Teratogenic Effects of Sodium Arsenate in Mice

Hood, Ronald D.; Bishop, Sally L.

doi:10.1080/00039896.1972.10666051

Cited by 121 publications

(36 citation statements)

References 6 publications

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“…For example, inorganic arsenicals were widely used in agricultural products, including pesticides and herbicides. Arsenic is a well established teratogen in rodents (Ferm et al, 1971;Hood and Bishop, 1972;Beaudoin, 1974;Machado et al, 1999). Exposure of mouse embryos in culture to 3-4 M sodium arsenite results in open neural tubes (Chaineau et al, 1990;Tabocova et al, 1996), and developmental exposure of arsenic to the dam in rodent models causes exencephaly (Morrissey and Mottet, 1983).…”

Section: Discussionmentioning

confidence: 99%

Arsenite-Induced Apoptosis in Cortical Neurons Is Mediated by c-Jun N-Terminal Protein Kinase 3 and p38 Mitogen-Activated Protein Kinase

2000

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c-Jun N-terminal protein kinase (JNK) and p38 mitogenactivated protein kinase are activated by stress and are implicated in regulation of apoptosis in several tissues. However, their contribution to stress-induced apoptosis in CNS neurons is not well defined. Here we investigated the role of JNK and p38 in cortical neuron apoptosis caused by sodium arsenite treatment. Sodium arsenite is an environmental toxicant that causes developmental defects in the CNS. Treatment of cortical neurons with sodium arsenite activated p38 and JNK3 but not JNK1 or JNK2. It also induced c-Jun phosphorylation. Furthermore, sodium arsenite induced cortical neuron apoptosis. This apoptosis was attenuated by SB203580, an inhibitor of p38, and by CEP-1347, an inhibitor of JNK activation. Expression of dominant-interfering mutants of the JNK or p38 pathways inhibited apoptosis induced by arsenite, whereas expression of constitutive active mutants for either pathway induced apoptosis. Moreover, the caspase inhibitor zVAD-fluoromethylketone as well as expression of bcl-2 or bcl-xL inhibited cortical neuron apoptosis induced by arsenite or by constitutive activation of JNK or p38. These data indicate that both JNK and p38 contribute to arsenite-induced apoptosis in primary CNS neurons, and this apoptosis requires the bcl-2-caspase pathway. This is the first evidence that a specific JNK isoform is differentially activated by stress and contributes to neuronal apoptosis.

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Section: Discussionmentioning

confidence: 99%

Arsenite-Induced Apoptosis in Cortical Neurons Is Mediated by c-Jun N-Terminal Protein Kinase 3 and p38 Mitogen-Activated Protein Kinase

2000

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“…Acute or chronic experimental exposure to iAs during development (Hood and Bishop, 1972;Piamphongsant, 1999) or adulthood Shila et al, 2005) has been reported to affect the CNS. Interestingly, compared to a non-exposed control group, adult rats exposed to ~77 mg/L iAs for 60 days were found to accumulate iAs in a brain region-specific manner following the descendent order cortex-striatum-hippocampus-hypothalamus-cerebellum (Shila et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

Locomotor activity and sensory – motor developmental alterations in rat offspring exposed to arsenic prenatally and via lactation

Gumilar

Lencinas

Bras

et al. 2015

Neurotoxicology and Teratology

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Please cite this article as: Fernanda Gumilar, Ileana Lencinas, Cristina Bras, Leda Giannuzzi, Alejandra Minetti, Locomotor activity and sensory-motor developmental alterations in rat offspring exposed to Arsenic prenatally and via lactation, Neurotoxicology and Teratology (2015), doi: 10.1016/j.ntt.2015 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.A C C E P T E D M A N U S C R I P T an open field were assessed in 90-day-old offspring. Results show that rats exposed to low iAs concentrations through drinking water during early development evidence a delay in the development of sensory-motor reflexes. A C C E P T E D M A N U S C R I P T ACCEPTED MANUSCRIPTBoth FOB procedure and open-field tests showed a decrease in locomotor activity in adult rats. This study reveals that exposure to the above-mentioned iAs concentrations produces dysfunction in the CNS mechanisms whose role is to regulate motor and sensory development and locomotor activity.

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“…Ayrıca, Grup A, B ve C kendi içlerinde de 6 alt gruba (Al-6, Bl-6 ve Cl-6) bölündü; K ve deneme alt gruplarının her birinde 12 yumurta bulundurullarda verim ve ağırlık kazancının azalmasına, kansızlığa, kemiklerde erimeye ve şekil bozukluklarına, özellikle karaciğer, böbrek ve dal ak olmak üzere, organlarda bozukluklara sebep olabilirler (6,7,11,22,29,35,36). Başta arsenik, kurşun ve civa olmak üzere, metallerin bir çoğunun memeli, kanatlı ve balık embriyoları üzerinde güçlü teratojenik etkileri vardır (3, 10,15,16,18). Yalnız bu çalışmaların çoğunda metallerin teratojenik etkilerine ayrı ayrı bakıl-mıştır.…”

Section: Introductionunclassified

AĞIR METALLERİN TAVUK EMBRİYOLARINDA TERATOJENİK ETKİLERİ: 1. Arsenik ve Kurşunun Ayrı Ayrı ve Birlikte Kullanılmasının Etkileri

Sezai;ALABAY¹

1995

Ankara Üniversitesi Veteriner Fakültesi Dergisi

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Teratogenic Effects of Sodium Arsenate in Mice

Cited by 121 publications

References 6 publications

Arsenite-Induced Apoptosis in Cortical Neurons Is Mediated by c-Jun N-Terminal Protein Kinase 3 and p38 Mitogen-Activated Protein Kinase

Arsenite-Induced Apoptosis in Cortical Neurons Is Mediated by c-Jun N-Terminal Protein Kinase 3 and p38 Mitogen-Activated Protein Kinase

Locomotor activity and sensory – motor developmental alterations in rat offspring exposed to arsenic prenatally and via lactation

AĞIR METALLERİN TAVUK EMBRİYOLARINDA TERATOJENİK ETKİLERİ: 1. Arsenik ve Kurşunun Ayrı Ayrı ve Birlikte Kullanılmasının Etkileri

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