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Role of the Pituitary in Modulating Hepatic Monoamine Oxidase Activity

Laboratory of Environmental Toxicology, National Institute of Environmental Health Sciences,Research Triangle Park North Carolina 27709

Address requests for reprints to: Dr. Coral A. Lamartiniere, Laboratory of Environmental Toxicology, National Institute of Environmental Health Sciences, P.O. Box 12233, Research Triangle Park, North Carolina 27709.

Abstract

The activity of monoamine oxidase was measured in a liver mitochondrial fraction from gonadectomized and hypophysectomized rats. The effects of 17β-estradiol and testosterone propionate administration on hepatic monoamine oxidase (MAO) activity in these animals were also studied. The regulation of hepatic MAO was studied using ectopic pituitary transplants under the kidney capsule of hypophysectomized, gonadectomized rats.

MAO activity is normally 50% higher in adult females than in males. Ovariectomy has no effect on adult female MAO activity, but castration of the adult male increases MAO activity to the intact female level. The administration of testosterone propionate to the male castrate restores the intact male MAO level. Enzyme activity was elevated in both adult male and female rats after hypophysectomy, but the sex difference in MAO activity was maintained in the absence of the pituitary. Gonadectomy had no effect on these elevated levels. Transplantation of an age-matched pituitary (of male or female origin) into hypophysectomized, ovariectomized females restored the elevated MAO activity to the intact female level, but implantation of prepubertal male pituitaries did not restore female MAO to the intact level. Transplantation from a male or female donor into the hypophysectomized, castrated male recipient was also without effect on the increased level of MAO activity.

Our results suggest that hepatic MAO activity is partially regulated by a pituitary factor or factors, as yet unidentified, which suppress enzyme activity. In the adult female, release of this pituitary factor appears to be independent of hypothalamic control. Release of this factor in the male seems to be dependent on the hypothalamus and stimulated by testosterone. (Endocrinology 106: 798, 1980)

Received April 30, 1979.