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© 1994 Oxford University Press

research-article

Immunotoxicological Profile of Morphine Sulfate in B6C3F1 Female Mice1

DAVID G. LEVIER*, J. ANN MCCAY*, MALVIN L. STERN*, LOUIS S. HARRIS*, DENNIS PAGE{dagger}, RONNETTA D. BROWN*, DEBORAH L. MUSGROVE*, LEON F. BUTTERWORTH*, KIMBER L. WHITE, JR.{ddagger} and ALBERT E. MUNSON*

*Departmenl of Pharmacology and Toxicology, Medical College of Virginia/Virginia Commonwealth University Box 613, Richmond, Virginia 23298 {dagger}Department of Pathology, School of Dentistry, Medical College of Virginia/Virginia Commonwealth University Box 613, Richmond, Virginia 23298 {ddagger}Department of Biostalistics, Medical College of Virginia/Virginia Commonwealth University Box 613, Richmond, Virginia 23298

Received April 20, 1993; accepted November 5, 1993

This study was undertaken to investigate a number of immune parameters which may be compromised with exposure to morphine sulfate. Mice were implanted subcutaneously with 8-, 25-, or 75-mg morphine sulfate pellets. Placebo pellets of identical makeup to the 75-mg morphine pellet (without morphine of course) were used as a control. Twenty-four hours after implantation of a 75-mg morphine pellet, blood levels reached a peak of 1610 ng/ml. Corticosterone increased in parallel with morphine and reached a peak level of 966 ng/ml 24 hr after implantation. The dose response of morphine to increase corticosterone, however, was fiat. The weight of the lymphoid organs, spleen and thymus, and the liver were significantly reduced in the morphine-treated groups. Morphine treatment was associated with an increase in serum albumin, SGPT, BUN, and alkaline phosphatase indicative of hepatic damage. In contrast to increased serum proteins, the C3 component of complement was reduced in a dose-dependent manner. Leukocyte number in the peripheral blood was significantly reduced, while erythro-cyte number and hematocrit were both increased. The number of B cells and T cells was decreased in morphine-treated animals. However, the percentage of T cells relative to B cells was increased. The primary IgM antibody response to the T-depen-dent antigen, sheep red blood cells, was decreased. Natural killer cell activity was reduced in response to morphine, as was the phagocytic capacity of Kupffer cells. Host-resistance models of Listeria monocytogenes or Streptococcus pneumoniae showed an increased resistance following administration of morphine. This increased host resistance, however, was not due to an increase in antimicrobial action of sera obtained from mice treated with morphine. The majority of morphine's effects on the immune system exhibited a flat dose response, suggesting that these effects may be mediated secondarily through corticosterone.


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