Tissue distribution and turnover of [3H]riboflavin during respiratory infection in mice.

Studies in children and mice suggest that respiratory infections cause a mobilization of riboflavin from the tissues to the blood, resulting in increased urinary loss of this vitamin. To verify this observation, the tissue distribution and turnover of [3H]riboflavin were investigated in control and low-riboflavin-fed mice infected with Klebsiella pneumoniae. Infection significantly reduced [3H]riboflavin levels in the liver and kidney of low-riboflavin-fed mice and in the liver of control mice. Such changes were not observed in tissues such as muscle, small intestine, and brain. Urinary excretion of [3H]riboflavin increased significantly during the acute phase of infection and the biological half-life of [3H]riboflavin was shorter in the low-riboflavin-fed group. The results confirm that the mobilization of riboflavin from tissues to blood during infection results in a deterioration of riboflavin status. Thus, the study supports the hypothesis that respiratory infection is a nondietary factor contributing to the high prevalence of subclinical riboflavin deficiency in children of developing countries like India.