author(s):  
Thierry CRESTEIL ◽  
Philippe BEAUNE ◽  
Jean-Paul LEROUX

Xenobiotica ◽  
1992 ◽  
Vol 22 (5) ◽  
pp. 515-522 ◽  
Author(s):  
G. J. M. Horbach ◽  
J. G. Van Asten ◽  
I. M. C. M. Rietjens ◽  
P. Kremers ◽  
C. F. A. Van Bezooijen

1983 ◽  
Vol 32 (15) ◽  
pp. 2309-2318 ◽  
Author(s):  
Marcel Delaforge ◽  
Maryse Jaouen ◽  
Daniel Mansuy

1990 ◽  
Vol 68 (3) ◽  
pp. 370-373 ◽  
Author(s):  
D. S. Riddick ◽  
J. E. Mackie ◽  
T. E. Massey ◽  
G. S. Marks

Various rat liver cytochrome P-450 (P-450) isozymes are targets for mechanism-based inactivation by 3,5-diethoxycarbonyl-2,6-dimethyl-4-ethyl-1,4-dihydropyridine (4-ethyl DDC). Unlike rat liver, which contains multiple P-450 isozymes, rabbit lung contains only three major isozymes referred to as forms 2, 5, and 6. We have examined the ability of 4-ethyl DDC to destroy P-450 heme in hepatic and pulmonary microsomes from untreated and β-naphthoflavone (βNF)-treated rabbits. This compound destroyed 31% of the P-450 in either hepatic microsomal preparation, but was ineffective at lowering P-450 and heme levels in pulmonary microsomes when examined at a range of concentrations (0.45 – 5.0 mM). These data suggest that rabbit pulmonary P-450 forms 2, 5, and 6 are not targets for destruction by 4-ethyl DDC, despite the ability of this compound to inactivate rat liver P-450c, the orthologue of rabbit lung form 6.Key words: 3,5-diethoxycarbonyl-2,6-dimethyl-4-ethyl-1,4-dihydropyridine, cytochrome P-450, mechanism-based inactivation, rabbit pulmonary microsomes.


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