Opioid growth factor is present in human and mouse gastrointestinal tract and negatively regulates dna synthesis. Zagon, Ian S., Yan Wu, Patricia J. McLaughlin. Department of Neuroscience and Anatomy, The Pennsylvania State University, College of Medicine, Hershey, Pennsylvania 17033
APStracts 3:0415R, 1996.
Native opioid peptides serve as growth factors in a number of normal and neoplastic cells and tissues. This study investigated the influence of opioids on circadian rhythm-dependent DNA synthesis in mouse esophagus during homeostatic renewal. In contrast to a labeling index (LI) of approximately 24.0% at 0630 hours and 5.5% 1600 hours, disruption of opioid-receptor interaction by the potent opioid antagonist naltrexone (NTX) (10 mg/kg) in mice resulted in an elevation of 49% in DNA synthesis of esophageal epithelial cells at 1600 hours but had no effect at 0630 hours. Mice subjected to [Met5] -enkephalin (1 mg/kg) had a LI that was decreased 23% from control levels at 0630 hours but was unaffected at 1600 hours. This decrease in DNA synthesis was blocked by concomitant administration of naloxone (10 mg/kg); naloxone alone had no influence on cell replicative processes. In tissue culture studies, NTX and OGF markedly increased and decreased, respectively, the LI from control values. Both OGF and its receptor, _, were detected in all but the cornified layer of mouse esophageal epithelium, and in the epithelial cells of the stomach and small and large intestines. In addition, both peptide and receptor were observed in the basal and suprabasal cells of human esophageal epithelium. These results indicate that an endogenous opioid peptide (OGF) and its receptor (_) reside in gastrointestinal epithelium and play a role in cellular renewal processes in a tonically inhibitory, direct, and circadian rhythm -dependent fashion.

Received 8 August 1996; accepted in final form 13 November 1996.
APS Manuscript Number R465-6.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 31 December 1996