结缔组织对某些重金属的反应。3银和抗坏血酸的膳食补充剂。组织学和超微结构。

G Ellender, K N Ham
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引用次数: 0

摘要

将载银离子交换树脂珠植入大鼠耳廓疏松结缔组织,产生局部反应。最初病变包括局部坏死和组织破坏,主要是小圆形细胞浸润。随后的组织被拖延和混乱。成纤维细胞发育粗内质网的大池。基质中含有大小不一的胶原原纤维,取向不佳,基质呈浓缩颗粒状。在成纤维细胞和巨噬细胞细胞质的膜结合液泡中发现了扭曲的胶原原纤维。银色病变的异常表明胶原蛋白生物合成紊乱。银干扰结缔组织基质成分的生物合成和组装。在大量补充抗坏血酸的饮食中,大鼠对银珠的反应在时间尺度、组织反应和组织组织方面接近于对照组(钠负载珠)。形成的胶原基质比正常饮食的大鼠更有组织,密度更大。然而,修复组织保留了一些银毒性遗留的形态学特征,特别是修复延迟和成纤维细胞和巨噬细胞内致密的细胞内原纤维。过量的抗坏血酸部分地改善了银的作用,可能是通过补偿由释放的银引起的抗坏血酸的分解代谢。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Connective tissue responses to some heavy metals. III. Silver and dietary supplements of ascorbic acid. Histology and ultrastructure.

Silver-loaded ion exchange resin beads implanted into loose connective tissue of the rat pinna produced a local reaction. Initially the lesion comprised local necrosis and tissue disruption with predominantly small round cell infiltration. The subsequent organization was delayed and disordered. Fibroblasts developed grossly dilated cisternae of the rough endoplasmic reticulum. The matrix contained poorly orientated collagen fibrils of varying size and ground substance appeared condensed and granular. Distorted collagen fibrils were identified within membrane-bound vacuoles in the cytoplasm of both fibroblasts and macrophages. Abnormalities of the silver lesion were indicative of disordered collagen biosynthesis. Silver interfered with the biosynthesis and assembly of matrix components of the connective tissue. The reaction to silver beads in rats maintained on a diet heavily supplemented with ascorbic acid approached that of the control (sodium-loaded bead) with respect to the time scale, tissue reaction and tissue organization. The collagen matrix which formed was more organized and of greater density than that in the rat maintained on a normal diet. However, the repair tissue retained some of the morphological features of the legacy of silver toxicity, in particular delayed repair and dense intracellular fibrils within fibroblasts and macrophages. The excess of ascorbic acid partially ameliorated the effect of silver, possibly by compensating catabolysis of ascorbic acid caused by the presence of the released silver.

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