Desvendado o mecanismo de ação rápida do herbicida amônio-glufosinato

O amônio-glufosinato é um herbicida de contato, não-seletivo e de amplo espectro de controle sobre plantas daninhas. No Brasil e no mundo, este herbicida é amplamente utilizado em dessecação pré-plantio, culturas perenes ou em pós-emergência de culturas anuais contendo a tecnologia Liberty Link.

Uma das características marcantes do amônio-glufosinato é o seu rápido efeito de dessecação sobre plantas suscetíveis. Apesar de ser um herbicida inibidor da glutamina sintetase, as causas do rápido efeito (ação de contato) sobre as plantas eram atribuídas ao acúmulo de amônia e à inibição da fotossíntese.

No entanto, uma pesquisa recentemente publicada por pesquisadores da Universidade do Colorado nos Estados Unidos, mostrou que a rápida ação do amônio-glufosinato sobre plantas daninhas deve-se ao acúmulo de espécies reativas de oxigênio.

Em altas concentrações, estas formas reativas de oxigênio são extremamente tóxicas para as plantas pelo fato delas reagirem com lipídios na membrana plasmática, causando o extravasamento celular.

Esta descoberta pode abrir portas para o desenvolvimento de estratégias de controle e manejo da resistência com o uso deste herbicida.

Para saber mais sobre a pesquisa, o artigo encontra-se disponível para leitura no link aqui

Reactive oxygen species trigger the fast action of glufosinate

Abstract

Main conclusion Glufosinate is primarily toxic to plants due to a massive light-dependent generation of reactive oxygen species rather than ammonia accumulation or carbon assimilation inhibition.

Glutamine synthetase (GS) plays a key role in plant nitrogen metabolism and photorespiration. Glufosinate (C5H12NO4P) targets GS and causes catastrophic consequences leading to rapid plant cell death, and the causes for phytoxicity have been attributed to ammonia accumulation and carbon assimilation restriction. This study aimed to examine the biochemical and physiological consequences of GS inhibition to identify the actual cause for rapid phytotoxicity. Monocotyledonous and dicotyledonous species with different forms of carbon assimilation (C3 versus C4) were selected as model plants. Glufosi-nate sensitivity was proportional to the uptake of herbicide between species. Herbicide uptake also correlated with the level of GS inhibition and ammonia accumulation in planta even with all species having the same levels of enzyme sensitivity invitro. Depletion of both glutamine and glutamate occurred in glufosinate-treated leaves; however, amino acid starvation would be expected to cause a slow plant response. Ammonia accumulation in response to GS inhibition, often reported as the driver of glufosinate phytotoxicity, occurred in all species, but did not correlate with either reductions in carbon assimilation or cell death. This is supported by the fact that plants can accumulate high levels of ammonia but show low inhibition of carbon assimilation and absence of phytotoxicity. Glufosinate-treated plants showed a massive light-dependent generation of reactive oxygen species, followed by malondialdehyde accumulation. Consequently, we propose that glufosinate is toxic to plants not because of ammonia accumulation nor carbon assimilation inhibition, but the production of reactive oxygen species driving the catastrophic lipid peroxidation of the cell membranes and rapid cell death.

Keywords: Glutamine synthetase, Phosphinothricin, Ammonia accumulation, Photosynthesis, Light dependent, Lipid peroxidation

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Fonte: Hudson K. Takano