Abstract
Treatment with 0.5% ( w w) dietary clofibrate, a peroxisome proliferator, for 14 days induced microsomal carboxylesterase activities for five substrates including malathion, clofibrate, diethylsuccinate, diethylphthalate, and p-nitrophenylacetate in liver and kidney of male Swiss-Webster mice and Sprague-Dawley rats. The induction was substrate, tissue, and species dependent. The carboxylesterase activity was induced in mouse from 1.2- to 2.2-fold (liver) and from 1.1- to 1.7-fold (kidney) depending upon substrate used. Analogous values from rat ranged from 1.0- to 1.4-fold (liver) and from 1.1- to 1.8-fold (kidney). Enzyme activities were either decreased or not affected in testes of treated mice and rats. Substituted trifluoroketones ("transition-state" inhibitors of carboxylesterase) were found to be very potent inhibitors of clofibrate-metabolizing carboxylesterase(s) and to be potentially useful in distinguishing among isozymes. The inhibition data suggested that changes in carboxylesterase activity following clofibrate treatment were both qualitative and quantitative.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 361-369 |
| Number of pages | 9 |
| Journal | Toxicology and Applied Pharmacology |
| Volume | 89 |
| Issue number | 3 |
| DOIs | |
| State | Published - 1987 |
Fingerprint
ASJC Scopus subject areas
- Pharmacology
- Toxicology
Cite this
Apparent induction of microsomal carboxylesterase activities in tissues of clofibrate-fed mice and rats. / Ashour, Mohamed Bassem A; Moody, David E.; Hammock, Bruce D.
In: Toxicology and Applied Pharmacology, Vol. 89, No. 3, 1987, p. 361-369.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Apparent induction of microsomal carboxylesterase activities in tissues of clofibrate-fed mice and rats
AU - Ashour, Mohamed Bassem A
AU - Moody, David E.
AU - Hammock, Bruce D.
PY - 1987
Y1 - 1987
N2 - Treatment with 0.5% ( w w) dietary clofibrate, a peroxisome proliferator, for 14 days induced microsomal carboxylesterase activities for five substrates including malathion, clofibrate, diethylsuccinate, diethylphthalate, and p-nitrophenylacetate in liver and kidney of male Swiss-Webster mice and Sprague-Dawley rats. The induction was substrate, tissue, and species dependent. The carboxylesterase activity was induced in mouse from 1.2- to 2.2-fold (liver) and from 1.1- to 1.7-fold (kidney) depending upon substrate used. Analogous values from rat ranged from 1.0- to 1.4-fold (liver) and from 1.1- to 1.8-fold (kidney). Enzyme activities were either decreased or not affected in testes of treated mice and rats. Substituted trifluoroketones ("transition-state" inhibitors of carboxylesterase) were found to be very potent inhibitors of clofibrate-metabolizing carboxylesterase(s) and to be potentially useful in distinguishing among isozymes. The inhibition data suggested that changes in carboxylesterase activity following clofibrate treatment were both qualitative and quantitative.
AB - Treatment with 0.5% ( w w) dietary clofibrate, a peroxisome proliferator, for 14 days induced microsomal carboxylesterase activities for five substrates including malathion, clofibrate, diethylsuccinate, diethylphthalate, and p-nitrophenylacetate in liver and kidney of male Swiss-Webster mice and Sprague-Dawley rats. The induction was substrate, tissue, and species dependent. The carboxylesterase activity was induced in mouse from 1.2- to 2.2-fold (liver) and from 1.1- to 1.7-fold (kidney) depending upon substrate used. Analogous values from rat ranged from 1.0- to 1.4-fold (liver) and from 1.1- to 1.8-fold (kidney). Enzyme activities were either decreased or not affected in testes of treated mice and rats. Substituted trifluoroketones ("transition-state" inhibitors of carboxylesterase) were found to be very potent inhibitors of clofibrate-metabolizing carboxylesterase(s) and to be potentially useful in distinguishing among isozymes. The inhibition data suggested that changes in carboxylesterase activity following clofibrate treatment were both qualitative and quantitative.
UR - http://www.scopus.com/inward/record.url?scp=0023184183&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0023184183&partnerID=8YFLogxK
U2 - 10.1016/0041-008X(87)90155-4
DO - 10.1016/0041-008X(87)90155-4
M3 - Article
VL - 89
SP - 361
EP - 369
JO - Toxicology and Applied Pharmacology
JF - Toxicology and Applied Pharmacology
SN - 0041-008X
IS - 3
ER -