Phagocytosis in riboflavin- or pyridoxine-deficient rats

Abstract The effect of riboflavin or pyridoxine deficiency on phagocytosis was examined in rats to elucidate the mechanism of impaired wound healing in these deficiencies reported earlier. Phagocytic ingestion by peritoneal leukocytes was 60.4% and 68%, respectively, in riboflavin- or pyridoxine-deficient rats compared with weight-matched control animals. Lactate production, which is a measure of glycolytic activity and exocytic degranulation, were also reduced to 74% and 65%, respectively, in riboflavin deficiency but were unaltered in pyridoxine deficiency. Food restriction per se increased production of superoxide anion by leukocytes by two fold, and it was further increased by 1.5 fold during particle uptake only in pyridoxine deficiency. However, postphagocytic digestive events, as judged by the activities of acid phosphatase and collagenase in the incised wound, were not affected in either deficiency. Thus, impaired phagocytosis other than reduced collagenization (reported earlier) may contribute to the adverse effects of vitamins B 2 or B 6 deficiencies on wound healing.