Zhonghua yu fang yi xue za zhi [Chinese journal of preventive medicine] · 1999
[Effects of methylmercury on embryonic cell behavior and expression of related gene].
Аннотация на английскомСтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Li Y, Li S, Zhao R, Chen X, Pan Q, Sun M, Li Z
Аннотация
OBJECTIVE: To explore the mechanism of embryonic developmental toxicity of methyl mercury at cellular and gene levels.
METHODS: Effects of methylmercury on embryonic cell behavior and gene expression in rats were observed with in vitro (0, 0.05, 0.10, 0.20, 0.40, 0.80 and 1.60 mg/L of methylmercury) and in vivo (0, 0.2, 0.4, 0.8, 1.6 and 3.2 mg/L of methylmercury) rat models, in situ hybridization and TdT-induced dUTP nick end labeling techniques.
RESULTS: Methylmercury could pass through yolk-sac placenta quickly, and inhibit placenta development and blood vessel differentiation there at higher concentration. There was a dose-response relationship between concentration of methylmercury and its embryonic developmental toxicity. Its developmental toxicity mainly characterized as patent neural tube and anomalous flexion. Methylmercury could induce excessive apoptosis of embryonic cells, inhibit apparently the synthesis of cellular DNA and RNA and damage its cellular ultrastructure. It also could induce significantly the expression of heat shock protein 70 mRNA and inhibit the expression of fibronectin and p16 mRNA. There was relationship between heat shock protein 70 mRNA, Ca(2+), apoptosis and teratogenesis.
CONCLUSION: Disturbance of embryonic cell behavior and related gene expression played important roles in developmental toxicity caused by methylmercury.
METHODS: Effects of methylmercury on embryonic cell behavior and gene expression in rats were observed with in vitro (0, 0.05, 0.10, 0.20, 0.40, 0.80 and 1.60 mg/L of methylmercury) and in vivo (0, 0.2, 0.4, 0.8, 1.6 and 3.2 mg/L of methylmercury) rat models, in situ hybridization and TdT-induced dUTP nick end labeling techniques.
RESULTS: Methylmercury could pass through yolk-sac placenta quickly, and inhibit placenta development and blood vessel differentiation there at higher concentration. There was a dose-response relationship between concentration of methylmercury and its embryonic developmental toxicity. Its developmental toxicity mainly characterized as patent neural tube and anomalous flexion. Methylmercury could induce excessive apoptosis of embryonic cells, inhibit apparently the synthesis of cellular DNA and RNA and damage its cellular ultrastructure. It also could induce significantly the expression of heat shock protein 70 mRNA and inhibit the expression of fibronectin and p16 mRNA. There was relationship between heat shock protein 70 mRNA, Ca(2+), apoptosis and teratogenesis.
CONCLUSION: Disturbance of embryonic cell behavior and related gene expression played important roles in developmental toxicity caused by methylmercury.
Предметные рубрики MeSH
AnimalsCulture TechniquesCyclin-Dependent Kinase Inhibitor p16Dose-Response Relationship, DrugEmbryo, MammalianEmbryonic and Fetal DevelopmentFemaleFibronectinsGene ExpressionHSP70 Heat-Shock ProteinsMaleMethylmercury CompoundsNeural Tube DefectsPregnancyPrenatal Exposure Delayed EffectsRNA, MessengerRatsRats, Sprague-Dawley