Pyrimidine metabolism in Tritrichomonas foetus

C. C. Wang, R. Verham, Fu Tzeng Sin Fu Tzeng, S. Aldritt, H. W. Cheng

研究成果: 雜誌貢獻文章

38 引文 斯高帕斯(Scopus)

摘要

The anaerobic parasitic protozoa Tritrichomonas foetus is found incapable of de novo pyrimidine biosynthesis by its failure to incorporate bicarbonate, aspartate, or orotate into pyrimidine nucleotides or nucleic acids. Uracil phosphoribosyltransferase in the cytoplasm provides the major pyrimidine salvage for the parasite. Exogenous uridine and cytidine are mostly converted to uracil by uridine phosphorylase and cytidine deaminase in T. foetus prior to incorporation. T. foetus cannot incorporate labels from exogenous uracil or uridine into DNA; it has not detectable dihydrofolate reductase or thymidylate synthetase and is resistant to methotrexate, pyrimethamine, trimethoprim, and 5-bromovinyldeoxyuridine at millimolar concentrations. It has an enzyme thymidine phosphotransferase in cellular fraction pelleting at 100,000 x g that can convert exogenous thymidine to TMP via a phosphate donor such as p-nitrophenyl phosphate or nucleoside 5'-monophosphate. Thymidine salvage in T. foetus is thus totally dissociated from other pyrimidine salvage.

原文英語
頁(從 - 到)2564-2568
頁數5
期刊Proceedings of the National Academy of Sciences of the United States of America
80
發行號9 I
出版狀態已發佈 - 1983
對外發佈Yes

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ASJC Scopus subject areas

  • Genetics
  • General

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