Cultured peripheral blood mononuclear leukocytes from anorexia nervosa patients are refractory to visible light.

Cultured human peripheral blood mononuclear leukocytes [PBML] from patients with anorexia nervosa [AN] did not respond to light stimulation as PBML of normal controls [NC] did. During winter, visible light increased [3H]thymidine incorporation into DNA of NC-PBML stimulated with phytohemagglutinin [PHA]. This effect was enhanced by 10(-7) M melatonin. PHA-stimulated DNA synthesis of PBML from AN patients failed to respond to photic stimulation during winter, and their proliferative response to melatonin was significantly blunted. In vitro photic stimulation of NC-PBML reduced melatonin while increasing both serotonin and 5-hydroxyindole 3-acetic acid [HIAA] production in both basal and PHA-stimulated conditions. In contrast AN-PBML, that in darkness enhanced the oxidative deamination of serotonin into HIAA more than NC-PBML, did not switch their indole metabolism in response to light. Light did not inhibit the binding of both melatonin and serotonin to AN-PBML as occurred in NC-PBML. The present data suggest that AN-PBML do not respond to light in vitro, because of a failure in the regulation of serotonin and melatonin metabolism.