Aleo J J, Padh H, Subramoniam A
J Periodontol. 1984 Nov;55(11):642-7. doi: 10.1902/jop.1984.55.11.642.
The uptake of Ca2+ by endotoxin-challenged 3T6 fibroblasts, in vitro, was studied. In recent years, the role of calcium in cell injury ultimately leading to cell death has attracted a fair amount of interest. The purpose of the study was to determine whether the direct toxic action of endotoxin is related to a disturbance in Ca2+ homeostasis. Increased calcium uptake in endotoxin-challenged cells was found to be directly related to the bacterial source and method of extraction of endotoxin, the cell density of the culture and the pH of the medium. The effect of endotoxin on calcium uptake was completely reversed by polymyxin B which is known to neutralize the endotoxicity of lipopolysaccharides. These results imply that the increased calcium uptake may be one of the mechanisms by which endotoxin causes direct tissue damage. The potential significance of these data to periodontal disease is discussed.
研究了内毒素刺激的3T6成纤维细胞在体外对Ca2+的摄取。近年来，钙在最终导致细胞死亡的细胞损伤中的作用引起了相当多的关注。该研究的目的是确定内毒素的直接毒性作用是否与Ca2+稳态紊乱有关。发现内毒素刺激的细胞中钙摄取增加与内毒素的细菌来源和提取方法、培养物的细胞密度以及培养基的pH值直接相关。多粘菌素B可完全逆转内毒素对钙摄取的影响，已知多粘菌素B可中和脂多糖的内毒素毒性。这些结果表明，钙摄取增加可能是内毒素导致直接组织损伤的机制之一。讨论了这些数据对牙周疾病的潜在意义。
