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Lack of Protective Effects of Dietary Silicon on Aluminium‐Induced Maternal and Developmental Toxicity in Mice
Author(s) -
Bellés Montserrat,
Albina M. Luisa,
Sánchez Domènec J.,
Domingo Jose L.
Publication year - 1999
Publication title -
pharmacology & toxicology
Language(s) - English
Resource type - Journals
eISSN - 1600-0773
pISSN - 0901-9928
DOI - 10.1111/j.1600-0773.1999.tb01055.x
Subject(s) - toxicity , developmental toxicity , gestation , medicine , silicon , ossification , pregnancy , endocrinology , toxicology , surgery , biology , metallurgy , materials science , genetics
In recent years, it has been demonstrated that oral aluminium (A1) 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 A1 absorption. The aim of the present study was to assess whether dietary silicon could prevent against A1‐induced maternal and developmental toxicity in mice. On gestation days 6–15. A1 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 adiministration at 236 mg/l significantly reduced the percentage of A1‐induced deaths, abortions and early deliveries, neither 118 nor 236 mg/l of silicon produced significant ameliorations on A1‐induced foetotoxicity. Under the current experimental conditions dietary silicon was not effective in protecting against A1‐induced developmental toxicity.

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