Lead and Aroclor 1254 disrupt reproductive neuroendocrine function in Atlantic croaker

Abstract

We have previously shown that lead (lead chloride) and a polychlorinated biphenyl (PCB) mixture (Aroclor 1254) can alter hypothalamic serotonin (5-hydroxytryptamine, 5-HT) content, and pituitary gonadotropin II (GTH II) release in vitro, in the Atlantic croaker ( Micropogonias undulatus). In the present study we investigated whether impairment of the hypothalamic 5-HT pathway involves alterations in tryptophan hydroxylase (TPH), the rate-limiting enzyme in 5-HT biosynthesis, or monoamine oxidase (MAO), the catabolic enzyme. Aroclor 1254 (1 mg/kg body wt. for 30 days) significantly inhibited hypothalamic TPH activity without altering MAO activity, and caused a significant decline in 5-HT content. On the other hand, lead exposure (15 mg/kg body wt. for 30 days) only induced a slight decrease in hypothalamic 5-HT content and TPH activity, and a minor increase in MAO activity. However, both Aroclor 1254 and lead significantly inhibited the GTH II response to stimulation 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 metabolism. 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 growth.