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Deprenyl inhibits tumor growth, reduces
serum prolactin, and suppresses brain monoamine metabolism in rats with
carcinogen-induced mammary tumors
ThyagaRajan S, Quadri SK
Neuroendocrine Research Laboratory,
Kansas State University, Manhattan, KS USA.
sthyagarajan@som.llu.edu
Endocrine 1999 Jun; 10(3):225-32
ABSTRACT
Previously, we have reported that L-deprenyl
decreased the incidence of mammary tumors and pituitary tumors in old
acyclic rats. The objective of the present study was to investigate the
effects of L-deprenyl, a monoamine oxidase-B (MAO-B) inhibitor, treatment on
the development and growth of tumors and on the metabolism of catecholamines
and indoleamine in the medial basal hypothalamus (MBH) and the striatum (ST)
of rats bearing 7,12-dimethylbenzanthracene (DMBA)-induced mammary tumors.
Female Sprague-Dawley rats with DMBA-induced mammary tumors were injected
(sc) daily with 0.25 mg or 5.0 mg of deprenyl/kg BW or the vehicle (saline;
control) for 12 wk. Tumor diameter, tumor number, body weight, and feed
intake were measured every week of the treatment period. Serum PRL and
the concentrations of catecholamines, indoleamine, and their metabolites
were measured by RIA and HPLC, respectively. Treatment with 5.0 mg
deprenyl decreased the tumor diameter, tumor number, and serum prolactin (PRL)
level. Although the body weight increased in all three groups, the
body weight gain in the 5.0 mg group was smaller than that in the control
and 0.25 mg groups. Deprenyl treatment had no effect on feed intake.
The concentrations of dihydroxyphenylacetic acid (DOPAC) and homovanillic
acid (HVA) were decreased in the MBH and the ST, and the concentration of
5-hydroxyindoleacetic acid (5-HIAA) was decreased in the MBH of deprenyl-treated
rats. Treatment with 5.0 mg deprenyl enhanced the concentrations of
norepinephrine (NE) and serotonin (5-HT) in the MBH and in the ST, and the
concentration of dopamine (DA) in the MBH. These results suggest that the
suppression of the development and growth of DMBA-induced mammary tumors by
chronic deprenyl treatment may be mediated through alterations in the
synthesis and metabolism of catecholamines and indoleamine in the MBH and
inhibition of PRL secretion.
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