Per cent stimulation of GR activity by FAD in vitro and PNP oxidase activity 
were measured in G6PD deficiency, heterozygous beta-thalassaemia and controls. 
It is confirmed that, in contrast to the high stimulation of GR by FAD commonly 
found in in thalassaemia indicating red-cell deficiency of FAD, and shown here 
to be greater in the Italian subjects, GR is usually saturated with FAD in G6PD 
deficiency, leading to high in vitro activity. Unexpectedly, on the other hand, 
low FMN-dependent PNP oxidase activity due to red-cell deficiency of FMN, 
confirmed by response to oral riboflavin, was found in the majority of subjects 
with G6PD deficiency, similar to that found in heterozygous beta-thalassaemia. 
Whereas this is explained in thalassaemia by an inherited slow red-cell 
metabolism of riboflavin to FMN, it is suggested that in G6PD deficiency an 
increased rate of red-cell metabolism of FMN to FAD leads to the low FMN and 
high FAD. When G6PD deficiency occurs with heterozygous beta-thalassaemia, GR is 
usually saturated with FAD as in G6PD deficiency alone, unless there is an 
inherited, very slow red-cell metabolism of riboflavin to FMN. The part played 
by GR in haemolytic crises in G6PD deficiency is discussed.