Polycyclic aromatic compounds are ubiquitously distributed pollutants in the aquatic and terrestrial environment containing harmful properties on creatures such as carcinogenicity, teratogenicity and toxicity, but are not so well analyzed yet. In the present study, the embryotoxic and teratogenic effects of selected hydroxylated and methylated PACs on the embryonal development of Danio rerio as an aquatic model organism were analyzed with the Fish Embryo Toxicity Test (FET) and the Tail Length Test (TLT) to obtain information on the toxic and teratogenic impact of the tested PACs on the environment. Two of the five tested PACs, 9-MA and DMBA, showed embryotoxic respectively teratogenic effects on the embryonal development of the zebrafish. The embryotoxicity of 9-MA was indicated in the high mortality rate of the exposed zebrafish embryos, whereas the teratogenic effect of DMBA was revealed in the emergence of sub-lethal malformations during the embryonal development such as a shortened tail length, tail curvatures, tail tip deformity or the formation of edema on the yolk sac and pericard as well as abnormal heartbeat and blood circulation. The high mortality rate of the zebrafish embryos exposed to 9-MA did not increase over the exposure time of 96h, which suggests that the chorion of the zebrafish egg could not protect the embryo at all against the strong embryotoxic effect of 9-MA. The sub-lethal malformations of the zebrafish embryos exposed to DMBA could be induced to the metabolic activation of AhR-agonist DMBA through the AhR-pathway or the accumulation of the neurotransmitter Acetylcholine due to the inhibitory function of DMBA on the ACh-Esterase, which caused a neuromuscular system defect or uncontrolled contractions of the axis musculature. Further research, may focus on the mode of action of PACs such as 9-MA and DMBA and their impact on organisms in order to take reasonable precautions to avoid or to diminish the uptake of PACs from the environment.

No description available.

Locoweed, a well-known teratogenic plant affecting livestock, is prevalent in mountain regions of the Western United States. Two common species (Astragalus lentiginosus and A. wootoni), administered to pregnant rats, induced behavioral deviations in their offspring. Treated mothers consumed less feed and gained less wieght during gestation than controls when gavaged locoweed at the rate of 1 gram whole plant per day on days 7 through 17 of gestation. A. lentiginosus reduced pup weight at birth (13% less than controls) and this weight reduction (as much as 29% less than controls) continued at least four weeks. A. lentiginosus also reduced number of offspring born alive (34.9% less than controls) and number which survived until weaning (86.4% less than controls). No gross malformations were observed in the offspring of loco-treated dams. however, when the pups were subjected to behavioral testing (beginning at 30 days of age), deviations were observed. there was considerable difference among the treatment groups when tested with the activity wheel (P=.0000). Water-intubated controls did not differ from non-fed controls, but the two loco-treated groups differed in opposite directions from controls. A. lentiginosus offspring were more active (26.5%) overall than other groups, and had an abnormal pattern of activity in the day to evening night activity totals. A. wootoni offpsring were less active (25%) than other groups in the activity wheel. Significant differences among groups were also observed in the open-field test. The trend was toward decreased activity (P=.027; 31 and 43% less than controls - A. lentiginosus and A. wootoni respectively) and increased number of fecal boluses (P=.06; 45.5 and 19.3% more than controls - A. lentiginosus and A. wootoni respectively) in the loco-treated offspring. There were no significant differences in avoidance conditioning in a two-way shuttle box among the groups, though the loco offspring made fewer avoidance responses than controls. Alizarin Red-S staining of fetuses revealed no skeletal defects in the pups. Microscopic examination of maternal tissues showed the kidney and liver degenerative changes which are typical of locoweed intoxication: primarily vacuolation of proximal tubular epithelium and of the hepatocytes. Tissues from pups on day of birth also showed mild kidney and liver changes. Older pups had no visible microscopic deviations from normal. The results indicate that the locoweed teratogen produces behavioral deviations in the offspring of rats in the absence of gross malformations.

No description available.

No description available.

Leung, Chun Yin. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2011. / Includes bibliographical references (leaves 155-169). / Abstracts in English and Chinese. / Title Page --- p.i / Acknowledgements --- p.ii / Table of Content --- p.iii / List of Figures --- p.viii / List of Graphs --- p.x / List of Tables x --- p.iv / Abbreviations --- p.xvii / Abstract --- p.xviii / Abstract (Chinese) --- p.xx / Chapter Chapter 1: --- General Introduction / Chapter 1.1 --- Introduction to retinoids --- p.2 / Chapter 1.2 --- Role of endogenous retinoic acid in embryonic development --- p.3 / Chapter 1.3 --- Regulation of retinoic acid in embryonic development --- p.5 / Chapter 1.3.1 --- Retinoic acid synthesis and degradation --- p.5 / Chapter 1.3.2 --- Retinoic acid signaling --- p.8 / Chapter 1.4 --- Effect of excess vitamin AJ RA on embryogenesis --- p.8 / Chapter 1.4.1 --- Examples of human animal studies --- p.9 / Chapter 1.4.2 --- Mechanisms of retinoid teratogenesis --- p.11 / Chapter 1.4.2.1 --- Apoptosis --- p.11 / Chapter 1.4.2.2 --- Altered proliferation --- p.12 / Chapter 1.4.2.3 --- Altered cell migration --- p.12 / Chapter 1.4.2.4 --- Altered differentiation --- p.13 / Chapter 1.4.3 --- Critical period of RA administration caused specific Malformations --- p.14 / Chapter 1.5 --- Effect of vitamin A/ RA deficiency on embryogenesis --- p.15 / Chapter 1.6 --- Excess and deficiency of RA cause similar types of malformations --- p.17 / Chapter 1.6.1 --- Retinoic acid-induced renal malformations mouse model --- p.18 / Chapter 1.7 --- Strategy of thesis --- p.19 / Chapter Chapter 2: --- General Materials and Methods / Chapter 2.1 --- Mouse maintenance and mating methods --- p.23 / Chapter 2.2 --- All-trans retinoic acid preparation and injection --- p.23 / Chapter 2.3 --- Whole mount in situ hybridization --- p.24 / Chapter 2.3.1 --- Riboprobe synthesis --- p.24 / Chapter 2.3.1.1 --- Bacterial culture --- p.24 / Chapter 2.3.1.2 --- DNA plasmids extraction --- p.24 / Chapter 2.3.1.3 --- Linearization of plasmid --- p.25 / Chapter 2.3.1.4 --- Purification of linearized plasmid --- p.26 / Chapter 2.3.1.5 --- In vitro transcription and labeling --- p.26 / Chapter 2.3.2 --- Sample collection --- p.27 / Chapter 2.3.3 --- Hybridization --- p.28 / Chapter 2.3.4 --- Post hybridization wash and antibody development --- p.29 / Chapter 2.3.4.1 --- Embryo powder preparation --- p.30 / Chapter 2.3.4.2 --- Pre-absorption of antibody --- p.30 / Chapter 2.3.5 --- Post-antibody and staining --- p.31 / Chapter 2.4 --- Real-time quantitative reverse transcription -polymerase chain reaction (RT-PCR) --- p.32 / Chapter 2.4.1 --- Sample collection --- p.32 / Chapter 2.4.2 --- RNA extraction --- p.32 / Chapter 2.4.3 --- Reverse transcription into cDNA --- p.33 / Chapter 2.4.4 --- Quantitative real-time PCR --- p.33 / Chapter 2.4.5 --- Preparation of cDNA standards --- p.34 / Chapter 2.5 --- High pressure liquid chromatography (HPLC) --- p.35 / Chapter 2.5.1 --- Chromatographic system --- p.35 / Chapter 2.5.2 --- Standards preparation --- p.35 / Chapter 2.5.3 --- Embryo sample collection and preparation --- p.36 / Chapter 2.5.4 --- HPLC conditions --- p.36 / Chapter 2.5.5 --- Sample recovery --- p.37 / Chapter 2.5.6 --- Bradford assay --- p.38 / Chapter 2.6 --- RA-responsive cell line --- p.38 / Chapter 2.6.1 --- Cell culture --- p.39 / Chapter 2.6.2 --- Seeding and loading sample to 96-well plate --- p.40 / Chapter 2.6.3 --- X-gal staining --- p.41 / Chapter Chapter 3: --- Time and Dose Responses to RA / Chapter 3.1 --- Introduction --- p.43 / Chapter 3.1.1 --- Time response to RA --- p.43 / Chapter 3.1.2 --- Dose response to RA --- p.45 / Chapter 3.1.3 --- Other factors affecting susceptibilities to RA --- p.46 / Chapter 3.2 --- Experimental design --- p.48 / Chapter 3.3 --- Materials and methods --- p.50 / Chapter 3.3.1 --- Time response to RA --- p.50 / Chapter 3.3.2 --- Dose response to RA --- p.50 / Chapter 3.3.3 --- Examination of fetuses --- p.51 / Chapter 3.3.4 --- Statistical analysis --- p.51 / Chapter 3.4 --- Results --- p.53 / Chapter 3.4.1 --- Time response --- p.53 / Chapter 3.4.1.1 --- Time response to RA-induced resorption --- p.53 / Chapter 3.4.1.2 --- Time response to RA-induced renal malformations --- p.54 / Chapter 3.4.1.3 --- Time response to RA-induced changes in growth parameters --- p.57 / Chapter 3.4.1.4 --- Time response to RA-induced non-renal malformations --- p.60 / Chapter 3.4.2 --- Dose response --- p.64 / Chapter 3.4.2.1 --- Dose response to RA-induced resorption --- p.64 / Chapter 3.4.2.2 --- Dose response to RA-induced renal malformations --- p.65 / Chapter 3.4.2.3 --- Dose response to RA-induced changes in growth parameters --- p.68 / Chapter 3.4.2.4 --- Dose response to RA-induced non-renal malformations --- p.71 / Chapter 3.5 --- Discussion --- p.74 / Chapter Chapter 4: --- Effect of Teratogenic Dose of RA on RA Synthesis and Endogenous RA Levels in the Embryo / Chapter 4.1 --- Introduction --- p.79 / Chapter 4.1.1 --- RA synthesis in embryo --- p.79 / Chapter 4.1.2 --- Detection of endogenous RA in embryo --- p.81 / Chapter 4.2 --- Experimental design --- p.83 / Chapter 4.3 --- Materials and methods --- p.84 / Chapter 4.3.1 --- Localization of mRNA transcripts in whole embryo by in situ hybridization --- p.84 / Chapter 4.3.2 --- Vibratome sectioning --- p.85 / Chapter 4.3.2.1 --- Preparation of Gloop --- p.85 / Chapter 4.3.2.2 --- Sample preparation and sectioning --- p.85 / Chapter 4.3.3 --- Quantification of mRNA expression levels in whole embryo and in metanephros by real-time RT-PCR --- p.86 / Chapter 4.3.4 --- Detection of RA levels in whole embryo by HPLC --- p.87 / Chapter 4.3.5 --- Detection of RA levels in metanephros by RA-responsive cell line --- p.87 / Chapter 4.3.6 --- Statistical analysis --- p.88 / Chapter 4.4 --- Results --- p.89 / Chapter 4.4.1 --- Comparison of mRNA expression levels of different iso forms of RA synthesizing enzymes Raldh and RA catabolizing enzymes Cyp26 between embryos of RA-treated and vehicle-treated control mice at various time points after treatment --- p.89 / Chapter 4.4.2 --- Comparison of mRNA expression levels of different iso forms of RA synthesizing enzymes Raldh and RA catabolizing enzymes Cyp26 between metanephroi of embryos of RA-treated and vehicle-treated control mice at various time points after treatment --- p.93 / Chapter 4.4.3 --- Comparison of the in situ hybridization pattern of different iso forms of Raldh between embryos of RA-treated and vehicle-treated control mice at different time points after treatment --- p.95 / Chapter 4.4.3.1 --- In situ hybridization pattern of Raldh 1 --- p.96 / Chapter 4.4.3.2 --- In situ hybridization pattern of Raldh2 --- p.97 / Chapter 4.4.3.3 --- In situ hybridization pattern of Raldh3 --- p.100 / Chapter 4.4.4 --- Comparison of the in situ hybridization pattern of Cyp26al and Cyp26bl between embryos of RA-treated and vehicletreated control mice at different time points after treatment --- p.101 / Chapter 4.4.4.1 --- In situ hybridization pattern of Cyp26al --- p.101 / Chapter 4.4.4.2 --- In situ hybridization pattern of Cyp26bl --- p.102 / Chapter 4.4.5 --- Comparison of RA levels between embryos of RA-treated and vehicle-treated control mice at different time points after treatment --- p.103 / Chapter 4.4.6 --- Comparison of RA levels between metanephroi of embryos of RA-treated and vehicle-treated control mice at different time points after treatment --- p.105 / Chapter 4.5 --- Discussion --- p.106 / Chapter Chapter 5: --- Effect of Supplementation with Low Doses of RA on RA Teratogenesis / Chapter 5.1 --- Introduction --- p.111 / Chapter 5.1.1 --- RA supplementation --- p.111 / Chapter 5.1.2 --- Wilms' tumor suppressor gene Wtl --- p.112 / Chapter 5.1.3 --- Apoptosis --- p.113 / Chapter 5.2 --- Experimental design --- p.115 / Chapter 5.3 --- Materials and methods --- p.117 / Chapter 5.3.1 --- Oral gavage of low dose of RA --- p.117 / Chapter 5.3.2 --- Determination of Wtl expression level by real-time quantitative RT-PCR --- p.117 / Chapter 5.3.3 --- Preparation of paraffin sections and TUNEL staining --- p.118 / Chapter 5.3.3.1 --- Sample collection --- p.118 / Chapter 5.3.3.2 --- "Dehydration, embedding and sectioning" --- p.118 / Chapter 5.3.3.3 --- TUNEL staining --- p.119 / Chapter 5.3.4 --- Statistical analysis --- p.121 / Chapter 5.4 --- Results --- p.122 / Chapter 5.4.1 --- Time response to RA supplementation in rescuing kidney development --- p.122 / Chapter 5.4.2 --- Dose response to RA supplementation in rescuing kidney development --- p.127 / Chapter 5.4.3 --- RA supplementation restored various growth parameters --- p.132 / Chapter 5.4.4 --- RA supplementation rescued non-renal malformations --- p.134 / Chapter 5.4.5 --- Wtl expression in the metanephros after RA supplementation --- p.142 / Chapter 5.4.6 --- Apoptotic cell death in the metanephros after RA supplementation --- p.143 / Chapter 5.5 --- Discussion --- p.145 / Chapter Chapter 6: --- Conclusion and Future Perspectives --- p.150 / References --- p.155 / Figures / Graphs

A percepção de risco teratogênico equivocada pode levar à privação de uso de medicamentos seguros e à relutância ou não adesão ao tratamento farmacológico durante a gestação. Estudos prévios realizados em países desenvolvidos sugerem que a percepção de risco teratogênico ao uso de medicamentos é superestimada por gestantes, não gestantes e profissionais de saúde. Grande parte destes estudos foi realizada em centros de aconselhamento teratogênico e utilizou apenas uma técnica de aferição da percepção de risco (Escalas Visuais Analógicas). Com o objetivo de caracterizar a percepção de risco teratogênico por gestantes e mulheres em idade fértil, conduzimos um estudo que combinou métodos qualitativos e quantitativos de investigação. Participaram da pesquisa usuárias de serviços de saúde da rede básica municipal de Porto Alegre. Em termos qualitativos, foram realizados dois grupos focais com gestantes. Os dados quantitativos resultaram da realização de entrevistas estruturadas com 287 mulheres em idade fértil divididas em dois grupos: gestantes e não gestantes. A percepção de risco de malformações congênitas na população geral e as percepções de risco teratogênico das exposições a paracetamol, metoclopramida, misoprostol e radioterapia na gestação foram aferidas por duas técnicas: Escalas Visuais Analógicas (EVA) e perguntas numéricas. A concordância entre as duas técnicas de aferição foi avaliada pela análise gráfica de Bland-Altman. Não encontramos concordância entre as medidas obtidas por EVA e por pergunta para nenhuma das percepções de risco em estudo. As medianas das percepções de risco teratogênico medidas por EVA foram superiores às obtidas através da pergunta numérica, para todas as variáveis. Para ambas as técnicas de aferição, as medianas das percepções de risco teratogênico ao paracetamol e à metoclopramida foram mais baixas que para o risco de malformações congênitas na população geral. Já as medianas das percepções de risco ao misoprostol e à radioterapia apresentaram os maiores valores. Não foram encontradas diferenças significativas nas percepções de risco entre gestantes e não gestantes. A lógica acionada pelas mulheres na estimação do risco teratogênico é a da classificação dos medicamentos em fortes e fracos. Dentro desta lógica, os medicamentos e as exposições percebidos por elas como fracos não apresentam riscos, enquanto que aqueles percebidos como fortes são vistos como perigosos e devem ser evitados na gestação. Concluímos que o uso de EVA leva à superestimação das percepções de risco teratogênico. Além disso, frente à dificuldade em operar a lógica probabilística na estimação de risco, as mulheres operam uma lógica própria, classificando os medicamentos em fortes ou fracos. / An erroneous perception of teratogenic risk can lead to the non-use of safe medications and reluctance to or abstaining from pharmacological treatment during pregnancy. Previous studies conducted in developed countries suggest that the perception of teratogenic risk in the use of medications is overestimated by pregnant women, non-pregnant women and health professionals. Most of these studies were performed in teratogen counseling centers and only used one technique for measuring risk perception (Visual Analogue Scales). In order to characterize the perception of teratogenic risk by pregnant women and women of childbearing age, we conducted a study that combined qualitative and quantitative research methods. Public health care users from the city of Porto Alegre participated in the research. In qualitative terms, two focus groups were carried out with pregnant women. The quantitative data was derived from structured interviews with 287 women of childbearing age divided into two groups: pregnant and non-pregnant women. The perception of risk of congenital malformations in the general population and the perception of teratogenic risk through exposure to acetaminophen, metoclopramide, misoprostol and radiation therapy during pregnancy were measured via two techniques: Visual Analogue Scales (VAS) and numerical questions. The agreement between the two measurement techniques was evaluated using Bland-Altman graphic analysis. We did not find an agreement between the measurements obtained through VAS and those obtained through questions for any of the risk perceptions in the study. The medians of the perceptions of teratogenic risk measured by VAS were higher than those obtained by numerical questions, for all variables. For both measurement techniques, the medians of the perceptions of teratogenic risk with acetaminophen and metoclopramide were lower than those for the risk of congenital malformations in the general population. However, the medians of the perceptions of risk with misoprostol and radiation therapy presented the highest values. There were no significant differences in risk perceptions among pregnant and non-pregnant women. The logic employed by women in estimating teratogenic risk is the classification of drugs according to strong and weak. According to this logic, the drugs and exposure to them, perceived by these women as weak, do not present risks, while those perceived as strong are seen as hazardous and should be avoided during pregnancy. Our conclusion is that the use of VAS leads to the overestimation of teratogenic risk perceptions. Moreover, given the difficulty to engage in probabilistic logic for estimating risk, women engage in their own logic, classifying medications as strong or weak.

In 1996, the Institute of Medicine made an initial step towards addressing the confusion and controversy regarding the diagnosis of fetal alcohol syndrome (FAS) by proposing a classification scheme and calling for research to evaluate its validity and clinical utility. Previous research evaluated memory, executive functions, and behaviour problems in FAS. Prior to the present study, however, there had not been an empirical evaluation of the existence of a spectrum of diagnostic subgroups or an evaluation of subgroup functioning on neuropsychological components of attention during the pre-teen and adolescent years. Part 1 of this study used categorical data regarding diagnostic domains to determine if an a priori spectrum of four subgroups could be identified. This spectrum included FAS and three fetal alcohol effect (FAE) subgroups, which were defined using teratogenic theory, previous research findings, and logic. The sample consisted of 112 children with a confirmed history of excessive prenatal alcohol exposure. Part 2 evaluated the continuity and comparability of the CNS dysfunction subgroups exhibited by assessing neuropsychological components of attention using models by Mirsky and Conners. The sample consisted of 30 children and subgroups were matched on age, sex, and living situation. Results identified 3 of the 4 potential subgroups. All subgroups exhibited a clinically significant attention deficit. After adjusting for IQ, the FAS and FAE subgroups had comparable levels of functioning on all components of attention with one exception. On the sustain component, the FAE subgroups had more difficulties than the FAS subgroup in maintaining a consistent response-speed in response to changes in the length of time between targets. This study provides empirical and theoretical support for the validity and clinical utility of a spectrum of fetal alcohol subgroups consistent with the IOM's classification. It furthers a theoretical understanding of the dose-response effects of alcohol as a teratogenic agent. It suggests that attention regulation functions are especially vulnerable to the damage caused by prenatal alcohol exposure. The findings emphasize the importance of obtaining a history of prenatal alcohol exposure in individuals presenting with neuropsychological difficulties, and developing treatment programs for pregnant women with an alcohol addiction.

Pre-gestational diabetes increases the risk of congenital malformation in the offspring and both morbidity and mortality in the diabetic mother and her offspring. During pregnancy, high glucose levels act as a teratogen through several cellular and biochemical pathways and increased production of reactive oxygen species (ROS) has a central role in diabetic embryopathy. The aim of this work was to investigate the importance of genetic predisposition for congenital malformations and to study the genes involved in the teratogenic process of diabetic pregnancy. The crossbreeding of two rat strains, with both low and high incidence of diabetes-induced malformations, indicated that strain-specific maternal factors, such as disturbed serum levels of amino acids, triglycerides, and β-hydroxybutyrate, were associated with malformation. In addition, disturbed fetal expression of genes involved in ROS defense and development (Shh, Bmp4, Ret and Gdnf) in mandible and heart, and decreased activity of Gapdh and Aldose Reductase were associated with the teratogenic process, and the trans-generational heredity of the mother determined the type of malformations induced by maternal diabetes. In rat embryos, a diabetic environment in utero changed the expression of genes involved in ROS defense (Nrf2, Gpx1 and Cat), development of mandible and heart (Msx2, Shh, Bmp4, Ret and Gdnf), and neural tube closure and apoptosis (Pax3 and p53). The changes were divergent with tissue-specific alterations of gene expression in developing mandible, heart anlage, and whole embryo. Disruption of the Receptor for Advanced Glycation End products (RAGE) had a protective effect against diabetic embryopathy in mice, and the blockage of RAGE diminished ROS production in the offspring: this supported oxidative stress being a necessary etiological component in diabetic embryopathy. Maternal metabolic state and genetic susceptibility influence fetal outcome in experimental diabetic pregnancy. Disturbed protection against oxidative stress and tissue-specific derangements in the expression of developmental genes play pivotal roles in the teratogenic mechanism, and enhanced levels of Advanced Glycation End products (AGE) and RAGE-induced oxidative stress are involved in diabetic dysmorphogenesis.

A percepção de risco teratogênico equivocada pode levar à privação de uso de medicamentos seguros e à relutância ou não adesão ao tratamento farmacológico durante a gestação. Estudos prévios realizados em países desenvolvidos sugerem que a percepção de risco teratogênico ao uso de medicamentos é superestimada por gestantes, não gestantes e profissionais de saúde. Grande parte destes estudos foi realizada em centros de aconselhamento teratogênico e utilizou apenas uma técnica de aferição da percepção de risco (Escalas Visuais Analógicas). Com o objetivo de caracterizar a percepção de risco teratogênico por gestantes e mulheres em idade fértil, conduzimos um estudo que combinou métodos qualitativos e quantitativos de investigação. Participaram da pesquisa usuárias de serviços de saúde da rede básica municipal de Porto Alegre. Em termos qualitativos, foram realizados dois grupos focais com gestantes. Os dados quantitativos resultaram da realização de entrevistas estruturadas com 287 mulheres em idade fértil divididas em dois grupos: gestantes e não gestantes. A percepção de risco de malformações congênitas na população geral e as percepções de risco teratogênico das exposições a paracetamol, metoclopramida, misoprostol e radioterapia na gestação foram aferidas por duas técnicas: Escalas Visuais Analógicas (EVA) e perguntas numéricas. A concordância entre as duas técnicas de aferição foi avaliada pela análise gráfica de Bland-Altman. Não encontramos concordância entre as medidas obtidas por EVA e por pergunta para nenhuma das percepções de risco em estudo. As medianas das percepções de risco teratogênico medidas por EVA foram superiores às obtidas através da pergunta numérica, para todas as variáveis. Para ambas as técnicas de aferição, as medianas das percepções de risco teratogênico ao paracetamol e à metoclopramida foram mais baixas que para o risco de malformações congênitas na população geral. Já as medianas das percepções de risco ao misoprostol e à radioterapia apresentaram os maiores valores. Não foram encontradas diferenças significativas nas percepções de risco entre gestantes e não gestantes. A lógica acionada pelas mulheres na estimação do risco teratogênico é a da classificação dos medicamentos em fortes e fracos. Dentro desta lógica, os medicamentos e as exposições percebidos por elas como fracos não apresentam riscos, enquanto que aqueles percebidos como fortes são vistos como perigosos e devem ser evitados na gestação. Concluímos que o uso de EVA leva à superestimação das percepções de risco teratogênico. Além disso, frente à dificuldade em operar a lógica probabilística na estimação de risco, as mulheres operam uma lógica própria, classificando os medicamentos em fortes ou fracos. / An erroneous perception of teratogenic risk can lead to the non-use of safe medications and reluctance to or abstaining from pharmacological treatment during pregnancy. Previous studies conducted in developed countries suggest that the perception of teratogenic risk in the use of medications is overestimated by pregnant women, non-pregnant women and health professionals. Most of these studies were performed in teratogen counseling centers and only used one technique for measuring risk perception (Visual Analogue Scales). In order to characterize the perception of teratogenic risk by pregnant women and women of childbearing age, we conducted a study that combined qualitative and quantitative research methods. Public health care users from the city of Porto Alegre participated in the research. In qualitative terms, two focus groups were carried out with pregnant women. The quantitative data was derived from structured interviews with 287 women of childbearing age divided into two groups: pregnant and non-pregnant women. The perception of risk of congenital malformations in the general population and the perception of teratogenic risk through exposure to acetaminophen, metoclopramide, misoprostol and radiation therapy during pregnancy were measured via two techniques: Visual Analogue Scales (VAS) and numerical questions. The agreement between the two measurement techniques was evaluated using Bland-Altman graphic analysis. We did not find an agreement between the measurements obtained through VAS and those obtained through questions for any of the risk perceptions in the study. The medians of the perceptions of teratogenic risk measured by VAS were higher than those obtained by numerical questions, for all variables. For both measurement techniques, the medians of the perceptions of teratogenic risk with acetaminophen and metoclopramide were lower than those for the risk of congenital malformations in the general population. However, the medians of the perceptions of risk with misoprostol and radiation therapy presented the highest values. There were no significant differences in risk perceptions among pregnant and non-pregnant women. The logic employed by women in estimating teratogenic risk is the classification of drugs according to strong and weak. According to this logic, the drugs and exposure to them, perceived by these women as weak, do not present risks, while those perceived as strong are seen as hazardous and should be avoided during pregnancy. Our conclusion is that the use of VAS leads to the overestimation of teratogenic risk perceptions. Moreover, given the difficulty to engage in probabilistic logic for estimating risk, women engage in their own logic, classifying medications as strong or weak.