氟苯尼考,作为氯霉素的替代品,可以与70S核糖体的50S亚基中的23SrRNA的A位点紧密结合,从而抑制蛋白质合成和细菌增殖。由于在水产养殖和兽医学中的广泛使用,氟苯尼考已在全球水生环境中被检测到。近年来,人们对氟苯尼考对目标和非目标生物的影响和健康风险的担忧日益增加。尽管氟苯尼考的生态毒性在不同的物种中得到了广泛的报道,尚未尝试审查氟苯尼考毒性的当前进展,hormesis,及其对生物群的健康风险。在这项研究中,进行了全面的文献综述,以总结氟苯尼考对包括细菌在内的各种生物的影响,藻类,无脊椎动物,鱼,鸟,和哺乳动物。产生抗生素抗性细菌并传播抗生素抗性基因,与hormesis密切相关,由于过度使用或滥用包括氟苯尼考在内的抗生素而引起的紧迫的环境健康问题。在几种藻类中暴露于μg/L-mg/L的氟苯尼考引起的蜂群效应,和染色体可能作为氟苯尼考诱导作用的目标;然而,根本的分子机制是完全缺乏的。暴露于高水平(mg/L)的氟苯尼考改变了生物异源代谢,抗氧化系统,和能量代谢,导致肝毒性,肾毒性,免疫毒性,发育毒性,生殖毒性,致肥胖效应,和不同动物物种的兴奋。线粒体和相关的能量代谢被认为是动物中氟苯尼考毒性的主要目标,尽管需要进一步深入调查以揭示长期影响(例如,整个生命周期的影响,氟苯尼考的多代效应),尤其是在环境层面,以及潜在的机制。这将有助于评估潜在的毒副反应,并为氟苯尼考的环境风险评估和监管构建不良结果途径。
Florfenicol, as a replacement for chloramphenicol, can tightly bind to the A site of the 23S rRNA in the 50S subunit of the 70S ribosome, thereby inhibiting protein synthesis and bacterial proliferation. Due to the widespread use in aquaculture and veterinary medicine, florfenicol has been detected in the aquatic environment worldwide. Concerns over the effects and health risks of florfenicol on target and non-target organisms have been raised in recent years. Although the ecotoxicity of florfenicol has been widely reported in different species, no attempt has been made to
review the current research progress of florfenicol toxicity, hormesis, and its health risks posed to biota. In this study, a comprehensive literature
review was conducted to summarize the effects of florfenicol on various organisms including bacteria, algae, invertebrates, fishes, birds, and mammals. The generation of antibiotic resistant bacteria and spread antibiotic resistant genes, closely associated with hormesis, are pressing environmental health issues stemming from overuse or misuse of antibiotics including florfenicol. Exposure to florfenicol at μg/L-mg/L induced hormetic effects in several algal species, and chromoplasts might serve as a target for florfenicol-induced effects; however, the underlying molecular mechanisms are completely lacking. Exposure to high levels (mg/L) of florfenicol modified the xenobiotic metabolism, antioxidant systems, and energy metabolism, resulting in hepatotoxicity, renal toxicity, immunotoxicity, developmental toxicity, reproductive toxicity, obesogenic effects, and hormesis in different animal species. Mitochondria and the associated energy metabolism are suggested to be the primary targets for florfenicol toxicity in animals, albeit further in-depth investigations are warranted for revealing the long-term effects (e.g., whole-life-cycle impacts, multigenerational effects) of florfenicol, especially at environmental levels, and the underlying mechanisms. This will facilitate the evaluation of potential hormetic effects and construction of adverse outcome pathways for environmental risk assessment and regulation of florfenicol.