RESUMEN
OBJECTIVE: Study the cytotoxicity of toluene and its mechanism, the hippocampus neurons were primarily cultured and were exposed to toluene in vitro. METHODS: The neurons from newborn SD rat's hippocampus were primarily cultured for two weeks, then administered with toluene (3, 6, 9 mmol/L), with blank control group and excipient group being also set up. 24 hours later, Morphology and viability of the cells, the LDH activity, [Ca2+]i, and cell apoptosis were examined. RESULTS: Protuberances of neurons of the toluene-exposed groups were damaged; the bodies of the neurons became round and swollen; the number of the cells decreased; the LDH activity of neurons of high-dose group increased significantly compared with control group (P < 0.05). [Ca2+]i of toluene-exposed groups also increased significantly compared with control group(P < 0.05) in a dose-dependent manner; after diltizem as antagonist of calcium tunnel was added, no increase of [Ca2+]i was found; and evident apoptosis of the exposed cells were also found. CONCLUSION: Toluene was toxic to the neurons after being administered in vitro, which might be ascribed to higher lipid solubility of toluene and it's ability to increase calcium influx, the latter facilitating apoptosis.
Asunto(s)
Apoptosis/efectos de los fármacos , Hipocampo/citología , Tolueno/toxicidad , Animales , Animales Recién Nacidos , Calcio/metabolismo , Células Cultivadas , Neuronas/citología , Ratas , Ratas Sprague-DawleyRESUMEN
OBJECTIVE: To explore the molecular mechanism of cleft palate induced by chemicals. METHODS: Retinoic acid was used as a known teratogen to induce cleft palate in ICR mice and a suppression subtractive hybridization (SSH) technique was applied to identify differentially expressed genes that related to cleft palate of ICR mice. RESULTS: 14 reverse differently and 9 forward differentially expressed clones were obtained. Some clones were selected to be sequenced and aligned to GenBank. CONCLUSION: In this study, suppressed Gpc3 and Insulin-Induced protein 1 could affect growth of palate shelves and resulted in cleft palate by reducing the size of the palate shelves. Down-regulation of Ptprs interfered with a cell signal pathway and down-regulation of Tn C inhibited the cell de-adhesion and expression of Egfr, then suppressed Egfr prevented the normal expression of MMPs that influenced the medial edge epithelium disruption and caused cleft palate. Tn C could bind to Ptprs and Gpcs, and HSPGs were ligands for Ptrps. Up-regulate of Rps25 might play a role in cleft palate by excessively apoptosis.
Asunto(s)
Fisura del Paladar/inducido químicamente , Fisura del Paladar/genética , Tretinoina/toxicidad , Animales , Apoptosis , Fisura del Paladar/patología , Regulación hacia Abajo , Femenino , Perfilación de la Expresión Génica , Regulación del Desarrollo de la Expresión Génica , Glipicanos , Proteoglicanos de Heparán Sulfato/genética , Masculino , Proteínas de la Membrana/genética , Ratones , Ratones Endogámicos ICR , Hibridación de Ácido Nucleico , Tenascina/genética , Regulación hacia ArribaRESUMEN
The estrogenic activity of 5 polycyclic aromatic hydrocarbons(PAHs) of rat uterine wet weight bioassy and estrogen receptor binding bioassy are determined. The results show that penzo(a)pyrene, 7,12-dimethyl benz(a)anthracene and pentacene could statistically increase uterine wet weight of immature female rats(P < 0.01 or P < 0.05) while benz(a)anthracene and chrysene can not significantly increase uterine wet weight(P > 0.05). Penzo(a)pyrene, 7,12-dimethyl benz(a)anthracene and pentacene effectively inhibit the specific 3H-estradial binding to rat uterine estrogen receptor(P < 0.01). Whereas benz(a)anthracene and chrysene can not inhibit the specific 3H-estradial binding to rat uterine estrogen receptor(P > 0.05). The results from this study indicate that penzo(a)pyrene, 7,12-dimethyl benz(a) anthracene and pentacene have significant estrogenic activity.
