Final answer:
Cholesterol is not an appropriate target for antifungal drugs; instead, ergosterol synthesis and components unique to fungal cells like chitin and β(1→3) glucan are targeted. The targets for antifungal drugs are more limited due to the similarity between human and fungal cells.
Step-by-step explanation:
The target that is not appropriate for antifungal drugs is cholesterol. Antifungal drugs aim to disrupt the biosynthesis of ergosterol, a component of the fungal cell membrane that is analogous to cholesterol in human cells. Therefore, targeting cholesterol would be inappropriate, as it would affect human cells as well. Additionally, some antifungal drugs target other specific components of fungi, such as chitin in the cell wall and β(1→3) glucan, which are absent in human cells.The targets for antifungal drugs are limited compared to antibiotics or antivirals because human cells and fungal cells are more similar to each other than to bacterial or viral cells. This similarity makes it challenging to find targets that are unique to fungi without affecting human cells, leading to possible toxic side effects.
Disruption of ergosterol biosynthesis is an effective mode of action for antifungal drugs because ergosterol is not found in human cell membranes, making drugs targeting this pathway selectively toxic to fungi.The correct answer is c) DNA replication. Antifungal drugs target various components in fungal cells to disrupt their normal function. Ergosterol synthesis, cell wall synthesis, and microtubule formation are all appropriate targets for antifungal drugs. Ergosterol is a component of fungal cell membranes, and antifungal drugs can interfere with its synthesis or bind to it to disrupt the cell membrane integrity. Cell wall synthesis is another target, as some antifungal drugs can inhibit the production of cell wall-specific components like β(1→3) glucan. Microtubule formation can also be disrupted by antifungal drugs.