Increased hepatic and reduced prostatic prolactin (PRL) binding in iron deficiency and during neuroleptic treatment: correlation with changes in serum PRL and testosterone.

Iron deficiency (ID) induced in 21 day old male rats for 28 days caused a 7 fold increase in hepatic prolactin (PRL)-specific binding and a parallel 3 fold rise in serum PRL, as expected from both the reported reduction in central dopaminergic (DA) activity and PRL's up-regulating effect on its own liver receptors. Similarly, serum testosterone was increased by 80%. Prostatic PRL binding was slightly reduced (by 27%), possibly because of masking by the raised hormone levels, although more likely by a more generalized reduction in proliferation during ID, as indicated by the 50% prostatic weight loss. Chronic treatment with neuroleptics also increased hepatic PRL binding in accord with their anti DA activity: chlorpromazine (10 mg/kg) or fluphenazine (5 mg/kg) injected daily (i.p.) for 21 days followed by a 3 day drug-free period resulted in 26 and 10 fold increases, respectively. The parallel reductions of serum levels of PRL (by 40%) and of testosterone (by 70%) by both drugs is indicative of the drug withdrawal supersensitivity normally observed in the caudate nucleus DA receptor. A testicular peripheral effect of the neuroleptics probably further accounted for the reduction in testosterone synthesis, reinforcing the induction of liver PRL binding by these drugs and explaining their negative effects on prostate PRL binding and weight. These findings stress the importance of monitoring hormone levels in ID and during treatment with neuroleptics, in order to avoid endocrine side-effects.