Effects of Drugs and Chemicals on the Fetus and Newborn (First of Two Parts)

Hill, Lyndon M.; Kleinberg, Fredric

doi:10.1016/s0025-6196(12)62060-6

Cited by 25 publications

(4 citation statements)

References 84 publications

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“…[88][89][90][91][92][93] The other chemicals that we tested, namely SA, WAF, HU, PHT, IM, BA, and THA, have been reported to induce craniofacial malformations in mammals, but there have been no reports about the cellular and molecular mechanisms of these malformations. 39,41,45,47,59,63,94 In the present study, we showed that all of these teratogens affected craniofacial morphogenesis as well as CNC development at the cellular level. Our large-scale analysis of numerous teratogens revealed that they caused aberrant CNC development and led to craniofacial malformation.…”

Section: Teratogens Act As Environmental Factors That Disrupt the Dev...mentioning

confidence: 49%

“…In accord with this possibility, RA, MTX, VPA, CAF, and DEX have been reported to affect CNC development in mammals and other vertebrates 88‐93 . The other chemicals that we tested, namely SA, WAF, HU, PHT, IM, BA, and THA, have been reported to induce craniofacial malformations in mammals, but there have been no reports about the cellular and molecular mechanisms of these malformations 39,41,45,47,59,63,94 …”

Section: Discussionmentioning

confidence: 69%

“…The teratogens used in our experiments are well known to induce multiple craniofacial disorders, such as micrognathia, cleft palate, microcephaly, eye defects, and ear abnormalities based on epidemiological data and experiments in mammals. 39,41,43,45,47,61,63,64,86,87 However, there is limited information about the cellular and molecular mechanisms of craniofacial malformations caused by teratogens.…”

Section: Teratogens Act As Environmental Factors That Disrupt the Dev...mentioning

confidence: 99%

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Chemical‐induced craniofacial anomalies caused by disruption of neural crest cell development in a zebrafish model

Liu

Narumi

Ikeda

et al. 2020

Developmental Dynamics

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Background: Craniofacial anomalies are among the most frequent birth defects worldwide, and are thought to be caused by gene-environment interactions. Genetically manipulated zebrafish simulate human diseases and provide great advantages for investigating the etiology and pathology of craniofacial anomalies. Although substantial advances have been made in understanding genetic factors causing craniofacial disorders, limited information about the etiology by which environmental factors, such as teratogens, induce craniofacial anomalies is available in zebrafish. Results: Zebrafish embryos displayed craniofacial malformations after teratogen treatments. Further observations revealed characteristic disruption of chondrocyte number, shape and stacking. These findings suggested aberrant development of cranial neural crest (CNC) cells, which was confirmed by gene expression analysis of the CNC. Notably, these observations suggested conserved etiological pathways between zebrafish and mammals including human. Furthermore, several of these chemicals caused malformations of the eyes, otic vesicle, and/or heart, representing a phenocopy of neurocristopathy, and these chemicals altered the expression levels of the responsible genes. Conclusions: Our results demonstrate that chemical-induced craniofacial malformation is caused by aberrant development of neural crest. This study indicates that zebrafish provide a platform for investigating contributions of environmental factors as causative agents of craniofacial anomalies and neurocristopathy.

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Section: Teratogens Act As Environmental Factors That Disrupt the Dev...mentioning

confidence: 49%

Section: Discussionmentioning

confidence: 69%

Section: Teratogens Act As Environmental Factors That Disrupt the Dev...mentioning

confidence: 99%

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Chemical‐induced craniofacial anomalies caused by disruption of neural crest cell development in a zebrafish model

Liu

Narumi

Ikeda

et al. 2020

Developmental Dynamics

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“…Cerca de 0,5% de mulheres gestantes são epilépticas e precisam usar anticonvulsivantes continuamente já que com a interrupção do tratamento podem surgir crises convulsivas e conseqüente risco fetal por hipóxia intra-uterina 1,2 . Entretanto, drogas antiepilépticas eficientes como o ácido valpróico e a carbamazepina têm apresentado efeito teratogênico em humanos 3,4 .…”

Section: Introductionunclassified

Desenvolvimento pré-embrionário em ratas tratadas com oxcarbazepina nos quatro primeiros dias após a inseminação

Guerra¹,

Oliveira²,

Peters³

2000

Rev. Assoc. Med. Bras.

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. A oxcarbazepina (OXC) é uma nova droga anticonvulsivante, estruturalmente relacionada à carbamazepina, que exibe espectro farmacológico e potência semelhantes à da carbamazepina, porém com menor freqüência de efeitos colaterais [7][8][9][10] . Há relato de um caso de tratamento monoterápico com OXC (300mg/ 3 vezes ao dia), efetuado inadvertidamente desde o terceiro mês de gestação, que resultou em um recém-nascido saudável 11 . Além disso, um estudo retrospectivo de 947 pacientes tratadas com OXC mostrou que em 12 gestações, nove recém-nascidos eram saudáveis 12 , não havendo informações sobre os três casos restantes.São escassos os estudos em animais de laboratório, visando a avaliação do potencial teratogênico da OXC. Há um relato de que seria desprovida de efeitos sobre a fertilidade de ratos e de camundongos; de teratogenicidade e, que nenhum efeito cognitivo indesejável seria evidenciável, quando a administração ocorreu no estágio final da gestação ou no período de lactação 13 . A referência trata de trabalhos do laboratório produtor do medicamento, apresentados em relatórios internos e sobre os quais não foram encontradas publicações na literatura. Outra publicação menciona que não ocorreu diferença significativa no índice de malformações, quando foram comparadas ratas controles e tratadas com 1.100mg de OXC/Kg/dia 14 . Não foram encontrados estudos visando a fase inicial do desenvolvimento embrionário, quando a morte do pré-embrião, pode não ser detectada e, assim, confundida com infertilidade.

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Current Concepts in the Treatment of Rheumatoid Arthritis

Baker

Rabinowitz

1986

The Journal of Clinical Pharma

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The treatment of RA is complex and often frustrating. The pathologic process of RA is composed of acute inflammation, chronic immunologic phenomenon, and chronic connective tissue degradation. It is important to understand not only the pathophysiology of RA but also the mechanism of action of our therapeutic drugs so that treatment can be tailored to affect the important aspects of the process leading to end-organ damage. Despite the many drugs available, therapy is still unsatisfactory. Many drugs work in only certain patients. This could be secondary to variability in the disease state or to difference in drug metabolism. A better understanding of both disease and therapeutic agents may lead to better use of our present agents and development of new, more effective treatment modalities.

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Effects of Drugs and Chemicals on the Fetus and Newborn (First of Two Parts)

Cited by 25 publications

References 84 publications

Chemical‐induced craniofacial anomalies caused by disruption of neural crest cell development in a zebrafish model

Chemical‐induced craniofacial anomalies caused by disruption of neural crest cell development in a zebrafish model

Desenvolvimento pré-embrionário em ratas tratadas com oxcarbazepina nos quatro primeiros dias após a inseminação

Current Concepts in the Treatment of Rheumatoid Arthritis

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