L-Glufosinate

Glufosinate-ammonium, the second largest transgene crop resistant herbicide, is classified as a mobile persistent pollutant by the U.S. Environmental Protection Agencybecause of its slow decomposition and easy mobile transfer in a water environment. The chronic and multigeneration toxicity of this compound to environmental organisms are alarming. In this study, racemic glufosinate-ammonium and the effective isomer, l-glufosinate-ammonium, were used as the test agents. The developmental, neurotoxic and reproductive toxicities of Caenorhabditis elegans to their parents and progeny were studied by continuous exposure in water at concentrations of 0.1, 1, 10 and 100 μg/L. The causes of toxicity differences were analysed from oxidative stress and transcription levels. Through oxidative stress of C. elegans, racemic glufosinate-ammonium and l-glufosinate-ammonium both mediated the developmental toxicity (shortened developmental cycle, reduced body length and width, promoted ageingand decreased longevity), neurotoxicity (inhibited head swinging, body bending frequency and acetylcholinesterase [AchE] activity) and reproductive toxicity (significant reductions in the number of eggs and offspring in vivo and induced apoptosis of gonadal cells). These phenomena caused oxidative damage (protein and membrane lipid peroxidation) and further induced apoptosis. The changes in various indicators caused by racemic glufosinate-ammonium exposure were more significant than those caused by l-glufosinate-ammonium exposure, and the reproduction-related indicators were more significant than the developmental and neurological indicators. A continuous accumulation of toxicity was observed after multiple generations of continuous exposure. These research results provide a data reference for the ecotoxicological evaluation and risk assessment of glufosinate-ammonium and contribute to the revision and improvement of the related environmental policies of glufosinate-ammonium.

Weed interference in the crop field is one of the major biotic stresses causing dramatic crop yield losses, and the development of herbicide-resistant crops is critical for weed control in the application of herbicide technologies. To identify herbicide-resistant germplasms, we screened 854 maize inbreed lines and 25,620 seedlings by spraying them with 1 g/L glufosinate. One plant (L336R), possibly derived from a natural variation of line L336, was identified to have the potential for glufosinate tolerance. Genetic analysis validated that the glufosinate tolerance of L336R is conferred by a single locus, which was tentatively designated as ZmGHT1. By constructing a bi-parental population derived from L336R, and a glufosinate sensitive line L312, ZmGHT1 was mapped between molecular markers M9 and M10. Interestingly, genomic comparation between the two sequenced reference genomes showed that large scale structural variations (SVs) occurred within the mapped region, resulting in 2.16 Mb in the inbreed line B73, and 11.5 kb in CML277, respectively. During the fine mapping process, we did not detect any additional recombinant, even by using more than 9500 F2 and F3 plants, suspecting that SVs should also have occurred between L336R and L312 in this region, which inhibited recombination. By evaluating the expression of the genes within the mapped interval and using functional annotation, we predict that the gene Zm00001eb361930, encoding an aminotransferase, is the most likely causative gene. After glufosinate treatment, lower levels of ammonia content and a higher activity of glutamine synthetase (GS) in L336R were detected compared with those of L336 and L312, suggesting that the target gene may participate in ammonia elimination involving GS activity. Collectively, our study can provide a material resource for maize herbicide resistant breeding, with the potential to reveal a new mechanism for herbicide resistance.

Glufosinate-ammonium, a widely used chiral herbicide, has become the focus of attention because of its toxicity toward non-target organisms and its degradation behavior in the environment. With the introduction of L-glufosinate-ammonium products, the toxicity and environmental behavior of rac-glufosinate-ammonium and L-glufosinate-ammonium have become the subject of increasing interest. The overall goal of this study was to investigate the differences in toxicity and biodegradation of rac-glufosinate-ammonium and L-glufosinate-ammonium in an aquatic organism, Scenedesmus obliquus. The toxicity of rac-glufosinate-ammonium and L-glufosinate-ammonium to S. obliquus was compared by measuring EC50, malondialdehyde (MDA) content, protein content and antioxidant enzyme activity. The 96-h EC50 values of rac-glufosinate-ammonium and L-glufosinate-ammonium were 57.22 μg/mL and 25.55 μg/mL, respectively, which indicated that L-glufosinate-ammonium was more toxic to S. obliquus than rac-glufosinate-ammonium. Based on the MDA content, protein content, and antioxidant enzyme (SOD and CAT) activity, we found that L-glufosinate-ammonium could cause more serious oxidative damage than rac-glufosinate-ammonium. The residual amount of glufosinate-ammonium and its metabolites in the culture medium and S. obliquus were determined by HPLC-HRMS. Comparison of glufosinate-ammonium concentrations in algae-free and algae-containing media, showed that glufosinate-ammonium degradation in the S. obliquus system was significantly increased, and the degradation rate of L-glufosinate-ammonium was faster than that of D-glufosinate-ammonium. No enantiomerization was observed for pure L-glufosinate-ammonium treatment. N-acetyl-glufosinate was identified as the main metabolite of glufosinate-ammonium.