Rungby J
Department of Neurobiology, University of Aarhus.
Dan Med Bull. 1990 Oct;37(5):442-9.
Exposure of foetal and adult rats to silver results in a long-lasting deposition of the metal in many structures of the nervous system. A brief anatomical description of the localization of silver deposits as they are visualized by autometallography is provided. The consequences of silver in the nervous system were evaluated by volumetric measurements on developing rat hippocampi which showed that silver induced a decrease in the total volume of hippocampal pyramidal cells. The toxicity of silver at the cellular level was studied in a test-system of cultured macrophages. High doses of silver caused coagulation necrosis, whereas lower concentrations resulted in a cytotoxic and possibly a cytostatic effect without affecting cell structure. The processing of silver which resulted in lysosomal accumulations was affected by the metal itself in a dose-dependent fashion (autointerference). Other basic macrophage functions (protein-production, phagocytosis, migration) were not affected by silver at concentrations which did not cause acute cell death. Biochemically, silver causes an increase in lipid peroxidation, which was evident only in liver tissue. Coagulation necrosis and, to some extent, long-term effects on cell viability could be reversed by inorganic selenium, which was tested as a detoxicant. On the other hand, pre-exposure of animals to selenium greatly enhanced the silver-induced lipid peroxidation. Furthermore, the co-exposure to silver and nickel resulted in a synergistically increased lipid peroxidation.
将胎儿和成年大鼠暴露于银会导致该金属在神经系统的许多结构中长期沉积。本文提供了通过自动金相显微镜观察到的银沉积物定位的简要解剖学描述。通过对发育中的大鼠海马体进行体积测量来评估银在神经系统中的影响，结果表明银会导致海马锥体细胞总体积减少。在培养巨噬细胞的测试系统中研究了银在细胞水平的毒性。高剂量的银会导致凝固性坏死，而较低浓度则会产生细胞毒性作用，甚至可能是细胞生长抑制作用，且不影响细胞结构。导致溶酶体积累的银处理过程受到金属本身剂量依赖性方式的影响（自干扰）。在不会导致急性细胞死亡的浓度下，银不会影响巨噬细胞的其他基本功能（蛋白质产生、吞噬作用、迁移）。从生化角度来看，银会导致脂质过氧化增加，这仅在肝脏组织中明显。作为解毒剂进行测试的无机硒可以逆转凝固性坏死以及在一定程度上对细胞活力的长期影响。另一方面，动物预先暴露于硒会大大增强银诱导的脂质过氧化。此外，银和镍共同暴露会导致脂质过氧化协同增加。
