Deoxycytidine excretion by mouse peritoneal macrophages

Its implication in modulation of immunological functions

T. S. Chan, B. D. Lakhchaura

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

Pyrimidine excretion by macrophages was studied in order to identify the potential immunoregulatory effector molecules. Deoxycytidine was found in the culture medium of thioglycollate-elicited mouse peritoneal macrophages, along with thymidine, which was shown by others to be a possible immunoregulatory substance. The identification of deoxycytidine was based on: (1) cochromatography with the authentic compound in four different solvents, (2) UV absorption spectral analysis, and (3) the enzymatic peak shift method. Phagocytosis of nucleated chicken erythrocytes, but not enucleated sheep erythrocytes, increased deoxycytidine excretion. The macrophages lacked both deoxycytidine kinase and deoxycytidine deaminase, which is consistent with their excretory pattern. Since it has been known that deoxycytidine can protect cells against cytotoxic effects of thymidine, we propose that deoxycytidine has a role in preventing immunosuppression by thymidine. In patients with adenosine deaminase deficiency, however, immunosuppression caused by combined toxicity of thymidine and deoxyadenosine may not be adequately prevented by deoxycytidine.

Original languageEnglish (US)
Pages (from-to)28-32
Number of pages5
JournalJournal of Cellular Physiology
Volume111
Issue number1
StatePublished - 1982

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Deoxycytidine
Macrophages
Peritoneal Macrophages
Modulation
Thymidine
deoxycytidine deaminase
Immunosuppression
Deoxycytidine Kinase
Thioglycolates
Erythroblasts
Adenosine Deaminase
Phagocytosis
Spectrum analysis
Toxicity
Culture Media
Chickens
Sheep
Erythrocytes
Molecules

ASJC Scopus subject areas

  • Cell Biology
  • Clinical Biochemistry
  • Physiology

Cite this

Deoxycytidine excretion by mouse peritoneal macrophages : Its implication in modulation of immunological functions. / Chan, T. S.; Lakhchaura, B. D.

In: Journal of Cellular Physiology, Vol. 111, No. 1, 1982, p. 28-32.

Research output: Contribution to journalArticle

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