Fluoroquinolone antibiotic enrofloxacin (ENR) is frequently detected in agricultural environments. The hormesis and detrimental effects of ENR on crops have been extensively observed. However, the molecular mechanisms underlying these crops' responses to ENR remain limited. Here, integrated physiological, transcriptomic, and metabolomic analysis revealed the key metabolic pathway responses underlying the ENR-induced effects on rice. The results showed that ENR mainly affected three metabolic pathways: 'biosynthesis of amino acids', "tryptophan metabolism", and 'phenylpropanoid/flavonoid biosynthesis'. A low level of ENR treatment promoted root elongation and enhanced the antioxidant capacity by increasing the phytohormone gibberellin A3 and the flavonol quercetin-3-O-neohesperidoside, respectively. However, the high dose of ENR significantly stimulated ROS production, inhibited photosynthesis, and ultimately impaired plant growth. In response to high ENR toxicity, plants accumulated more quercetin derivatives as antioxidants and produced defense-related substances, such as N-hydroxytryptamine, indole-3-acetonitrile, and jasmonic acid, to combat biotic stress. In conclusion, this study provides new insights into the molecular mechanism accounting for the ecological effects of antibiotic pollution in farmland.
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