|Ecological hazards:||hazardous to amphibians|
|Organic Gardening:||not permitted|
|Formulations (Brands):||Roundup, Rodeo, TOP UP48|
Glyphosate (N-(phosphonomethyl) glycine, C3H8NO5P) is a non-selective herbicide used to kill weeds, especially perennials.
Glyphosate is the primary ingredient in Monsanto's popular herbicide, Roundup. Many crops have been genetically engineered to be resistant to it. The chemical is only absorbed by the leaves of plants and it is not absorbed by roots from the soil.
Glyphosate is an aminophosphonic analogue of the natural amino acid glycine and the name is a contraction of glycine, phospho-, and -ate.
Glyphosate kills plants by inhibiting the enzyme 5-enolpyruvoyl-shikimate-3-phosphate synthase (EPSPS), which forms the aromatic amino acids: phenylalanine, tyrosine and tryptophan. EPSPS catalyzes the reaction of shikimate 3-phosphate (S3P) and phosphoenolpyruvate (PEP) to form ESP and phosphate. The aromatic amino acids are also used to make secondary metabolites such as folates, ubiquinones and naphthoquinones. The shikimate pathway is not present in animals. CAS: 1071-83-6
Glyphosate is applied as a spray or a paint. Concentrations depend on the particular formulation used.
There are concerns about the effects of glyphosate (and Roundup) on non-plant species. For more information, see Roundup.
Glyphosate binds tightly to soil so it does not end up passing through the soil and ending up in the aquifers. It is rapidly metabolized in the soil by dephosphorylation.
However, it should be noted that the government of Denmark banned spraying of glyphosate in Sept 2003 after groundwater concentrations over 5 times the allowed limit were discovered. Furthermore, glyphosate groundwater residues are documented in Canada, the Netherlands and also in the USA, as well as, off coast in many marine environments. (For more information please see http://www.national-toxic-encephalopathy-foundation.org/roundup.pdf)
In-vitro studies (Walsh, et al. 2000) have shown glyphosate to have an effect on progesterone production in mammalian cells and can affect mortality of placental cells in-vitro (Richard, et al. 2005). Whether these studies classify glyphosate as an endocrine disruptor is a matter of debate.
Some feel that in-vitro studies are insufficient, and are waiting to see if animal studies show a change in endocrine activity, since a change in a single cell line may not occur in an entire organism. Additionally, current in-vitro studies expose cell lines to concentrations orders of magnitude greater than would be found in real conditions, and through pathways that would not be experienced in real organism. Current toxicological studies of higher order mammals (EU 2002) have suggested no endocrine disruption even at high doses.
Others feel that in-vitro studies, particularly ones identifying not only an effect, but a chemical pathway, are sufficient evidence to classify glyphosate as an endocrine disruptor, on the basis that even small changes in endocrine activity can have lasting effects on an entire organism that may be difficult to detect through whole organism studies alone. Further research on the topic has been planned, and should shed more light on the debate.
Some microorganisms have a version of 5-enolpyruvoyl-shikimate-3-phosphate synthetase (EPSPS) that is resistant to glyphosate inhibition. The version used in genetically modified crops was isolated from Agrobacterium strain CP4 (CP4 EPSPS) that was resisitant to glyphosate. The CP4 EPSPS gene was cloned and inserted into soybeans. The CP4 EPSPS gene was engineered for plant expression by fusing the 5' end of the gene to a chloroplast transit peptide derived from the petunia EPSPS. This transit peptide was used because it had shown previously an ability to deliver bacterial EPSPS to the chloroplasts of other plants. The plasmid used to move the gene into soybeans was PV-GMGTO4. It contained three bacterial genes, two PC4 EPSPS genes, and a gene encoding beta-glucuronidase (GUS) from Escherichia coli as a marker. The DNA was injected into the soybeans using the particle acceleration method. Soybean cultivar A54O3 was used for the transformation. The expression of the GUS gene was used as the initial evidence of transformation. GUS expression was detected by a staining method in which the GUS enzyme converts a substrate into a blue precipitate. Those plants that showed GUS expression were then taken and sprayed with glyphosate and their tolerance was tested over many generations.
In 1996, genetically modified soybeans were available commercially(). This greatly improved the ability to control weeds in soybean fields since glyphosate could be sprayed on fields without hurting the crop. As of 2004, glyphosate was used on 80% of U.S. soybean fields to eliminate weeds.
- EU (2002). Review report for the active substance glyphosate. Retrieved October 28, 2005.
- U.S. EPA ReRegistration Decision Fact Sheet for Glyphosate. http://www.epa.gov/oppsrrd1/REDs/factsheets/0178fact.pdf]. Retrieved Nov 13, 2005.
- Walsh, et al (2000). "Roundup inhibits steroidogenesis by disrupting steroidogenic acute regulatory (stAR) protein expression.". Environmental Health Perspectives 108-N8: 769–776.
- Sophie Richard, Safa Moslemi, Herbert Sipahutar, Nora Benachour, Gilles-Eric Seralini (2005). "Differential effects of glyphosate and Roundup on human placental cells and aromatase". Environmental Health Perspectives 113-N6: 716–720.
- JP Giesy, KR Solomon, S Dobson (2000). "Ecotoxicological Risk Assessment for Roundup Herbicide". Reviews of Environmental Contamination and Toxicology 167: 35–120.
- GM Williams, R Kroes, JC Munro (2000). "Safety evaluation and risk assessment of the herbicide Roundup and its active ingredient, glyphosate, for humans". Regulatory Toxicology and Pharmacology 31-N2: 117–165.
- KR Solomon, DG Thompson (2003). "Ecological risk assessment for aquatic organisms from over-water uses of glyphosate". Journal of Toxicology and Environmental Health 6: 289–324.
- World Health Organization. (1994) Environmental Health Critera 159: Glyphosate.