Urinary excretion ofD-glucaric acid, an indicator of drug metabolizing enzyme activity, in patients with impaired renal function

1980 ◽  
Vol 18 (3) ◽  
pp. 255-261 ◽  
Author(s):  
D. Kampf ◽  
I. Roots ◽  
A. G. Hildebrandt
Keyword(s):  
Renal Function ◽  
Enzyme Activity ◽  
Urinary Excretion ◽  
Impaired Renal Function ◽  
Glucaric Acid ◽  
Drug Metabolizing Enzyme ◽  
Metabolizing Enzyme

scholarly journals Urinary excretion of aflatoxin M1 after administration of aflatoxin B1 in sucrose- or starch-rich diets

1978 ◽  
Vol 40 (2) ◽  
pp. 397-401 ◽  
Author(s):  
A. Wise ◽  
M. Suzangar ◽  
M. Messripour ◽  
J. Mohammadi
Keyword(s):  
Urinary Excretion ◽  
Aflatoxin B1 ◽  
Aflatoxin M1 ◽  
Sprague Dawley ◽  
Drug Metabolizing Enzyme ◽  
Sprague Dawley Rats ◽  
Metabolizing Enzyme ◽  
Aflatoxin B

1. Male Sprague–Dawley rats were given 630 g/kg sucrose or starch with 2 mg/kg aflatoxin B1 for periods of 75, 145 and 200 d, and the 24 h urinary excretion of aflatoxin M1 was measured.2. Less aflatoxin M1 was excreted by the rats fed on the sucrose-rich diet compared to those fed on the starch-rich diet. This difference was especially marked when expressed per g metabolizing tissue.3. It is concluded that sucrose probably decreases the activity of aflatoxin B1 metabolism in a similar way to its previously found effect on the drug-metabolizing enzyme.

scholarly journals Hepatic drug-metabolizing enzyme activity in rats pretreated with (−)-emetine or (±)-2,3-dehydroemetine

1970 ◽  
Vol 117 (3) ◽  
pp. 491-498 ◽  
Author(s):  
H. H. Miller ◽  
R. K. Johnson ◽  
J. D. Donahue ◽  
W. R. Jondorf
Keyword(s):  
Enzyme Activity ◽  
Female Rats ◽  
Inhibitory Effects ◽  
Hepatic Drug ◽  
Azo Reduction ◽  
Drug Metabolizing Enzyme ◽  
Metabolizing Enzyme ◽  
Sodium Phenobarbital ◽  
Stimulation Of

1. Pretreatment of female rats with (−)-emetine or (±)-2,3-dehydroemetine (at 18μmol/kg body wt. for 24h) prolongs the hexobarbital-induced sleeping-time of the treated animals. 2. This effect is not observed on pretreating animals with other compounds closely related to (−)-emetine, such as (−)-isoemetine or (+)-O-methylpsychotrine. 3. Liver microsomal drug-metabolizing enzyme activity in vitro as measured by N-demethylation of aminopyrine and azo-reduction of Neoprontosil is inhibited in rats pretreated with (−)-emetine or with (±)-2,3-dehydroemetine. 4. These inhibitory effects on drug metabolism in vitro are not observed in corresponding experiments involving pretreatment of rats with (−)-isoemetine or (+)-O-methylpsychotrine. 5. Co-administration of emetine or 2,3-dehydroemetine and sodium phenobarbital or 1,1-dichloro-2-o-chlorophenyl-2-p-chlorophenylethane to rats abolishes or greatly diminishes the stimulation of drug-metabolizing enzyme activity in vitro usually obtained by the administration of phenobarbital or 1,1-dichloro-2-o-chlorophenyl-2-p-chlorophenylethane alone. 6. Further, in rats pretreated with sodium phenobarbital and subsequently injected with emetine or 2,3-dehydroemetine the pre-stimulated drug-metabolizing enzyme activity in vitro is diminished. 7. The inhibitory effects on drug-metabolizing enzyme activity after pretreatment with (−)-emetine or (±)-2,3-dehydroemetine do not appear to be related to NADPH generation.

Aryl hydrocarbon receptor-mediated induction of microsomal drug-metabolizing enzyme activity by indirubin and indigo

2004 ◽  
Vol 318 (2) ◽  
pp. 571-578 ◽  
Author(s):  
Kazumi Sugihara ◽  
Shigeyuki Kitamura ◽  
Tsuyoshi Yamada ◽  
Takashige Okayama ◽  
Shigeru Ohta ◽  
...  
Keyword(s):  
Enzyme Activity ◽  
Aryl Hydrocarbon Receptor ◽  
Aryl Hydrocarbon ◽  
Drug Metabolizing Enzyme ◽  
Metabolizing Enzyme
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