Journal article
Genistein and daidzein induce neurotoxicity at high concentrations in primary rat neuronal cultures
Journal of biomedical science, v 14(2)
01 Mar 2007
PMID: 17245525
Featured in Collection : UN Sustainable Development Goals @ Drexel
Abstract
It is known that estrogen can protect neurons from excitotoxicity. Since isoflavones possess estrogen-like activity, it is of interest to determine whether isoflavones can also protect neurons from glutamate-induced neuronal injury. Morphological observation and lactate dehydrogenase (LDH) release assay were used to estimate the cellular damage. It is surprising that, contrary to estrogen, isoflavones, specifically genistein and daidzein, are toxic to primary neuronal culture at high concentration. Treatment of neurons with 50 mu M genistein and daidzein for 24 h increased LDH release by 90% and 67%, respectively, indicating a significant cellular damage. Under the same conditions, estrogen such as 17 beta-estradiol did not show any effect on primary culture of brain cells. At 100 mu M, both genistein and daidzein increased LDH release by 2.6- and 3-fold, respectively with a 30-min incubation. Furthermore, both genistein and daidzein at 50 mu M increased the intracellular calcium level, [Ca2+](i), significantly. To determine their mode of action, genistein and daidzein were tested on glutamate and GABA(A) receptor binding. Both genistein and daidzein were found to have little effect on glutamate receptor binding, while the binding of [H-3]muscimol to GABA(A) receptors was markedly inhibited. However, 17 beta-estradiol did not affect GABA(A) receptor binding suggesting that the toxic effect of genistein and daidzein could be due to their inhibition of the GABA(A) receptor resulting in further enhancement of excitation by glutamate and leading to cellular damage.
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Details
- Title
- Genistein and daidzein induce neurotoxicity at high concentrations in primary rat neuronal cultures
- Creators
- Ying Jin - Florida Atlantic UniversityHeng Wu - Florida Atlantic UniversityEric M. CohenJianning Wei - Florida Atlantic UniversityHong Jin - University of KansasHoward Prentice - Florida Atlantic UniversityJang-Yen Wu - Florida Atlantic University
- Publication Details
- Journal of biomedical science, v 14(2)
- Publisher
- Springer Nature
- Number of pages
- 10
- Grant note
- R01NS037851 / NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA; NIH National Institute of Neurological Disorders & Stroke (NINDS) NS37851 / NINDS NIH HHS; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA; NIH National Institute of Neurological Disorders & Stroke (NINDS)
- Resource Type
- Journal article
- Language
- English
- Academic Unit
- Neurobiology and Anatomy; Physical Therapy (and Rehabilitation Sciences)
- Web of Science ID
- WOS:000245806700011
- Scopus ID
- 2-s2.0-34247223636
- Other Identifier
- 991020545117804721
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- Collaboration types
- Domestic collaboration
- Web of Science research areas
- Cell Biology
- Medicine, Research & Experimental