This study explored nitrogen (N)-dependent interaction between Microcystis and chloramphenicol (CAP) along 20 day-test. Results showed that 5 mg/L N largely alleviated inhibitory effects of CAP on Microcystis growth, while 50 and 0.5 mg/L N exacerbated growth-inhibition by CAP especially in early (before day 8) and mid–late stage, respectively. At each N level, CAP-induced antioxidant defense and cell damage extents were negatively correlated to growth state in each stage, and CAP-biodegradation coincided with Microcystis growth and glutathione synthesis dynamics, implying that antioxidant defense, cell damage and CAP-removal closely linked to N-dependent Microcystis growth under CAP-stress. Microcystin (MC)-production and -release under CAP-stress were also N-dependent. Although Microcystis growth was greatly-inhibited by prolonged CAP-stress at 0.5 mg/L N, delayed CAP-loss and high MC-release at 0.5 mg/L N should be emphasized during Microcystis-dominated cyanobacterial blooms (MCBs) and CAP co-occurrence. This study had great implication in risk assessment for MCBs–CAP co-occurrence in different waters.

中文翻译：

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在各种与环境相关的氮水平下，产毒微囊藻对氯霉素-应力的生长和细胞响应。

这项研究探索了20天试验中微囊藻和氯霉素（CAP）之间氮（N）依赖性的相互作用。结果表明，5 mg / LN在很大程度上减轻了CAP对微囊藻生长的抑制作用，而50和0.5 mg / LN分别加剧了CAP的生长抑制作用，尤其是在早期（第8天之前）和中后期。在每个氮水平上，CAP诱导的抗氧化防御和细胞损伤程度与每个阶段的生长状态均呈负相关，并且CAP生物降解与微囊藻的生长和谷胱甘肽合成动力学相吻合，这表明抗氧化防御，细胞损伤和CAP去除紧密相关。 N依赖性微囊藻在CAP压力下增长。CAP胁迫下微囊藻毒素（MC）的产生和释放也是N依赖性的。尽管在0.5 mg / LN的条件下长时间的CAP胁迫极大地抑制了微囊藻的生长，但在以微囊藻为主导的蓝细菌水华（MCBs）和CAP共存的过程中，应强调延迟的CAP丢失和0.5 mg / LN的高MC释放。这项研究在不同水域对MCBs-CAP共存的风险评估中具有重要意义。