We have previously shown that lead (lead chloride) and a polychlorinated bi
phenyl (PCB) mixture (Aroclor 1254) can alter hypothalamic serotonin (5-hyd
roxytryptamine, 5-HT) content, and pituitary gonadotropin II (GTH II) relea
se in vitro, in the Atlantic croaker (Micropogonias undulatus). In the pres
ent study we investigated whether impairment of the hypothalamic 5-HT pathw
ay involves alterations in tryptophan hydroxylase (TPH), the rate-limiting
enzyme in 5-HT biosynthesis, or monoamine oxidase (MAO), the catabolic enzy
me. Aroclor 1254 (1 mg/kg body wt. for 30 days) significantly inhibited hyp
othalamic TPH activity without altering MAO activity, and caused a signific
ant decline in 5-HT content. On the other hand, lead exposure (15 mg/kg bod
y wt. for 30 days) only induced a slight decrease in hypothalamic 5-HT cont
ent and TPH activity, and a minor increase in MAO activity. However, both A
roclor 1254 and lead significantly inhibited the GTH II response to stimula
tion by a luteinizing hormone-releasing hormone analog (LHRHa) in vivo and
caused reduced gonadal growth. These results demonstrate that impairment of
hypothalamic serotonin metabolism by Aroclor 1254 involves inhibition of 5
-HT synthesis, whereas lead does not exert a profound influence on 5-HT met
abolism. The decline in 5-HT availability due to reduced 5-HT synthesis in
the PCB-exposed fish may result in disruption of the stimulatory 5-HT-GnRH
pathway controlling GTH II secretion leading to impairment of gonadal growt
h. (C) 2000 Elsevier Science Ltd, All rights reserved.