Purine nucleotide metabolism in resident and activated rat macrophages in vitro.

The overall purine metabolism was studied in detail in resident peritoneal macrophages (M phi) and in thioglycolate elicited peritoneal M phi in vitro. The salvage of purine bases (adenine, hypoxanthine and guanine) was active in both M phi populations, whereas purine biosynthesis de novo was low. Purine nucleosides (inosine, guanosine and adenosine) were efficiently degraded to uric acid and only adenosine was directly salvaged into nucleotides. Purine salvage was markedly increased in elicited M phi as compared to resident M phi whereas purine degradation pathways were enhanced only slightly. These results clearly indicate that salvage of purine bases is the main source for purine nucleotide biosynthesis in M phi, but nucleotide catabolism is the predominant pathway.