Adrenocortical Activation by 5-Fluorouracil and its Possible Reversal by Thymidine
5-Fluorouracil (FU) provokes a long lasting and dose-related increase of plasma corticosterone in the rat which may be considered a stress reaction involving CRH-ACTH release. Thymidine (TdR) believed to act as a specific and effective antidote against FU toxicity, administered i.m. or i.p. at different times before or after the i.p. or i.v. injection of 100 mg/kg FU on a molar basis 0.1 : 1–10.7 : 1 does not antagonize or, at the highest dosage seem to increase the FU induced adrenocortical activation. Thus, the FU adrenal activation is modulated by a mechanism not involving the block of the de novo thymidilate synthesis.
Key words5-Fluorouracil Thymidine Adrenocortical activation Thymidilate synthetase Thymine
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