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The Candida albicans cell membrane is a lipid bilayer embedded with proteins, crucial for maintaining homeostasis, mediating nutrient transport, and serving as a scaffold for enzymes involved in cell wall synthesis. This membrane is biochemically distinct from human cell membranes due to the presence of ergosterol, making it an attractive target for antifungal drugs. Disruption of the cell membrane results in loss of osmotic control and cell death, which is exploited by polyenes and azoles. Resistance mechanisms include changes in membrane lipid composition, upregulation of efflux pumps, and altered ergosterol biosynthetic pathways[3][9]. The membrane operates in close concert with the cell wall, and its integrity is essential for virulence, biofilm formation, and drug susceptibility in Candida albicans[3][4][9].
Azoles: Inhibit lanosterol 14-α-demethylase, blocking ergosterol synthesis, leading to increased membrane permeability[9]; Polyenes: Bind directly to ergosterol, forming pores in the membrane that cause leakage of cell contents and cell death[8][9]
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