Difference between revisions of "Glyphosate"

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:"Glyphosate inhibits plant growth by inhibiting the production of essential aromatic amino acids through competitive inhibition of the enzyme enolpyruvylshikimate phosphate (EPSP) synthase. This is a key enzyme in the shikimic acid pathway for the synthesis of chorismate..., which is a precursor for the essential amino acids phenylalanine, tyrosine, and tryptophan."<ref>John P. Giesy, Stuard Dobson, and Keith R. Solomon, 2000, "[http://www.colby.edu/biology/BI402B/Giesy%20et%20al%202000.pdf Ecotoxicological Risk Assessment for Roundup Herbicide]," Rev Environ Contam Toxicol 167:35-120.</ref>
 
:"Glyphosate inhibits plant growth by inhibiting the production of essential aromatic amino acids through competitive inhibition of the enzyme enolpyruvylshikimate phosphate (EPSP) synthase. This is a key enzyme in the shikimic acid pathway for the synthesis of chorismate..., which is a precursor for the essential amino acids phenylalanine, tyrosine, and tryptophan."<ref>John P. Giesy, Stuard Dobson, and Keith R. Solomon, 2000, "[http://www.colby.edu/biology/BI402B/Giesy%20et%20al%202000.pdf Ecotoxicological Risk Assessment for Roundup Herbicide]," Rev Environ Contam Toxicol 167:35-120.</ref>
  
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In other words, glyphosate prevents plants from making amino acids they need to survive. It does this by inhibiting an enzyme needed to make chorismate, a precursor to those amino acids.
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In other words, glyphosate prevents plants from making amino acids they need to survive. It does this by inhibiting an enzyme needed to make chorismate, a precursor to those amino acids. One of these amino acids, tryptophan, "is necessary for the synthesis of indolylacetic acid (IAA), the main growth promoter, that can explain the widespread field observation of reduced in depth root growth of plants."<ref>Preface "Glyphosate interactions with physiology, nutrition, and diseases of plants: Threat to agricultural sustainability?", European Journal of Agronomy 31 (2009) 111-113.</ref>
  
 
A 1984 study found plants that died following treatment with glyphosate were infected with pathogenic fungi, compared to control plants not treated with glyphosate but planted in the same media that did not yield pathogenic fungi.<ref>Gurmukh S. Johal and James E. Rahe, "[http://www.nationalorganiccoalition.org/resources/Biblio/glyphosatepathogenkillRahe.pdf Effect of soilborne plant-pathogenic fungi on the herbicidal action of glyphosate on bean seedlings]," ''Phytopathology'' (1984), 74:950-955.</ref> The study concluded that more research was needed but postulated that glyphosate inhibits the plant's defense mechanisms and/or increases nutrient leakage from treated plants.
 
A 1984 study found plants that died following treatment with glyphosate were infected with pathogenic fungi, compared to control plants not treated with glyphosate but planted in the same media that did not yield pathogenic fungi.<ref>Gurmukh S. Johal and James E. Rahe, "[http://www.nationalorganiccoalition.org/resources/Biblio/glyphosatepathogenkillRahe.pdf Effect of soilborne plant-pathogenic fungi on the herbicidal action of glyphosate on bean seedlings]," ''Phytopathology'' (1984), 74:950-955.</ref> The study concluded that more research was needed but postulated that glyphosate inhibits the plant's defense mechanisms and/or increases nutrient leakage from treated plants.

Revision as of 07:46, 11 April 2011

Glyphosate, N-phosphonomethyl glycine, is broad-spectrum herbicide, sold under the brand name Roundup. It is "the most widely used broad-spectrum herbicide on [a] global scale."[1] Some genetically engineered crops, sold as Roundup Ready Crops have their DNA altered to allow them to withstand glyphosate. Commercial formulations of glyphosate were first sold in 1974.[2]

How It Works

Glyphosate is absorbed through a plant's foliage and then transported throughout the stems, leaves, and roots of the entire plant.

"Glyphosate inhibits plant growth by inhibiting the production of essential aromatic amino acids through competitive inhibition of the enzyme enolpyruvylshikimate phosphate (EPSP) synthase. This is a key enzyme in the shikimic acid pathway for the synthesis of chorismate..., which is a precursor for the essential amino acids phenylalanine, tyrosine, and tryptophan."[3]

In other words, glyphosate prevents plants from making amino acids they need to survive. It does this by inhibiting an enzyme needed to make chorismate, a precursor to those amino acids. One of these amino acids, tryptophan, "is necessary for the synthesis of indolylacetic acid (IAA), the main growth promoter, that can explain the widespread field observation of reduced in depth root growth of plants."[4]

A 1984 study found plants that died following treatment with glyphosate were infected with pathogenic fungi, compared to control plants not treated with glyphosate but planted in the same media that did not yield pathogenic fungi.[5] The study concluded that more research was needed but postulated that glyphosate inhibits the plant's defense mechanisms and/or increases nutrient leakage from treated plants.

When more research was completed, "Rahe and coworkers documented that severe root infection associated with glyphosate-treated plants was due to disruption of synthesis of plant defense compounds, or phytoalexins, through the shikimate pathway there by predisposing plants to attack by soilborne fungal pathogens (Johal and Rahe, 1988; Lévesque et al., 1987).[6][7] Thus, infection by soilborne pathogens caused by the inability of plants to synthesize phytoalexins contributed to the overall herbicidal efficacy of glyphosate and was considered a “secondary mode of action” of glyphosate. These findings were significant because the release of glyphosate into the environment was found to have considerably more and far-reaching effects than the original notion that was limited to only the localized disruption of a specific metabolic pathway within a target plant."[8]

Impact on Non-Target Plants

Once glyphosate travels to a plant's roots, it is "released into the rhizosphere," (the area immediately around the roots), "where it is immobilized at the soil matrix or microbially degraded.[9] However, some of the glyphosate remains in dead plant tissues. A 2009 study found that non-target plants continue to be impacted by glyphosate toxicity up to three weeks after glyphosate application.[10]

Impacts of Glyphosate Drift

At sub-lethal doses of glyphosate, such as the amounts a plant might be exposed to from spray drift, plants are still impacted. A study examined sunflowers treated with small amounts of glyphosate (to simulate spray drift) found:[11]

"In conclusion, the results presented in this study showing that glyphosate is especially inhibitory to ferric reductase complement the recently published report (Eker etal., 2006) that glyphosate exerts a strong inhibitory influence on ferric reductase activity of Fe-deficient roots and impairs the uptake and translocation of Fe in plants. These impairments could be a major reason for the increasingly observed Fe deficiency chlorosis in cropping systems associated with widespread glyphosate usage as reported for different parts of the USA (Franzen etal., 2003; Jolley etal., 2004). Such strong interference of glyphosate with root uptake and root-to-shoot transport of Fe in crop plants may represent a potential threat to human and animal nutrition because of possible reduction of Fe in edible plants parts (e.g. seed/grain)."

In other words, low doses of glyphosate equal to the amount plants are exposed to in spray drift, can result in iron deficiencies in the plants. For crops destined as animal feed or as human food, this could result in decreased dietary iron.

Impact on Microorganisms

"Subsequent research on glyphosate interactions with soil microorganisms demonstrated that although glyphosate was metabolized by a segment of the microbial population, it was also toxic to several bacteria and fungi; the net effect glyphosate appeared to be a disruption of soil and root microbial community composition because selected components of the microbial community were stimulated while others were suppressed."[12][13][14]

Glyphosate in the Environment

Although glyphosate is highly soluble in water, its tendency to bond to soils makes it unlikely to leach into groundwater or runoff "significantly." (Studies have found about 1%-2% of glyphosate may runoff in rainfall after glyphosate is applied.[15])

Glyphosate in the Soil

Glyphosate can reach the soil by washing off the foliage of plants, via spray drift, by exudation from the roots of treated plants, or by the decomposition of treated plants. However, "risks of glyphosate toxicity to non-target organisms in soils are generally considered as marginal,since glyphosate is almost instantaneously inactivated by adsorption to clay minerals and cationic binding sites of the soil matrix (Piccoloetal.,1992;Dong-Meietal.,2004), while glyphosate in the soil solution is prone to rapid microbial degradation (Giesy et al., 2000)."[16][17] In other words, glyphosate residues in the soil are not considered hazardous as it either breaks down quickly or binds to minerals that make it no longer a threat to plants. Glyphosate that biodegrades usually breaks down into carbon dioxide and ammonium (NH4+).[18] In an analysis of 47 studies, 50% of glyphosate broke down in the soil in time periods ranging from 1.2 days to 197.3 days. The arithmetic mean amount of time was 32 days and the geometric mean was 17 days.[19]

Although glyphosate is mostly broken down by microbes or bound to the soil, a 2009 study found that "the root tissue of glyphosate-treated weeds represents a storage pool for glyphosate."[20]

Glyphosate in Water

Although most glyphosate applied to soil does not run off into waterways, sometimes glyphosate is applied to aquatic environments directly. In flowing water, it is dissipated via "tributary dilution, dispersion, and loss through processes such as absorption to suspended particulate matter or sediments and microbial degradation."[21] The half-life of glyphosate in water has been estimated to be from 7 to 14 days.[22]

Articles and resources

Related SourceWatch articles

References

  1. ↑ Tsehaye Tesfamariam, S. Bott, I. Cakmak, V. Römheld, G. Neumann, "Glyphosate in the rhizosphere – role of waiting times and different glyphosate binding forms in soils for phytoxicity to non-target plants," European Journal of Agronomy (2009), 31:126-132.
  2. ↑ John P. Giesy, Stuard Dobson, and Keith R. Solomon, 2000, "Ecotoxicological Risk Assessment for Roundup Herbicide," Rev Environ Contam Toxicol 167:35-120.
  3. ↑ John P. Giesy, Stuard Dobson, and Keith R. Solomon, 2000, "Ecotoxicological Risk Assessment for Roundup Herbicide," Rev Environ Contam Toxicol 167:35-120.
  4. ↑ Preface "Glyphosate interactions with physiology, nutrition, and diseases of plants: Threat to agricultural sustainability?", European Journal of Agronomy 31 (2009) 111-113.
  5. ↑ Gurmukh S. Johal and James E. Rahe, "Effect of soilborne plant-pathogenic fungi on the herbicidal action of glyphosate on bean seedlings," Phytopathology (1984), 74:950-955.
  6. ↑ Johal, G.S., Rahe, J.E., 1988. Glyphosate, hypersensitivity and phytoalexins accumulation in the incompatible bean anthracnose host-parasite interaction. Physiol. Mol. Plant Pathol. 32, 267-281
  7. ↑ Lévesque, C.A., Rahe, J.E., Eaves, D.M., 1987. Effects of glyphosate on Fusarium spp.: its influence on root colonization of weeds, propagule density in the soil, and crop emergence. Can. J. Microbiol. 33, 354-360.
  8. ↑ Preface "Glyphosate interactions with physiology, nutrition, and diseases of plants: Threat to agricultural sustainability?", European Journal of Agronomy 31 (2009) 111-113.
  9. ↑ Tsehaye Tesfamariam, S. Bott, I. Cakmak, V. Römheld, G. Neumann, "Glyphosate in the rhizosphere – role of waiting times and different glyphosate binding forms in soils for phytoxicity to non-target plants," European Journal of Agronomy (2009), 31:126-132.
  10. ↑ Tsehaye Tesfamariam, S. Bott, I. Cakmak, V. Römheld, G. Neumann, "Glyphosate in the rhizosphere – role of waiting times and different glyphosate binding forms in soils for phytoxicity to non-target plants," European Journal of Agronomy (2009), 31:126-132.
  11. ↑ Levent Ozturk, Atilla Yazici, Selim Eker, Ozgur Gokmen, Volker Römheld, and Ismail Cakmak, "Glyphosate inhibition of ferric reductase activity in iron deficient sunflower roots," New Phytologist (2008), 177:899-906.
  12. ↑ Preface "Glyphosate interactions with physiology, nutrition, and diseases of plants: Threat to agricultural sustainability?", European Journal of Agronomy 31 (2009) 111-113.
  13. ↑ Wardle, D.A., Parkinson, D.A., 1992. Influence of the herbicides 2,4-D and glyphosate on soil microbial biomass and activity: a field experiment. Soil Biol. Biochem. 24, 185-186.
  14. ↑ Busse, M.D., Ratcliffe, A.W., Shestak, C.J., Powers, R.F., 2001. Glyphosate toxicity and the effects of long-term vegetation control on soil microbial community. Soil Biol. Biochem. 33, 1777-1789.
  15. ↑ John P. Giesy, Stuard Dobson, and Keith R. Solomon, 2000, "Ecotoxicological Risk Assessment for Roundup Herbicide," Rev Environ Contam Toxicol 167:35-120.
  16. ↑ Tsehaye Tesfamariam, S. Bott, I. Cakmak, V. Römheld, G. Neumann, "Glyphosate in the rhizosphere – role of waiting times and different glyphosate binding forms in soils for phytoxicity to non-target plants," European Journal of Agronomy (2009), 31:126-132.
  17. ↑ John P. Giesy, Stuard Dobson, and Keith R. Solomon, 2000, "Ecotoxicological Risk Assessment for Roundup Herbicide," Rev Environ Contam Toxicol 167:35-120.
  18. ↑ John P. Giesy, Stuard Dobson, and Keith R. Solomon, 2000, "Ecotoxicological Risk Assessment for Roundup Herbicide," Rev Environ Contam Toxicol 167:35-120.
  19. ↑ John P. Giesy, Stuard Dobson, and Keith R. Solomon, 2000, "Ecotoxicological Risk Assessment for Roundup Herbicide," Rev Environ Contam Toxicol 167:35-120.
  20. ↑ Tsehaye Tesfamariam, S. Bott, I. Cakmak, V. Römheld, G. Neumann, "Glyphosate in the rhizosphere – role of waiting times and different glyphosate binding forms in soils for phytoxicity to non-target plants," European Journal of Agronomy (2009), 31:126-132.
  21. ↑ John P. Giesy, Stuard Dobson, and Keith R. Solomon, 2000, "Ecotoxicological Risk Assessment for Roundup Herbicide," Rev Environ Contam Toxicol 167:35-120.
  22. ↑ John P. Giesy, Stuard Dobson, and Keith R. Solomon, 2000, "Ecotoxicological Risk Assessment for Roundup Herbicide," Rev Environ Contam Toxicol 167:35-120.

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