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Riboflavin Deficiency and Glutathione Metabolism in Rats: Possible Mechanisms Underlying Altered Responses to Hemolytic Stimuli^1,2,

Department of Medicine, Memorial Sloan-Kettering Cancer Center and Cornell University Medical College, New York, NY 10021

Riboflavin deficiency suppresses parasitic growth in malaria. Three possible mechanisms have been proposed previously to explain the survival advantage of riboflavin-deficient hosts: a) enhanced fragility of red blood cells (RBC), b) decreased formation of reticulocytes and/or c) decreased concentrations of reduced glutathione (GSH) and ATP. The validity of these proposed mechanisms was tested by investigating whether riboflavin deficiency alters the hemolytic response to three stimuli: hydrogen peroxide (H₂O₂), a hypotonic medium or ferriprotoporphyrin IX (FP). Reticulocyte counts and concentrations of ATP and GSH were also determined. The percentage of hemolysis induced by H₂O₂ or FP was significantly less in riboflavin-deficient than in control animals. By contrast, hemolytic response to a hypotonic medium was enhanced during riboflavin deficiency. Despite diminished activity of glutathione reductase and normal glutathione peroxidase activity during riboflavin deficiency, the erythrocyte concentration of GSH was increased over that in control animals. Concentrations of ATP and hemoglobin in erythrocytes as well as the reticulocyte count were unaltered during riboflavin deficiency. Thus, diminished malarial parasitemia in riboflavin-deficient animals occurs despite greater resistance of RBC to either H₂O₂- or FP-induced hemolysis, and in the presence of a normal reticulocyte count and erythrocytes ATP concentration. Results of this study raise the possibility that Plasmodium parasites have greater requirements for flavin coenzymes, GSH or ATP than those of host erythrocytes, which may explain the apparent protection of the riboflavin-deficient host from malaria.

KEY WORDS: • riboflavin deficiency • hemolysis • reticulocytosis • lipid peroxidation • malaria • ATP • reduced glutathione

¹ Supported by Clinical Nutrition Research Unit Grant No. CA 29502 and Hypertension Training Grant No. HL 07379 from the National Institutes of Heath and by grants from the American Cancer Society, the American Federation for Aging Research, Inc., the Stella and Charles Guttman Foundation, the General Foods Fund and the Distilled Spirits Council of the U.S., Inc. The research was performed in the Nutrition Research Laboratory of Sloan-Kettering Institute.

² Portions of these studies were presented at the Annual Meeting of the American Society for Clinical Nutrition [Am. J. Clin. Nutr. 41: 845 (abs.), 1985].

Manuscript received 8 January 1988. Revision accepted 6 May 1988.