Effect of prostaglandin E in multiple experimental models: V. Effect on tumor/host interaction.
Prostaglandin E (PGE) has long been incriminated as a cause of the immunosuppression seen in cancer patients and for the increased rates of tumor growth due to the impairment of the immunologic response to the tumor. We have investigated the effect of PGE on tumor-host interaction by utilizing a parenterally administered long-acting PGE derivative, 16,16-dimethyl-prostaglandin E (dPGE). Administration of dPGE was found to decrease the rate of tumor growth but at a cost of decreasing tumor-free body mass. The dPGE did not alter resting metabolic rates but did alter some parts of brain dopamine metabolism and significantly decreased the serum level of multiple amino acids. In conclusion, elevated PGE levels may significantly alter metabolism in tumor patients.
Waymack
J P
JP
Shriners Burns Institute, Cincinnati, Ohio.
Chance
W T
WT
D000596:Amino Acids / Q000097:blood; D000818:Animals; D001835:Body Weight / Q000187:drug effects; D001923:Brain Chemistry / Q000187:drug effects; D004734:Energy Metabolism / Q000187:drug effects; D008297:Male; D009368:Neoplasm Transplantation; D018377:Neurotransmitter Agents / Q000378:metabolism; D011458:Prostaglandins E / Q000502:physiology*; D011459:Prostaglandins E, Synthetic / Q000494:pharmacology*; D051381:Rats; D011916:Rats, Inbred F344; D012513:Sarcoma, Experimental / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D014443:Tyrosine / Q000378:metabolism
D000596:Amino Acids; D018377:Neurotransmitter Agents; D011458:Prostaglandins E; D011459:Prostaglandins E, Synthetic; C017244:16,16-dimethylprostaglandin E; D014443:Tyrosine