ANTICONVULSANT-INDUCED CHANGES IN TISSUE MANGANESE, ZINC, COPPER, AND IRON CONCENTRATIONS IN WISTAR RATS

被引:10
作者
CRITCHFIELD, JW
CARL, FG
KEEN, CL
机构
[1] UNIV CALIF DAVIS, DEPT NUTR, DAVIS, CA 95616 USA
[2] UNIV CALIF DAVIS, DEPT INTERNAL MED, DAVIS, CA 95616 USA
[3] VET ADM MED CTR, DEPT MED RES 151, AUGUSTA, GA 30904 USA
[4] MED COLL GEORGIA, DEPT NEUROL, AUGUSTA, GA 30912 USA
来源
METABOLISM-CLINICAL AND EXPERIMENTAL | 1993年 / 42卷 / 07期
关键词
D O I
10.1016/0026-0495(93)90068-Y
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Human epileptics have been reported to have low blood manganese (Mn) concentrations in comparison to nonepileptics, an observation that is important because Mn deficiency can increase seizure susceptibility in experimental animals. Factors that have been suggested to contribute to the low blood Mn levels in epileptics include anticonvulsant use, seizure-induced tissue redistribution of Mn, and genetics; in the present study, the first of these possibilities was tested. Wistar rats were fed semipurified diets containing diphenylhydantoin ([DPH] 3 g/kg diet), phenobarbital ([PB] 2 g/kg diet), or primidone ([PRIM] 3 g/kg diet) for 7 weeks, at which time they were killed and tissues collected and analyzed for Mn, zinc (Zn), copper (Cu), and iron (Fe) concentrations. In comparison to pair-fed rats, DPH- and PRIM-fed rats had significantly elevated liver Mn concentrations, while Mn concentrations in blood, brain, heart, and kidney were unaffected by anticonvulsant exposure. Changes in the concentrations of Zn, Cu, and Fe in specific tissues were also found. Overall, these findings suggest that the anticonvulsants tested do not lead to significant derangements in the metabolism of Mn. © 1993.
引用
收藏
页码:907 / 910
页数:4
相关论文
共 26 条
[11]   ALTERATIONS IN TISSUE TRACE-ELEMENT AND ASCORBIC-ACID METABOLISM IN PHENYTOIN-FED RATS AND MICE [J].
DUBICK, MA ;
KEEN, CL .
JOURNAL OF NUTRITION, 1985, 115 (11) :1481-1487
[12]   BLOOD MANGANESE LEVELS IN CHILDREN WITH CONVULSIVE DISORDER [J].
DUPONT, CL ;
TANAKA, Y .
BIOCHEMICAL MEDICINE, 1985, 33 (02) :246-255
[13]   HYPERCUPREMIA INDUCED BY ANTI-EPILEPTIC DRUGS [J].
GHOSE, K ;
TAYLOR, A .
HUMAN TOXICOLOGY, 1983, 2 (03) :519-529
[14]   ZINC STATUS AND DELAYED CUTANEOUS HYPERSENSITIVITY IN HANDICAPPED-CHILDREN TREATED WITH ANTICONVULSANTS [J].
HIGASHI, A ;
CHEN, C ;
MATSUDA, I .
DEVELOPMENTAL PHARMACOLOGY AND THERAPEUTICS, 1987, 10 (01) :30-35
[15]   INFLUENCE OF MANGANESE ON SUSCEPTIBILITY OF RATS TO CONVULSIONS [J].
HURLEY, LS ;
ROSENTHAL, F ;
WOOLLEY, DE ;
TIMIRAS, PS .
AMERICAN JOURNAL OF PHYSIOLOGY, 1963, 204 (03) :493-&
[16]  
HURLEY LS, 1961, P SOC EXP BIOL MED, V106, P343, DOI 10.3181/00379727-106-26332
[17]  
KINYUA AM, 1988, TRACE ELEM MED, V5, P176
[18]   EFFECT OF VALPROIC ACID THERAPY ON ZINC-METABOLISM IN CHILDREN WITH PRIMARY EPILEPSY [J].
LERMANSAGIE, T ;
STATTER, M ;
SZABO, G ;
LERMAN, P .
CLINICAL NEUROPHARMACOLOGY, 1987, 10 (01) :80-86
[19]  
OLATUNBOSUN DA, 1978, NIGERIAN MED J, V8, P124
[20]   ZINC AND COPPER-METABOLISM IN PHENYTOIN THERAPY [J].
PALM, R ;
HALLMANS, G .
EPILEPSIA, 1982, 23 (05) :453-461