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Fungicide

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Fungicides are pesticides used to kill parasitic fungi or their spores.[1][2] Fungi can cause serious damage in agriculture, resulting in losses of yield and quality. Fungicides are used both in agriculture and to fight fungal infections in animals. Fungicides are also used to control oomycetes, which are not taxonomically/genetically fungi, although sharing similar methods of infecting plants. Fungicides can either be contact, translaminar or systemic. Contact fungicides are not taken up into the plant tissue and protect only the plant where the spray is deposited. Translaminar fungicides redistribute the fungicide from the upper, sprayed leaf surface to the lower, unsprayed surface. Systemic fungicides are taken up and redistributed through the xylem vessels. Few fungicides move to all parts of a plant. Some are locally systemic, and some move upward.[3][4]

Most fungicides that can be bought retail are sold in liquid form, the active ingredient being present at 0.08% in weaker concentrates, and as high as 0.5% for more potent fungicides. Fungicides in powdered form are usually around 90% sulfur.

Major fungi in agriculture

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Some major fungal threats to agriculture (and the associated diseases) are Ascomycetes ("potato late blight"), basidiomycetes ("powdery mildew"), deuteromycetes (various rusts), and oomycetes ("downy mildew").[1]

Types of fungicides

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Further information: List of fungicides

Like other pesticides, fungicides are numerous and diverse. This complexity has led to diverse schemes for classifying fungicides. Classifications are based on inorganic (elemental sulfur and copper salts) vs organic, chemical structures (dithiocarbamates vs phthalimides), and, most successfully, mechanism of action (MOA). These respective classifications reflect the evolution of the underlying science.

Traditional

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Captan, a phthalimide, is a major commercial fungicide.

Traditional fungicides are simple inorganic compounds like sulfur,[5] and copper salts. While cheap, they must be applied repeatedly and are relatively ineffective.[2] Other active ingredients in fungicides include neem oil, rosemary oil, jojoba oil, the bacterium Bacillus subtilis, and the beneficial fungus Ulocladium oudemansii.

Nonspecific

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In the 1930s dithiocarbamate-based fungicides, the first organic compounds used for this purpose, became available. These include ferbam, ziram, zineb, maneb, and mancozeb. These compounds are non-specific and are thought to inhibit cysteine-based protease enzymes. Similarly nonspecific are N-substituted phthalimides. Members include captafol, captan, and folpet. Chlorothalonil is also non-specific.[2]

Specific

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Specific fungicides target a particular biological process in the fungus.

Nucleic acid metabolism

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Cytoskeleton and motor proteins

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Respiration

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Some fungicides target succinate dehydrogenase, a metabolically central enzyme. Fungi of the class Basidiomycetes were the initial focus of these fungicides. These fungi are active against cereals.

Amino acid and protein synthesis

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Signal transduction

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Lipid synthesis / membrane integrity

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Melanin synthesis in cell wall

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Sterol biosynthesis in membranes

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Cell wall biosynthesis

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Host plant defence induction

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Mycoviruses

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Some of the most common fungal crop pathogens are known to suffer from mycoviruses, and it is likely that they are as common as for plant and animal viruses, although not as well studied. Given the obligately parasitic nature of mycoviruses, it is likely that all of these are detrimental to their hosts, and thus are potential biocontrols/biofungicides.[7]

Resistance

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See also: Antimicrobial resistance

Doses that provide the most control of the disease also provide the largest selection pressure to acquire resistance.[8]

In some cases, the pathogen evolves resistance to multiple fungicides, a phenomenon known as cross resistance. These additional fungicides typically belong to the same chemical family, act in the same way, or have a similar mechanism for detoxification. Sometimes negative cross-resistance occurs, where resistance to one chemical class of fungicides increases sensitivity to a different chemical class of fungicides. This has been seen with carbendazim and diethofencarb. Also possible is resistance to two chemically different fungicides by separate mutation events. For example, Botrytis cinerea is resistant to both azoles and dicarboximide fungicides.

A common mechanism for acquiring resistance is alteration of the target enzyme. For example, Black Sigatoka, an economically important pathogen of banana, is resistant to the QoI fungicides, due to a single nucleotide change resulting in the replacement of one amino acid (glycine) by another (alanine) in the target protein of the QoI fungicides, cytochrome b.[9] It is presumed that this disrupts the binding of the fungicide to the protein, rendering the fungicide ineffective. Upregulation of target genes can also render the fungicide ineffective. This is seen in DMI-resistant strains of Venturia inaequalis.[10]

Resistance to fungicides can also be developed by efficient efflux of the fungicide out of the cell. Septoria tritici has developed multiple drug resistance using this mechanism. The pathogen had five ABC-type transporters with overlapping substrate specificities that together work to pump toxic chemicals out of the cell.[11]

In addition to the mechanisms outlined above, fungi may also develop metabolic pathways that circumvent the target protein, or acquire enzymes that enable the metabolism of the fungicide to a harmless substance.

Fungicides that are at risk of losing their potency due to resistance include Strobilurins such as azoxystrobin.[12] Cross-resistance can occur because the active ingredients share a common mode of action.[13] FRAC is organized by CropLife International.[14][12]

Safety

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Fungicides pose risks for humans.[15]

Fungicide residues have been found on food for human consumption, mostly from post-harvest treatments.[16] Some fungicides are dangerous to human health, such as vinclozolin, which has now been removed from use.[17] Ziram is also a fungicide that is toxic to humans with long-term exposure, and fatal if ingested.[18] A number of fungicides are also used in human health care.

See also

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Further reading

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  • Haverkate, F.; Tempel, A.; Held, A. J. (1969). "Interaction of 2,4,5-trichlorophenylsulphonylmethyl thiocyanate with fungal spores". Netherlands Journal of Plant Pathology. 75 (5): 308–315. doi:10.1007/BF02015493. S2CID 23304303.

References

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  1. ^ a b Dreikorn, Barry A.; Owen, W. John (2000). "Fungicides, Agricultural". Kirk-Othmer Encyclopedia of Chemical Technology. doi:10.1002/0471238961.0621140704180509.a01. ISBN 978-0-471-48494-3.
  2. ^ a b c Franz Müller; Peter Ackermann; Paul Margot (2012). "Fungicides, Agricultural, 2. Individual Fungicides". Ullmann's Encyclopedia of Industrial Chemistry. Weinheim: Wiley-VCH. doi:10.1002/14356007.o12_o06. ISBN 978-3-527-30673-2.
  3. ^ Mueller, Daren. "Fungicides:Terminology". Iowa State University. Retrieved June 1, 2013.
  4. ^ Latijnhouwers, Maita; de Wit, Pierre; Govers, Francine (2003). "Oomycetes and fungi: similar weaponry to attack plants". Trends in Microbiology. 11 (10). Cell Press: 462–469. doi:10.1016/j.tim.2003.08.002. ISSN 0966-842X. PMID 14557029. S2CID 22200121.
  5. ^ C.Michael Hogan. 2011. Sulfur. Encyclopedia of Earth, eds. A.Jorgensen and C.J.Cleveland, National Council for Science and the environment, Washington DC Archived October 28, 2012, at the Wayback Machine
  6. ^ Thao, Hoang Thi Bich; Yamakawa, Takeo (April 2009). "Phosphite (phosphorous acid): Fungicide, fertilizer or bio-stimulator?". Soil Science and Plant Nutrition. 55 (2): 228–234. Bibcode:2009SSPN...55..228T. doi:10.1111/j.1747-0765.2009.00365.x.
  7. ^ Pearson, M.N.; Beever, R.E.; Boine, B.; Arthur, K. (2009). "Mycoviruses of filamentous fungi and their relevance to plant pathology". Molecular Plant Pathology (Review). 10 (1): 115–128. doi:10.1111/j.1364-3703.2008.00503.x. PMC 6640375. PMID 19161358. S2CID 34331588.
  8. ^ Metcalfe, R.J.; Shaw, M.W.; Russell, P.E. (2000). "The effect of dose and mobility on the strength of selection for DMI (sterol demethylation inhibitors) fungicide resistance in inoculated field experiments". Plant Pathology. 49: 546–557. doi:10.1046/j.1365-3059.2000.00486.x.
  9. ^ Sierotzki, Helge (2000). "Mode of resistance to respiration inhibitors at the cytochrome bc1 enzyme complex of Mycosphaerella fijiensis field isolates". Pest Management Science. 56 (10): 833–841. doi:10.1002/1526-4998(200010)56:10<833::AID-PS200>3.0.CO;2-Q.
  10. ^ Schnabel G, Jones AL (January 2001). "The 14alpha-Demethylasse(CYP51A1) Gene is Overexpressed in Venturia inaequalis Strains Resistant to Myclobutanil". Phytopathology. 91 (1): 102–110. doi:10.1094/PHYTO.2001.91.1.102. PMID 18944284.
  11. ^ Zwiers LH, Stergiopoulos I, Gielkens MM, Goodall SD, De Waard MA (July 2003). "ABC transporters of the wheat pathogen Mycosphaerella graminicola function as protectants against biotic and xenobiotic toxic compounds". Mol Genet Genomics. 269 (4): 499–507. doi:10.1007/s00438-003-0855-x. PMID 12768412.
  12. ^ a b "Fungicides Resistance Action Committee website".
  13. ^ "Fungal control agents sorted by cross resistance pattern and mode of action" (PDF). 2020. Archived from the original (PDF) on 2021-08-16. Retrieved 2020-09-04.
  14. ^ "Resistance Management". CropLife International. 2018-02-28. Archived from the original on 2020-12-10. Retrieved 2020-11-22.
  15. ^ Lini RS, Scanferla DT, de Oliveira NG, Aguera RG, Santos TD, Teixeira JJ, Kaneshima AM, Mossini SA (January 2024). "Fungicides as a risk factor for the development of neurological diseases and disorders in humans: a systematic review". Crit Rev Toxicol. 54 (1): 35–54. doi:10.1080/10408444.2024.2303481. PMID 38288970.
  16. ^ Brooks and, G.T; Roberts, T.R, eds. (1999). Pesticide Chemistry and Bioscience. Royal Society of Chemistry. doi:10.1533/9781845698416. ISBN 978-1-84569-841-6. OCLC 849886156.
  17. ^ Hrelia P, Fimognari C, Maffei F, Vigagni F, Mesirca R, Pozzetti L, Paolini M, Cantelli Forti G (September 1996). "The genetic and non-genetic toxicity of the fungicide Vinclozolin". Mutagenesis. 11 (5): 445–53. doi:10.1093/mutage/11.5.445. PMID 8921505.
  18. ^ National Center for Biotechnology Information. PubChem Compound Database; CID=8722, https://pubchem.ncbi.nlm.nih.gov/compound/8722 (accessed Jan. 13, 2019)
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