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The Role of Krebs Cycle Inhibition by Fluoroacetate

Harold Koenig, MD, PhD; Abdussamad Patel, PhD

Arch Neurol. 1970;23(2):155-160.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

THE PYRIMIDINE analog fluorouracil has been used extensively in the chemotherapy of malignant neoplasms since its introduction by Heidelberger and associates in 1957.¹ The carcinostatic property of fluorouracil seems to be due to anabolic reactions. Although fluorouracil is readily converted to acid-soluble fluorouracil nucleotides, undergoes incorporation into RNA, and interferes with RNA synthesis in mammalian tissues and tumor cells,² its major chemotherapeutic and toxic effects are attributable to an interference with DNA synthesis and cell division. The latter effect is due to inhibition of thymidylate synthetase, the enzyme which catalyzes the conversion of deoxyuridylate of thymidylate, by the fluorouracil derivative fluorodeoxyuridylate (FUDR).² Thus fluorouracil, like other agents which block DNA synthesis, is toxic chiefly to rapidly dividing normal cells, ie, epithelial cells of the alimentary tract and hematopoietic elements of bone marrow and lymphoid tissues.^3-5

Recently, Riehl and Brown⁶ described an acute neurological disorder . . . [Full Text PDF of this Article]

Author Affiliations
Chicago

From the Neurology Service, Veterans Administration Research Hospital, and the Department of Neurology, Northwestern University Medical School, Chicago.

Footnotes
Submitted for publication Jan 30, 1970; accepted Feb 12.

Reprint requests to Veterans Administration Research Hospital, Neurology Service, 333 E Huron St, Chicago 60611 (Dr. Koenig).

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