Toxicological Sciences, Vol 52, 68-79, Copyright © 1999 by Society of Toxicology
TE Stoker, CL Robinette and RL Cooper
The availability of prolactin (PRL) to the neonatal brain is known to
affect the development of the tuberoinfundibular (TIDA) neurons and, as a
consequence, lead to alterations in subsequent PRL regulation. Without
early lactational exposure to PRL (derived from the dam's milk), TIDA
neuronal growth is impaired and elevated PRL levels are present in the
prepubertal male. These observations, combined with the finding that
alterations in PRL secretion (i.e., hyperprolactinemia) in the adult male
rat have been implicated in the development of prostatitis, led us to
hypothesize that early lactational exposure to agents that suppress
suckling-induced PRL release would lead to a disruption in TIDA
development, altered PRL regulation, and subsequent prostatitis in the male
offspring. To test this hypothesis, suckling- induced PRL release was
measured in Wistar dams treated twice daily with the herbicide atrazine
(ATR, by gavage, on PND 1-4 at 0, 6.25, 12.5, 25, and 50 mg/kg body
weight), or twice daily with the dopamine receptor agonist bromocriptine
(BROM, sc, at 0.052, 0.104, 0.208, and 0.417 mg/kg); BROM is known to
suppress PRL release. Similarly, atrazine has also been reported to
suppress PRL in adult females. Serum PRL was measured on PND 3 using a
serial sampling technique and indwelling cardiac catheters. A significant
rise in serum PRL release was noted in all control females within 10 min of
the initiation of suckling. Fifty-mg/kg ATR inhibited suckling-induced PRL
release in all females, whereas 25 and 12.5 mg/kg ATR inhibited this
measure in some dams and had no discernible effect in others. The 6.25
mg/kg dose of ATR was without effect. BROM, used here as a positive
control, also inhibited suckling-induced PRL release at doses of 0.104 to
0.417 mg/kg, with no effect at 0.052 mg/kg. To examine the effect of
postnatal ATR and BROM on the incidence and severity of inflammation (INF)
of the lateral prostate of the offspring, adult males were examined at 90
and 120 days. While no effect was noted at 90 days of age, at 120 days,
both the incidence and severity of prostate inflammation was increased in
those offspring of ATR-treated dams (25 and 50 mg/kg). The 12.5 mg/kg ATR
and the two highest doses of BROM increased the incidence, but not the
severity, of prostatitis. Combined treatment of ovine prolactin (oPRL) and
25 or 50 mg/kg ATR on PND 1-4 reduced the incidence of inflammation
observed at 120 days, indicating that this increase in INF, seen after ATR
alone, resulted from the suppression of PRL in the dam. To determine
whether or not there is a critical period for these effects, dams were
dosed with 25 and 50 mg/kg on PND 6-9 and PND 11-14. Inflammation was
increased in those offspring from dams treated on PND 6-9, but this
increase was not significant. Dosing on PND 11-14 was without effect. These
data demonstrate that ATR suppresses suckling-induced PRL release and that
this suppression results in lateral prostate inflammation in the offspring.
The critical period for this effect is PND 1-9.
ARTICLES
Maternal exposure to atrazine during lactation suppresses suckling- induced prolactin release and results in prostatitis in the adult offspring
Endocrinology Branch, Reproductive Toxicology Division, National Health and Environmental Effects Research Laboratory, U.S. Environmental Protection Agency, Research Triangle Park, North Carolina, USA. Stoker.tammy@epa.gov
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