Ergosterol is a specific component of fungal biofilms and plays an important role in maintaining cell membrane integrity, fluidity and cellular resistance. Agricultural fungicides known to inhibit ergosterol biosynthesis include a variety of chemical structure types, among which pyridines, pyrimidines, piperazines, imidazoles, triazoles fungicides target 14α-demethylase (CytP-450 plus monooxygenase), also known as demethylation inhibitors (DMIs). The N atom of the agent binds to the coordination bond of the iron atom in the center of the enzyme's iron-sulfur protein, preventing the oxidative removal of methyl from the α-face of the 14th carbon position of the 24(28)-methylated dihydromethanosterol and interrupting the ergosterol biosynthetic pathway. It is now known that 14α-demethylase is the most important key enzyme in the fungal ergosterol biosynthetic pathway. The targets of action of morpholine and piperidine fungicides are ?8→7 isomerase and ?14-15 reductase. Allylamines such as terbinafine act on squaleneepoxidase, amines such as fenpropidin and spiroxamine act on △14-reductase, and hydroxyanilides act on △14-reductase. The hydroxyanilides fungicide fenhexamid acts on C-4 demethylase.
Sites of action of inhibitors of ergosterol biosynthesis
A. Sites of action of DMI-type fungicides B to C. Sites of action of morpholine- and piperidine-type fungicides
(1) lanosterol (2) 24-methylforked dihydromanosterol (3) 4,4-dimethylergosterol-8. 14,24(28)-trienol (4) 4,4-dimethylergosta-8,24(28)-dienol (5) ergosta-8,24(28)-dienol (6) epitestosterol (7) ergosta-5,7,24(28) is also a pheromone concerning genetic expression; therefore, ergosterol biosynthesis inhibitors can cause a variety of toxic symptoms in fungi.
(2) Effect on lecithin biosynthesis. Phospholipids and fatty acids are important components of the bilayer structure of cell membranes. The mechanism of action of the thio-catch phosphate ester class of isorhizobium, diquat, etc. is to inhibit lecithin biosynthesis in the cell membrane. By inhibiting the activity of S-adenosylhomocyanine methyltransferase, the methylation of phosphatidylethanolamine is prevented, so that the biosynthesis of phosphatidylcholine (lecithin) is blocked and the permeability of the cell membrane is changed. For example, altered permeability of the cell membrane reduces UDP-N-acetylglucosamine secretion, which further affects chitin biosynthesis.
(3) Effect on fatty acid biosynthesis. Fatty acids are important components of cell membranes. It is known that the target of inoculin fungicide is acetyl CoA carboxylase, a key enzyme in fatty acid biosynthesis, which interferes with fatty acid biosynthesis and alters cell membrane permeability.
(4) Direct action on the cell membrane. Organic sulfur fungicides and membrane subunits connected to the hydrophobic bond or metal bridge binding, resulting in the destruction of the structure of the biological membrane, cracks, pores, membrane loss of normal physiological functions. Fungicides containing heavy metal elements can act directly on the cell membrane ATP hydrolase, changing the membrane permeability.