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1.
Scanning ; 2017: 9650420, 2017.
Article in English | MEDLINE | ID: mdl-29109829

ABSTRACT

The aim of this study was to evaluate in fibroblast cultures the direct cytotoxic effects of etch-and-rinse, self-etch, and universal adhesive systems. The sterile glass cover slips (n = 3) were then immersed in culture medium to obtain the eluates for the experimental groups: (1) Adper™ Single Bond 2; (2) Ambar; (3) Adper™ Scotchbond™ Multi-Purpose; (4) Scotchbond™ Universal; (5) Ambar Universal; and (6) OptiBond All-In-One. As a negative control, sterile glass cover slips were immersed in culture medium only. After 24 h, the eluate obtained was applied on fibroblast culture. Cell viability and cell morphology were evaluated by MTT assay and SEM, respectively. Data were analyzed by Kruskal-Wallis and Mann-Whitney tests (α = 0.05). All adhesive systems except universal reduced cell viability in 3T3 cells to between 26.04% and 56.57%, and Scotchbond Universal and Ambar Universal reduced cell viability to 2.13% and 3.57%, respectively, when compared to the negative control. Cytoplasmic membrane shrinkage and cell-free areas with residual membrane fragments from dead cells were observed. In conclusion, improvements in universal adhesive system formulations and their mechanisms of action are not accompanied by increased toxicity compared with those in other systems, warranting commitment to the use of these dentin-pulp complexes.


Subject(s)
Cell Survival/drug effects , Dental Cements/toxicity , Fibroblasts/drug effects , Fibroblasts/physiology , 3T3 Cells , Animals , Cell Membrane/pathology , Cell Shape/drug effects , Fibroblasts/cytology , Formazans/analysis , Mice , Microscopy, Electron, Scanning , Tetrazolium Salts/analysis
2.
J. bras. patol. med. lab ; 45(6): 471-480, dez. 2009. tab, ilus
Article in English | LILACS | ID: lil-552204

ABSTRACT

INTRODUCTION AND OBJECTIVES: To investigate the effects of ethanol, diabetes mellitus and the combination of both on mouse fetuses. METHODS: We used 24 female Swiss mice, dividing them into four groups of 6 each: control (C), ethanol (E), diabetes (D) (blood glucose > 200 mg/dL) and diabetes + ethanol (DE). Diabetes was induced by alloxan (40 mg/kg) on day 7 of pregnancy. Groups E and DE received 4 g/kg of 25 percent v/v ethanol intraperitoneally, whereas groups C and D received saline. On day 18, all fetuses were harvested. RESULTS: In group DE the following anomalies were found: exencephaly, situs inversus totalis, situs inversus partialis, eyelid skin tag and one animal from group E had pulmonary artery hypoplasia. Ethanol administration partially reverted diabetes-fetal resorption caused by diabetes, yet it induced late fetal death. Both diabetes and ethanol reduced placental diameter and increased its weight. Ethanol had more effect on fetal length in males than in females, however, such bias was not found for diabetes. Ethanol prevented diabetes-induced tail shortening in both genders. CONCLUSIONS: These results show that, although ethanol might improve energy metabolism in early gestation, it causes cell damage that leads to cardiovascular, limb and neural tube defects, late fetal death and reduced placental size.


INTRODUÇÃO E OBJETIVOS: Investigar o efeito do etanol, do diabetes mellitus (DM) e da associação de ambos sobre os fetos de camundongo. MÉTODOS: Foram utilizadas 24 fêmeas de camundongos Swiss divididas em quatro grupos de seis animais cada: controle (C); etanol (E); diabetes (D) (glicemia > 200 mg/dl), e diabetes + etanol (DE). O diabetes foi induzido pela aloxana (40 mg/kg) no dia 7 da gestação. Os animais dos grupos E e DE receberam 4 g/kg de solução a 25 por cento v/v de etanol intraperitoneal (IP), enquanto os animais dos grupos C e D receberam salina. No dia 18, todos os fetos foram coletados. RESULTADOS: Foram encontradas as seguintes anomalias no grupo DE: exencefalia, situs inversus totalis, situs inversus partialis e apêndice cutâneo palpebral. Um animal do grupo E apresentou hipoplasia da artéria pulmonar. A administração de etanol reverteu parcialmente a reabsorção fetal induzida pelo diabetes, porém aumentou a morte fetal tardia. Ambos, diabetes e etanol, reduziram o diâmetro placentário e aumentaram o seu peso. O etanol teve mais efeito no comprimento de fetos machos, contudo isso não ocorreu com o diabetes. O etanol preveniu a redução da cauda induzida pelo diabetes em ambos os sexos. CONCLUSÃO: Esses resultados indicam que, embora o etanol possa melhorar o metabolismo energético no início da gestação, ele causa lesão celular que leva a defeitos cardiovasculares, dos membros e do tubo neural, além de morte fetal tardia e redução do tamanho da placenta.


Subject(s)
Animals , Female , Pregnancy , Mice , Diabetes, Gestational/chemically induced , Diabetes Mellitus, Experimental/chemically induced , Diabetes Mellitus/chemically induced , Neural Tube/abnormalities , Abnormalities, Drug-Induced , Alloxan/administration & dosage , Alloxan/toxicity , Ethanol/toxicity
3.
J. bras. patol. med. lab ; 45(1): 25-30, fev. 2009. graf, tab
Article in Portuguese | LILACS | ID: lil-518759

ABSTRACT

INTRODUÇÃO: A ingestão adequada de folato é essencial durante a embriogênese, e sua deficiência está associada à ocorrência de defeitos no fechamento do tubo neural. OBJETIVO: Determinar se a sacarose é um bom veículo para a suplementação de folato em camundongos. MATERIAL E MÉTODOS: Quarenta camundongos Swiss fêmeas foram divididos nos grupos: C: ração comercial + água ad libitum; DS: ração balanceada isenta de folato + folato adicionado à sacarose diluída na água por 14 dias; D/DS: ração balanceada isenta de folato + água com sacarose sem folato por 14 dias seguida de ração balanceada isenta de folato + folato adicionado à sacarose diluída na água por mais 14 dias; D: ração balanceada isenta de folato + água com sacarose sem folato por 14 dias. Os animais de todos os grupos experimentais receberam ração balanceada isenta de folato + folato adicionado à sacarose diluída na água durante os três dias do acasalamento e nos 15 dias restantes até o sacrifício. RESULTADOS: Os animais dos grupos D e D/DS apresentaram alopecia, palidez ocular e adinamia enquanto consumiam água com sacarose sem folato, sinais que foram revertidos quando receberam folato adicionado à sacarose diluída na água. Não houve diferença entre os grupos em relação a prenhez, implantes, fetos vivos, reabsorção, morte fetal tardia, nível sérico de folato e contagem de hemácias ao final do experimento, não tendo sido observadas anomalias congênitas em nenhum dos grupos. CONCLUSÃO: A sacarose é um meio adequado para a suplementação de folato na dieta.


Adequate folate intake is essential during embryogenesis and its deficiency is associated with neural tube defects. OBJECTIVE: To investigate if saccharose is a good vehicle for the supplementation of folate in mice. MATERIAL AND METHODS: 40 Swiss female mice were allocated into the following groups: C (commercial mouse food + ad libitum water); DS (folate-free balanced diet + saccharose with folate diluted in water for 14 days); D/DS (folate-free balanced diet + folate-free saccharose diluted in water for 14 days, followed by folate-free balanced diet + saccharose with folate diluted in water for 14 days); D (folate-free balanced diet + folate-free saccharose diluted in water for 14 days). Mice from all experimental groups received folate-free balanced diet + saccharose with folate diluted in water during their three-day mating period and thereafter 15 days until animals were put down. RESULTS: Mice from groups D and D/DS showed alopecia, pale eyes and adynamia while on folate-free saccharose water regimen. These symptoms disappeared after the introduction of saccharose with folate diluted in water. No statistical difference was noted among groups as to pregnancy, number of implants, live fetuses, reabsorption, late fetal death, serum folate levels and red blood cells count and no congenital abnormalities were identified in any groups by the end of the experiment. CONCLUSION: Saccharose is a suitable vehicle for the dietary supplementation of folate.


Subject(s)
Animals , Female , Pregnancy , Mice , Folic Acid/metabolism , Dietary Supplements , Folic Acid Deficiency/embryology , Food, Fortified , Sucrose/metabolism , Folic Acid/administration & dosage , Folic Acid/analysis , Folic Acid/blood , Neural Tube Defects/prevention & control , Folic Acid Deficiency/chemically induced , Models, Animal , Sucrose/administration & dosage
4.
Pathology ; 39(5): 495-503, 2007 Oct.
Article in English | MEDLINE | ID: mdl-17886100

ABSTRACT

INTRODUCTION: Ethanol is teratogenic, interferes with folic acid and is extensively used by young women. Our objective was to determine the effects of ethanol and/or folate deficiency on mouse fetuses. METHOD: In Experiment 1, pregnant mice receiving a commercial diet were divided into three groups: control (C), low ethanol dose (LE, 0.4 g/kg), and high ethanol dose (HE, 4.0 g/kg). In Experiment 2, pregnant mice receiving a folate-free diet (FFD) were divided into three groups: folate deficiency (FD), folate deficiency plus a low ethanol dose (FDLE), and folate deficiency plus a high ethanol dose (FDHE). Groups C and FD received saline and the remaining groups received ethanol administered i.p. from the 7th to the 9th gestational day (GD) and were sacrificed on the 18th GD. RESULTS: In Experiment 1, Group HE presented congenital anomalies, late fetal death (LFD), lower fetal length and weight and placental weight and diameter than Groups C and LE. In Experiment 2, there was a smaller number of live fetuses, a larger number of reabsorptions and LFD, a smaller length and lower fetal weight, placental weight and diameter in Groups FDLE and FDHE than in Group FD. CONCLUSION: In animals receiving a commercial diet, a high ethanol dose is deleterious to the pregnancy, inducing congenital anomalies, intrauterine growth restriction, reduction of the placenta and increased LFD, events that did not occur with the low dose. However, with a folate free diet, a low ethanol dose is as deleterious as a high dose.


Subject(s)
Central Nervous System Depressants/toxicity , Ethanol/toxicity , Fetal Growth Retardation/chemically induced , Fetus/drug effects , Folic Acid Deficiency/physiopathology , Prenatal Exposure Delayed Effects/physiopathology , Animals , Female , Mice , Pregnancy
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