, Volume 30, Issue 3, pp 233-244

In vitro OKT3-induced mitogenesis in selenium-deficient patients on a diet for phenylketonuria

Rent the article at a discount

Rent now

* Final gross prices may vary according to local VAT.

Get Access


Patients with phenylketonuria (PKU) are frequently deficient in the essential trace element selenium (Se), because of their very low protein diet. Using two approaches to investigate T-cell response to proliferative signaling, viz, mitogenesis caused by the monoclonal antibody OKT3 and the plant lectin phytohaemagglutinin (PHA), we demonstrated significantly reduced responses to optimal concentrations of OKT3 in a group of PKU patients with reduced serum Se compared with a normal group (p=0.0005) and with a group of PKU patients whose serum Se was normal (p=0.0023). The response of the Se-deficient group to optimal levels of PHA did not differ from that of the normal controls or from that of Se-normal PKU patients. A dose-dependent relationship between serum Se levels and mitogenic response was evident for OKT3 (r=0.34,p=0.0154), but not for PHA (r=−0.02,p=0.9086). We suggest that the reduced response to OKT3 mitogenesis in Se-deficient PKU patients is possibly the consequence of impaired Se-dependent metabolic activity, which affects mitogenic signaling via the T cell antigen receptor (TCR/CD3) complex.