1.Action of lombazole, and inhibitor of fungal ergosterol biosynthesis, on Staphylococcus epidermidis.
Barug D, Bastiaanse HB, van Rossum JM, Kerkenaar A. Antimicrob Agents Chemother. 1986 Aug;30(2):238-44.
Lombazole had no effect on respiration at any tested concentration and had little effect on the K+ permeability of Staphylococcus epidermidis. Of the major metabolic processes investigated in this bacterium, only de novo synthesis of the cell envelope was inhibited by lombazole well in advance of an effect on growth. The time course of inhibition indicated that lombazole exerted its primary effect via inhibition of lipid synthesis; other induced changes, such as reduced synthesis of lipoteichoic acid and cell wall components, were considered to be secondary effects. Although the precise site of action in S. epidermidis has to be established, the absence of alterations in lipid patterns after treatment with lombazole suggests the toxicant may affect an essential step in lipid biosynthesis. In Candida albicans, lombazole inhibited the sterol C-14 demethylation step in the ergosterol biosynthesis pathway.
2.Effect of the imidazole derivative lombazole on the ultrastructure of Staphylococcus epidermidis and Candida albicans.
Barug D, de Groot K. Antimicrob Agents Chemother. 1985 Nov;28(5):643-7.
Lombazole, an antimicrobial agent of the imidazole class, induced profound ultrastructural changes in Staphylococcus epidermidis and Candida albicans, as observed by freeze fracture electron microscopy. In S. epidermidis cells, the primary effect on ultrastructure was characterized by a distinct change in the morphology of the plasma membrane. Secondary effects of lombazole were cell wall thickening, accumulations of lipidlike material, abnormal cell division, severe change of shape, separation of the plasma membrane from the cell wall, and disruption of cells. The alterations in C. albicans were characterized by the deformation of and a decrease in the number of invaginations in the protoplasmic fracture face and corresponding ridges on the exoplasmic fracture face and by separation of the plasma membrane from the cell wall, leaving a gap which frequently contained small vesicles. Moreover, a considerable thickening of the cell wall occurred at localized regions.