Previous control studies carried out in children showed that respiratory
infection alters
riboflavin metabolism and leads to excessive urinary losses of the
vitamin. In order to understand the nature of biochemical changes in
riboflavin metabolism during respiratory
infection, a study was carried out using the mouse as the experimental model, and Klebsiella pneumoniae as the infective organism. Mice were fed on either a low (0.5 mg/kg)- or high (13.3 mg/kg)-
riboflavin semi-synthetic diet.
Infection resulted in a 5-6-fold higher excretion of
riboflavin in the urine of mice fed on the low-
riboflavin diet. Higher erythrocyte
FAD levels and lower liver
FAD levels were also observed during
infection. Of the four
enzymes involved in the synthesis and breakdown of the
flavin coenzymes studied, the activity of hepatic
flavokinase (
ATP:
riboflavin 5'-
phosphotransferase; EC 2.7.1.26) was significantly lower, and that of
FAD synthetase (
ATP:
FMN adenylyltransferase; EC 2.7.7.2) was higher during
riboflavin restriction and
infection. The activity of
FMN (
acid) phosphatase (EC 3.1.3.2) was unchanged, whereas
FAD (
nucleotide) pyrophosphatase (EC 3.6.1.9) activity was significantly higher both with the low-
riboflavin diet and during
infection.
Thyroid hormone is known to modulate
flavokinase activity and, hence, thyroid status was assessed. Plasma
triiodothyronine (T3) levels were not affected, but
thyroxine levels were lower in the mice fed on the low-
riboflavin diet. However, plasma T3 was significantly lower during
infection, suggesting a mechanistic role for the
hormone in the reduction of
flavokinase activity.