缺乏膳食硅对铝诱导的小鼠母体和发育毒性的保护作用。

M Bellés, M L Albina, D J Sánchez, J L Domingo
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引用次数: 16

摘要

近年来,研究表明,口服铝(Al)暴露可导致大鼠和小鼠生长迟缓、骨化延迟和胎儿畸形发生率增加。另一方面,也有人认为硅可能在限制口服铝吸收方面具有保护作用。本研究的目的是评估膳食硅是否可以预防铝引起的小鼠母体和发育毒性。在妊娠第6 ~ 15天,给3组妊娠动物灌胃非水合硝酸铝(398 mg/kg/d),并在妊娠第7 ~ 18天给3组妊娠动物灌胃浓度分别为0、118和236 mg/l的饮用水硅。另外三组孕鼠分别给予270.6 mg/kg硝酸钠(灌胃)和118和236 mg/l饮用水中的硅。虽然以236毫克/升的浓度施用硅可显著降低铝致死亡、流产和早产的百分比,但118毫克/升和236毫克/升的硅均未显著改善铝致胎儿毒性。在目前的实验条件下,饲粮硅对铝诱导的发育毒性没有有效的保护作用。
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Lack of protective effects of dietary silicon on aluminium-induced maternal and developmental toxicity in mice.

In recent years, it has been demonstrated that oral aluminium (Al) exposure can produce growth retardation, delayed ossification and an increased incidence of foetal abnormalities in rats and mice. On the other hand, it has been also suggested that silicon may have a protective effect in limiting oral Al absorption. The aim of the present study was to assess whether dietary silicon could prevent against Al-induced maternal and developmental toxicity in mice. On gestation days 6-15, Al nitrate nonahydrate (398 mg/kg/day) was given by gavage to three groups of pregnant animals, which also received silicon in drinking water at concentrations of 0, 118 and 236 mg/l on days 7-18 of gestation. Three additional groups of pregnant mice received respectively: 270.6 mg/kg of sodium nitrate (gavage), and silicon in drinking water at 118 and 236 mg/l. Although silicon administration at 236 mg/l significantly reduced the percentage of Al-induced deaths, abortions and early deliveries, neither 118 nor 236 mg/l of silicon produced significant ameliorations on Al-induced foetotoxicity. Under the current experimental conditions dietary silicon was not effective in protecting against Al-induced developmental toxicity.

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