MinireviewDevelopmental toxicity of valproic acid
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Cited by (32)
Role of environmental factors and epigenetics in autism spectrum disorders
2020, Progress in Molecular Biology and Translational ScienceCitation Excerpt :How VPA impacts the brain is still not well understood in the adult and even less so in the developing brain, however there are two interesting known molecular effects of VPA: (1) VPA acts on the GABA-ergic system, (2) VPA modulates an important factor of epigenetic regulation: the protein histone deacetylase. As early as 1969, it was understood that VPA leads to an increase of GABA in the brain which might inhibit the abnormal neuronal activity in epileptic centers in the brain (reviewed in Hammond et al. 1981 and in Cotariu and Saidman 1991)137,138 acting most probably through indirect effect on the cerebral enzymes that participate in the regulation of GABA.139 In the mouse, low doses of VPA (125–290 mg/kg) elevate GABA concentrations in the brain at the level of the synaptic terminals140,141 and valproate increases the level of GABA in the cerebro-spinal fluid in human.142
A scale out approach towards neural induction of human induced pluripotent stem cells for neurodevelopmental toxicity studies
2018, Toxicology LettersCitation Excerpt :For example, antiepileptic drugs direct their action towards targets located on the central nervous system (CNS), and their effects can induce negative effects on neurodevelopmental processes (Cotariu and Zaidman, 1991). The use of such compounds during pregnancy can increase the risk of malformations in the developing fetus, namely at the neural tube level, as well as growth retardation and microcephaly (Cotariu and Zaidman, 1991; 22). Valproic acid (VPA), for example, is an antiepileptic drug that is widely administered to treat neurologic disorders such as epilepsy and acute mania.
An adverse outcome pathway framework for neural tube and axial defects mediated by modulation of retinoic acid homeostasis
2015, Reproductive ToxicologyCitation Excerpt :These studies have proven useful in providing overall hazard information based on apical endpoints such as resorptions, prenatal death, growth retardation and malformations. Decades of experience with these studies have shown that the nature of apical endpoints cannot readily be extrapolated between species and not even between strains of the same species [2,8,9]. The relevance of apical animal findings for the human situation is therefore not always clear-cut.
The relative embryotoxicity of 1,3-dichloro-2-propanol on primary chick embryonic cells
2002, Toxicology in VitroContributions of dam and conceptus to differences in sensitivity to valproic acid among C57 black and SWV mice
1999, Reproductive Toxicology