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Pesticides
Published in José L. Tadeo, Analysis of Pesticides in Food and Environmental Samples, 2019
José L. Tadeo, Beatriz Albero, Rosa Ana Pérez
Another enzyme involved in amino acid synthesis and used as a target for herbicides is the glutamine synthetase (GS), which makes glutamine from glutamate and ammonia. This enzyme is present in plants, where it plays an important role in nitrogen assimilation, as well as in animals, as glutamate is a neurotransmitter that can be inactivated by GS. The mode of action of the herbicide glufosinate is the inhibition of the enzyme GS.
The genetically modified food credibility gap
Published in Charlotte Fabiansson, Stefan Fabiansson, Food and the Risk Society, 2016
Charlotte Fabiansson, Stefan Fabiansson
Herbicide resistance is the most prevalent genetically engineered trait introduced so far. Crops have been commercialised that are resistant to the herbicides glyphosate or glufosinate. As weeds have grown resistant to glyphosate, companies have started to develop crops engineered to become resistant to multiple herbicides to allow farmers to use a mixed group of two, three or four different chemicals (Batista and Oliveira 2009).
Chemistry and Agriculture: Helping to Feed the World
Published in Richard J. Sundberg, The Chemical Century, 2017
Glufosinate is derived from a tripeptide antibiotic called bialaphos. The herbicidal activity was discovered at Hoechst in Germany. Glufosinate is a structural analog of glutamic acid and is an inhibitor of glutamate synthesis, which is critical to ammonia metabolism in plants.
Elimination of glufosinate ammonium from aqueous solution with hollow fiber supported liquid membrane and mathematical modeling
Published in Chemical Engineering Communications, 2023
Sarunchana Hinoon, Worada Triemtung, Boonta Chutvirasakul, Mali Hunsom, Prakorn Ramakul
Glufosinate ammonium is a broad-spectrum herbicide used to inhibit weeds in many countries. These phosphorus-containing tripeptides are produced naturally as a component of bacteria-derived bactericidal and fungicidal compound. The ammonium salt of glufosinate is one of the most employed herbicides worldwide. Glufosinate ammonium inhibits plant glutamine synthetase, causing accumulation of ammonium ions that halt photosynthesis, resulting in plant death. It is used for plant control in forestry, agricultural and urban applications (Lewis et al. 2016; Schwartz et al. 2004). Glufosinate ammonium is currently in high demand because of the global prohibition of paraquat, a highly toxic herbicide and the expansion of green agriculture (Yang and Zhang, 2020). Glufosinate ammonium herbicide is safe under conditions of recommended use but rapidly contaminates water and soil and is not eco-friendly. Toxicity data have been shown that large amounts of glufosinate ammonium intake has toxic effects toward gastrointestinal tract, central nervous system, cardiovascular events, and respiratory system (EFSA, 2015). Glufosinate ammonium can also induce immunotoxicity and deformity of zebrafish embryos (Xiong et al. 2019).
Prognostic value of neutrophil to lymphocyte ratio in the diagnosis of neurotoxicity after glufosinate ammonium poisoning
Published in Journal of Toxicology and Environmental Health, Part A, 2022
Joochan Kim, Byeong Jo Chun, Jeong Mi Moon, Yongsoo Cho
Glufosinate ammonium irreversibly inhibits glutamine synthetase which catalyzes the synthesis of glutamine from glutamate and ammonia. Glutamine synthetase inhibition leads to the accumulation of intracellular ammonia (Takano and Dayan 2020). As serum ammonia levels increase, uptake of ammonia by the brain also rises (Sorensen 2013). Elevated brain ammonia levels may induce activation of N-methyl-D-aspartate receptors, which increase intracellular calcium ions and nitric oxide. Therefore, a rise in ammonia levels in the brain following glufosinate ammonium poisoning may elevate intracellular calcium ion and nitric oxide levels. This effect might inhibit glutamine synthetase in nearby astrocytes, increasing consumption and reducing synthesis of adenosine triphosphate with consequent neurotoxicity eventually leading to cell death (Rodrigo et al. 2009).