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对食用缺钙饮食的大鼠和猴子体内镁、钙和铝代谢的评估。

Evaluation of magnesium, calcium and aluminum metabolism in rats and monkeys maintained on calcium-deficient diets.

作者信息

Yasui M, Yase Y, Ota K, Garruto R M

机构信息

Division of Neurological Diseases, Wakayama Medical College, Japan.

出版信息

Neurotoxicology. 1991 Fall;12(3):603-14.

PMID:1745443
Abstract

The epidemiology of amyotrophic lateral sclerosis (ALS) in the Western Pacific indicates that low concentrations of calcium (Ca) and magnesium (Mg) and high levels of aluminum (Al) in soil and water in these foci are etiologically important. To determine the biochemical derangements and metal deposition induced by chronic dietary deficiencies of Ca, we maintained experimental animals on several regimens. Male Wistar rats, weighing 100g, were fed either a standard diet, low Ca diet, low Ca-Mg diet, or low Ca-Mg diet with high Al for 90 days. Ca, Mg and Al content was determined in central nervous system (CNS) tissues and bone using inductively coupled plasma emission spectrometry (ICP). In separate studies, five male Japanese macaques (Macaca fuscata), weighing 3.5 to 5 kg, were fed alternately with diets, normal in Ca, low in Ca, low in Mg, low in Ca-Mg, or low in Ca-Mg with added Al for four-week periods. Serum Ca, Mg, Al, parathyroid hormone (PTH), bone Gla-protein (BGP) and alkaline phosphatase (ALP) were measured after feeding each dietary regimen. Ca and Mg levels in lumbar vertebrae and femur were significantly reduced and bone Al levels were significantly increased in rats fed diets deficient in Ca alone or diets low in Ca-Mg with or without added Al. Al content in bones was also higher in rats fed the Ca deficient diets. In monkeys fed the low Ca-Mg diet with added Al, reduced levels of serum Ca and Mg, serum PTH, BGP, and ALP were apparent. Our data support the conjecture that deranged bone mineralization induced by chronic dietary deficiency of Ca accelerates mobilization of Ca and Mg from bone and deposition in brain.

摘要

西太平洋地区肌萎缩侧索硬化症(ALS)的流行病学研究表明,这些发病地区土壤和水中钙(Ca)和镁(Mg)浓度低以及铝(Al)含量高具有重要病因学意义。为了确定慢性饮食缺钙所致的生化紊乱和金属沉积,我们用几种饮食方案喂养实验动物。将体重100克的雄性Wistar大鼠分别喂以标准饮食、低钙饮食、低钙 - 镁饮食或添加高铝的低钙 - 镁饮食,持续90天。使用电感耦合等离子体发射光谱法(ICP)测定中枢神经系统(CNS)组织和骨骼中的钙、镁和铝含量。在单独的研究中,将5只体重3.5至5千克的雄性日本猕猴(Macaca fuscata),交替喂以钙正常、低钙、低镁、低钙 - 镁或添加铝的低钙 - 镁饮食,为期四周。在每种饮食方案喂养后,测定血清钙、镁、铝、甲状旁腺激素(PTH)、骨钙素(BGP)和碱性磷酸酶(ALP)。单独喂食缺钙饮食或含或不含添加铝的低钙 - 镁饮食的大鼠,腰椎和股骨中的钙和镁水平显著降低,骨铝水平显著升高。喂食缺钙饮食的大鼠骨骼中的铝含量也更高。在喂食添加铝的低钙 - 镁饮食的猕猴中,血清钙和镁、血清PTH、BGP和ALP水平明显降低。我们的数据支持这样的推测,即慢性饮食缺钙引起的骨矿化紊乱会加速钙和镁从骨骼中动员并沉积在大脑中。

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