Selenium and intractable epilepsy: Is there any correlation?

被引:56
作者
Ashrafi, Mahmood Reza
Shabanian, Reza [1 ]
Abbaskhanian, Ali
Nasirian, Abolfazl
Ghofrani, Mohammad
Mohammadi, Mahmood
Zamani, Gholam Reza
Kayhanidoost, Zarrin
Ebrahimi, Sara
Pourpak, Zahra
机构
[1] Univ Tehran Med Sci, Dept Pediat Neurol, Childrens Med Ctr, Tehran 14194, Iran
[2] Shahid Beheshti Univ Med Sci, Mofid Hosp, Tehran, Iran
关键词
D O I
10.1016/j.pediatrneurol.2006.09.001
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Oxidative stress and generation of reactive oxygen species are strongly implicated in a number of neuronal and neuromuscular disorders, including epilepsy. The functions of selenium as an antioxidant trace element are believed to be carried out by selenoproteins that possess antioxidant activities and the ability to promote neuronal cell survival. Because of this protective role of selenium against oxidative damage, a case-control study was designed to compare its serum level between intractable epileptic patients and normal subjects. Eighty patients who met the criteria of intractable epilepsy were compared with a normal control group of the same age, socioeconomic level, and place of living. Serum selenium level was measured with an atomic absorption spectrophotometer. The mean (+/- S.D.) of serum selenium were 68.88 (+/- 17.58) ng/mL and 85.93 (+/- 13.93) ng/mL in the patient and control groups respectively. Independent sample t test with P < 0.05 indicated a significant lower mean of serum selenium in the patient group compared with that of the normal control group. However, there was no association between serum selenium and some suggested predictive factors of intractable seizures, including age at the onset of seizures, neonatal seizure, neurologic impairment, and etiology of epilepsy. Measurement of serum selenium in patients with intractable epilepsy should be considered. (c) 2007 by Elsevier Inc. All rights reserved.
引用
收藏
页码:25 / 29
页数:5
相关论文
共 25 条
[1]   EVIDENCE FOR SPECIFIC SELENIUM TARGET TISSUES AND NEW BIOLOGICALLY IMPORTANT SELENOPROTEINS [J].
BEHNE, D ;
HILMERT, H ;
SCHEID, S ;
GESSNER, H ;
ELGER, W .
BIOCHIMICA ET BIOPHYSICA ACTA, 1988, 966 (01) :12-21
[2]  
Burk RF, 1999, MODERN NUTR HLTH DIS, P265
[3]   Low selenium diet increases the dopamine turnover in prefrontal cortex of the rat [J].
Castano, A ;
Ayala, A ;
RodriguezGomez, JA ;
Herrera, AJ ;
Cano, J ;
Machado, A .
NEUROCHEMISTRY INTERNATIONAL, 1997, 30 (06) :549-555
[4]   Etiology and clinical predictors of intractable epilepsy [J].
Chawla, S ;
Aneja, S ;
Kashyap, R ;
Mallika, V .
PEDIATRIC NEUROLOGY, 2002, 27 (03) :186-191
[5]   Selenium and selenoproteins in the brain and brain diseases [J].
Chen, J ;
Berry, MJ .
JOURNAL OF NEUROCHEMISTRY, 2003, 86 (01) :1-12
[6]   ANTIOXIDANTS AND DISEASE PREVENTION [J].
DIPLOCK, AT .
MOLECULAR ASPECTS OF MEDICINE, 1994, 15 (04) :293-+
[7]   A proposed diagnostic scheme for people with epileptic seizures and with epilepsy: Report of the ILAE Task Force on Classification and Terminology [J].
Engel, J .
EPILEPSIA, 2001, 42 (06) :796-803
[8]  
Jozanov-Stankov Olga, 1998, Journal of Environmental Pathology Toxicology and Oncology, V17, P251
[9]   Knowing when not to stop: Selenocysteine incorporation in eukaryotes [J].
Low, SC ;
Berry, MJ .
TRENDS IN BIOCHEMICAL SCIENCES, 1996, 21 (06) :203-208
[10]   FREE-RADICALS, ANTICONVULSANTS, AND THE NEURONAL CEROID-LIPOFUSCINOSES [J].
MAERTENS, P ;
DYKEN, P ;
GRAF, W ;
PIPPENGER, C ;
CHRONISTER, R ;
SHAH, A .
AMERICAN JOURNAL OF MEDICAL GENETICS, 1995, 57 (02) :225-228