THE MECHANISM OF BACTERIAL FRAGILITY PRODUCED BY 5-FLUOROURACIL: THE ACCUMULATION OF CELL WALL PRECURSORS

Abstract
Data is presented on the results of experiments designed to establish a possible correlation between the accumulation of N-acetylhexosamine esters and the presence of osmotic imbalance in bacteria. There is a significant increase of N-acetyl-hexoseamine esters in FU-treated cells (5-fluoracil). Isolation of the accumulated compounds showed two peaks in the UV each of which resolved into at least five components by paper chromatography. It appears that small amounts of FU become metabolized to some cell wall precursor and the product inhibits the enzyme complex of cell wall synthesis; this leads to the accumulation of large amounts of the normal precursor(s). The mechanism of FU-induced "osmotic imbalance" concerns a metabolic imbalance between cytoplasmic and cell wall synthesis accompanied by uninhibited cytoplasmic growth. After FU is removed the bacteria resume a sort of unbalanced growth leading to cellular disintergration.