Toxicity of cadmium to rat osteosarcoma cells (ROS 17/2.8): protective effect of 1 alpha,25-dihydroxyvitamin D3.

Toxicity of cadmium to rat osteosarcoma cells (ROS 17/2.8): protective effect of 1 alpha,25-dihydroxyvitamin D3.
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镉对大鼠骨肉瘤细胞的毒性(ROS 17/2.8):1α,25-二羟基维生素 D3 的保护作用。

DOI:
10.1016/0041-008x(90)90267-x
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发表时间:
1990
影响因子:
3.8
通讯作者:
Swanson,SA
Swanson,SA
中科院分区:
医学3区
文献类型:
--
作者:
Angle,CR;Thomas,DJ;Swanson,SA

文献摘要

被引文献

相似文献

维生素D摄入不足是慢性镉暴露引起临床和实验骨病的重要辅助因素。用等摩尔浓度的氯化镉和1α,25-(OH)2维生素D3的无血清培养基培养大鼠成骨肉瘤细胞(ROS 172.8),研究其相互作用。在培养液中单独添加镉后,10 pm时骨钙素分泌和细胞碱性磷酸酶活性均受到抑制,500 nm时DNA合成和脯氨酸并入胶原均受到抑制。在等摩尔镉和1α,25-(OH)2维生素D3存在的情况下,这四种反应与单独1α,25-(OH)2维生素D3的抑制浓度相似,直至500 mm镉的抑制浓度。10 nm的1α,25-(OH)2维生素d3和1 μm的镉都不能诱导细胞中金属硫蛋白的合成,这表明d3的保护作用与在ROS 172.8细胞中诱导金属硫蛋白样蛋白无关。在实验和临床镉诱导骨毒性研究中,无论D3存在与否,镉对成骨细胞功能的抑制浓度均低于骨中镉的全器官浓度。ROS 172.8细胞对镉的极端敏感性可能与缺乏金属硫蛋白合成有关。
Inadequate vitamin D intake is an important cofactor in clinical and experimental bone disease induced by chronic cadmium exposure. The interaction was investigated by culture of rat osteoblastic osteosarcoma cells (ROS 17 2.8 ) in a serum-free medium with equimolar concentrations of cadmium chloride and 1α,25-(OH)2vitamin D3. After addition of cadmium alone to culture medium, the unstimulated secretion of osteocalcin and cellular alkaline phosphatase activity were inhibited at 10 pm, and of DNA synthesis and proline incorporation into collagen at 500 nm. In the presence of equimolar amounts of cadmium and 1α,25-(OH)2vitamin D3, all four responses paralleled those of 1α,25-(OH)2vitamin D3alone up to the inhibitory concentration of 500 mm cadmium. Neither 10 nm 1α,25-(OH)2vitamin D3nor 1 μm cadmium induced synthesis of metallothionein in these cells indicating that the protective effect of D3was not related to the induction of a metallothionein-like protein in ROS 17 2.8 cells. In the presence or absence of D3, cadmium inhibited osteoblastic function at concentrations below the whole-organ concentration of cadmium in bone as reported in experimental and clinical cadmium-induced osteotoxicity. The extreme sensitivity of ROS 17 2.8 cells to cadmium may relate to the absence of metallothionein synthesis.