Abstract | BACKGROUND: METHODS: The control group received normal saline and the experimental group received VPA (500 mg/kg per day) by intraperitoneal injections for 7 days. Various clinical chemistry parameters in rat blood and free and total carnitine levels in plasma and tissue were determined. Mitochondria were isolated from rat liver and heart and the relative amount of each ACD protein was determined by immunoblot analysis. Total RNA was prepared from various tissues and the mRNA levels for various ACD were measured by slot-blot hybridization analysis using respective cDNA probes. RESULTS: CONCLUSIONS:
Valproic acid causes enhanced expression of fatty ACD mRNA, especially in the heart, by a feedback mechanism related to inhibition of beta-oxidation in rats fed ad libitum. However, it impairs the expression of ACD in the liver when there is a drastic change in nutritional state.
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Authors | M Kibayashi, M Nagao, S Chiba |
Journal | Pediatrics international : official journal of the Japan Pediatric Society
(Pediatr Int)
Vol. 41
Issue 1
Pg. 52-60
(Feb 1999)
ISSN: 1328-8067 [Print] Australia |
PMID | 10200137
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Anticonvulsants
- Fatty Acids
- Valproic Acid
- Acyl-CoA Dehydrogenase
- Acyl-CoA Dehydrogenase, Long-Chain
- Carnitine
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Topics |
- Acyl-CoA Dehydrogenase
- Acyl-CoA Dehydrogenase, Long-Chain
(analysis, drug effects)
- Animals
- Anticonvulsants
(adverse effects, metabolism)
- Carnitine
(blood)
- Chemical and Drug Induced Liver Injury
(etiology, metabolism)
- Drug Evaluation, Preclinical
- Fatty Acids
(metabolism)
- Male
- Mitochondria, Heart
(chemistry, metabolism)
- Mitochondria, Liver
(chemistry, metabolism)
- Oxidation-Reduction
- Rats
- Rats, Wistar
- Starvation
(metabolism)
- Valproic Acid
(adverse effects, metabolism)
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