• 1 January 1985
    • journal article
    • research article
    • Vol. 53 (1), 37-44
Abstract
The temporal relationship between glycosaminoglycan (GAG) accumulation and amyloid deposition was determined in 2 models of amyloid induction in the mouse. In the 1st model amyloid was induced rapidly using amyloid-enhancing factor and AgNO3 as an inflammatory stimulus. In the 2nd model amyloid was induced by daily injections of azocasein. Congo red staining was used to demonstrate amyloid, and both the sulfated Alcian blue and Alcian blue (pH 5.7)-MgCl2 methods were used to demonstrate GAG. In the rapid model, amyloid was 1st detected in the splenic perifollicular areas 36 h after induction. The initial presence of GAG was also seen at 36 h and in the exact locale where the amyloid was found. Amyloid was first seen in the liver about the central veins at 48 h. GAG in the liver appeared coincidentally with and in the same location as the amyloid. In the traditional model (azocasein injections) amyloid did not appear in the spleen until day 6-7, again with coincidental GAG deposition. Amyloid-associated GAG appear in the tissues together with the AA protein and are not a function of the tissue type. The appearance of the GAG is also not a function of the nature of the inflammatory agent or its length of action but appears to be part of the process involved in the deposition of the AA protein.