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Sources of Essential Oils
Published in K. Hüsnü Can Başer, Gerhard Buchbauer, Handbook of Essential Oils, 2020
Chlodwig Franz, Johannes Novak
Genetic engineering is defined as the direct manipulation of the genes of organisms by laboratory techniques, not to be confused with the indirect manipulation of genes in traditional (plant) breeding. Transgenic or GMOs are organisms (bacteria, plants, etc.) that have been engineered with single or multiple genes (either from the same species or from a different species), using contemporary molecular biology techniques. These are organisms with improved characteristics, in plants, for example, with resistance or tolerance to biotic or abiotic stresses such as insects, disease, drought, salinity, and temperature. Another important goal in improving agricultural production conditions is to facilitate weed control by transformed plant resistant to broadband herbicides like glufosinate. Peppermint has been successfully transformed with the introduction of the bar gene, which encodes phosphinothricin acetyltransferase, an enzyme inactivating glufosinate ammonium or the ammonium salt of glufosinate, phosphinothricin, making the plant insensitive to the systemic, broadspectrum herbicide Roundup (Roundup Ready mint) (Li et al., 2001).
Major component causing neurological toxicity in acute glufosinate ammonium poisoning: determination of glufosinate, 1-methoxy-2-propanol, and ammonia in serum and cerebrospinal fluid
Published in Clinical Toxicology, 2022
Seonghoon Yeon, Sung Hwa Kim, Juhyun Sim, Sunchun Kim, Yoonsuk Lee, Hyun Kim, Yong Sung Cha
The mechanism of this increase in serum ammonia concentration in GLA poisoning is not clearly understood. Glufosinate is available as an ammonium salt and thus may be a source of ingested free ammonia. However, there is no information regarding neurological effects of ammonia or ammonium compounds in humans after oral exposure [20]. Glufosinate is a glutamate analogue that reportedly inhibits GS in plants and blocks the synthesis of glutamine from glutamate and ammonia [9]. Glufosinate has also been reported to inhibit the activity of GS in vitro [21] through affecting the metabolic pathway of glutamic acid and the glutamic acid receptors in the brain [22]. Therefore, inhibition of GS by serum glufosinate in the acute phase of human GLA poisoning might lead to a further increase in ammonia levels in the brain, by inhibiting the already saturated GS. In animal studies, the metabolism of GLA was limited (up to 30% of the absorbed dose) and the main urinary and tissue residues were 3-[hydroxy(methyl)phosphinoyl] propionic acid, methylphosphinico butanoic acid, and 2-hydroxy-4-methylphosphinicobutanoic acid. In faeces, significant concentrations (up to 10%) of N-acetylglufosinate were detected, and there is no evidence of this metabolite having pathological findings suggesting a relationship with neurotoxicity [23]. A comparative study of the inhibition of GS in tissues from groups of ten male rats given diets containing N-acetylglufosinate and GLA was performed. The results indicated that orally administered GLA is approximately ten times more potent at inhibiting GS than N-acetylglufosinate [23].
Pesticide use, agricultural outputs, and pesticide poisoning deaths in Japan
Published in Clinical Toxicology, 2022
Michael Eddleston, Hiroshi Nagami, Chien-Yu Lin, Mark L. Davis, Shu-Sen Chang
A broad range of less hazardous pesticides (n = 529) are now registered in Japan. Recent reports of pesticide poisoning indicate that many cases now follow ingestion of the herbicides glyphosate [47] and glufosinate [48] and the insecticides fenitrothion [49,50] and imidacloprid [51]. These pesticides are of WHO hazard classes II and III, with lower case fatality than paraquat or Class I OP insecticides.