The antioxidants vitamin E and β-carotene protect against ethanol-induced neurotoxicity in embryonic rat hippocampal cultures
The antioxidants vitamin E and β-carotene protect against ethanol-induced neurotoxicity in embryonic rat hippocampal cultures
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DOI：
10.1016/s0741-8329(98)00051-2
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发表时间：
1999-02-01
期刊：
影响因子：
2.3
通讯作者：
Heaton, MB
中科院分区：
文献类型：
--
作者：
Mitchell, JJ;Paiva, M;Heaton, MB
胎儿酒精综合征的特征是许多神经系统异常，发育中的海马体非常脆弱。其他条件可以导致母亲的乙醇消费，包括氧化应激。关键的抗氧化剂，如维生素E，可以减少和抗氧化防御改变。将孕18天的大鼠海马培养物暴露于400至2400 mg/dl的乙醇（16 h）。MTT试验评估神经毒性。活力呈剂量依赖性降低。补充维生素E或β-胡萝卜素对所有乙醇浓度提供神经保护。维生素E完全改善400和800 mg/dl乙醇后的神经元损失。与非乙醇治疗相比，维生素E在1600、1800、2000和2400 mg/dl乙醇治疗期间将存活率提高至95%、79%、66%和75%。与未补充维生素E的乙醇处理相比，维生素E在1600、1800、2000和2400 mg/dl下使活力增加38%、23%、12%和29%。β-胡萝卜素完全改善了来自400 mg/dl乙醇的细胞损失，并且在1600 mg/dl下使存活率增加18%，在2000 mg/dl下增加12%。这项研究表明，在体外抗氧化神经保护对发展乙醇暴露，并建议，营养疗法纳入抗氧化剂可能有助于防止有害胎儿的影响，母亲酗酒。(C)1999 Elsevier Science Inc. All rights reserved.
Fetal alcohol syndrome is characterized by numerous nervous system anomalies with the developing hippocampus being highly vulnerable. Other conditions can result from maternal ethanol consumption including oxidative stress. Critical antioxidants, such as vitamin E, can be decreased and antioxidative defenses altered. Gestational day 18 rat hippocampal cultures were exposed to ethanol ranging from 400 to 2400 mg/dl (16 h). MTT assays assessed neurotoxicity. Viability was decreased dose dependently. Supplementation with vitamin E or beta-carotene afforded neuroprotection against all ethanol concentrations. Vitamin E completely ameliorated neuronal loss following 400 and 800 mg/dl ethanol. Vitamin E increased survival to 95%, 79%; 66%, and 75% during 1600, 1800, and 2000 and 2400 mg/dl ethanol compared to nonethanol treatment. Vitamin E increased viability by 38%, 23%, 12%, and 29% at 1600, 1800, 2000, and 2400 mg/dl compared to non-vitamin E-supplemented, ethanol treatment. beta-Carotene completely ameliorated cell loss from 400 mg/dl ethanol and increased survival by 18% at 1600 mg/dl and 12% at 2000 mg/dl. This study demonstrates in vitro antioxidative neuroprotection against developmental ethanol exposure and suggests that nutritional therapies incorporating antioxidants may help protect against deleterious fetal effects from maternal alcohol abuse. (C) 1999 Elsevier Science Inc. All rights reserved.