Abstract
Ascofuranone (AF) enhanced glucose consumption of splenocytes and macrophages, while it enhanced incorporation of [14C]acetate into macrophages but not into splenocytes. When using tumor cell lines, it inhibited the incorporation of [14C]acetate into lymphoma cell lines, YAC-1 and P388, and a thymoma, L5178Y, while it stimulated that into P388D1, which is derived from P388 and has macrophage-like characteristics. Incorporation of [14C]acetate into a mammary carcinoma FM3A was also stimulated by AF. In contrast, AF stimulated uptake of methylglucose in all cell lines tested. The effect of AF was further studied using mouse myeloid leukemia, M1 cells. AF slightly stimulated the incorporation of [14C]acetate into undifferentiated M1 cells, and strongly stimulated that of hydrocortisone-differentiated M1 cells. In contrast, AF suppressed the incorporation of [14C]acetate into retinoic acid-differentiated M1 cells. Glucose consumption of these three types of M1 cells was all stimulated. From these results, we conclude that AF specifically stimulates the incorporation of [14C]acetate into macrophages while it generally stimulates glucose uptake of the cells.
