摘要
N-棕榈酰基伏马毒素B 1(N-palmitoyl fumonisin B 1,NPF)是伏马毒素B 1经棕榈酰化而成的衍生物。作为一种新兴的隐蔽型真菌毒素,有关NPF的毒理学研究仍处于起步阶段,限制了相关健康风险评估的开展。本研究以斑马鱼为受试生物,首次考察了低、中、高3个亚致死浓度(1 mg·L^(-1)、3 mg·L^(-1)、9 mg·L^(-1))NPF急性暴露对斑马鱼的神经行为影响和氧化胁迫效应。结果表明,NPF暴露至5 dpf后,斑马鱼幼鱼的自发运动活跃度受到了显著抑制,3个浓度组的总运动距离和平均游速与对照组相比下降61%~90%;对明暗刺激的反应能力亦有所下降,但仅在高浓度组表现出显著性差异(比对照组下降49%);十字迷宫色彩偏好实验中,经低浓度NPF暴露至6 dpf后,斑马鱼幼鱼的色彩偏好有所改变,在4个颜色区块中呈均匀化分布;生化指标方面,NPF暴露至5 dpf后,斑马鱼体内的活性氧(ROS)水平呈浓度依赖性升高(比对照组升高36%~125%),3种抗氧化酶的活性则表现出不同的效应,其中,超氧化物歧化酶(SOD)的活性受到显著抑制(比对照组下降35%~65%),过氧化氢酶(CAT)的活性却表现为显著提高(比对照组提升200%~560%),而谷胱甘肽过氧化物酶(GPx)的活性略有上升但仅高浓度组有显著性差异,此外,神经递质乙酰胆碱代谢中的限速酶——乙酰胆碱酯酶(AChE)的活性亦受到显著抑制(比对照组降低28%~67%)。综上,本研究发现,经亚致死浓度的NPF急性暴露后,斑马鱼的运动行为受到了显著抑制,结合斑马鱼体内ROS水平以及抗氧化酶和乙酰胆碱酯酶的活性变化,推测NPF可通过诱导氧化应激对斑马鱼产生神经毒性,其作用机制则有待深层次的基因水平研究。上述研究结果有望为NPF的进一步神经毒理学研究和健康风险评估提供基础和参考依据。
N-palmitoyl fumonisin B 1(NPF)is derived from fumonisin B 1 by introduction of an palmitoyl group on its amino nitrogen.As an emerging modified mycotoxin,toxicological research on NPF is very limited,making it difficult to carry out health risk assessment on it.In the present study,neurobehavioral effects and oxidative stress of NPF on zebrafish(Danio rerio)embryos and larvae were investigated,using three sub-lethal concentrations(1 mg·L^(-1),3 mg·L^(-1),9 mg·L^(-1))of NPF.After exposure to NPF until 5 dpf,spontaneous locomotive activity of z ebrafish larvae was significantly inhibited,for all the three treatment groups,total movement distance and average swimming speed were significantly lowered by 61%-90%compared to the control group.Reactions to light-dark stimulation were also less active after exposure to NPF,but significant difference was only found in the high concentration group(9 mg·L^(-1)),which dropped by 49%,whereas in the low and medium concentration group,the response activities were slightly lowered with no statistical difference.After exposure to NPF until 6 dpf,the color preference of zebrafish larvae in cross-mazes was changed,their original preference to blue and avoidance to yellow and green were all attenuated.Regarding the biochemical markers,after exposure to NPF until 5 dpf,the levels of reactive oxygen species(ROS)were dose-dependently elevated by 36%-125%compared to the control.In the meantime,the activities of antioxidant enzymes exhibited different trends,the activity of superoxide d ismutase(SOD)was significantly inhibited by 35%-65%compared to the control,in contrast,the activity of c atalase(CAT)significantly increased by 200%-560%,as for glutathione peroxidase(GPx),its activity slightly i ncreased,but significant difference to control was only observed in the high concentration group(9 mg·L^(-1)).In addition,concerning the rate-limiting enzyme for the metabolism of neurotransmitter acetylcholine,i.e.a cetylcholinesterase(AChE),its activity was also significantly inhibited by 28%-67%compared to the control.In summary,the present study reported the first investigation of behavioral aberration and oxidative stress induced by NPF in zebrafish.The results showed that after acute exposure to sub-lethal concentrations of NPF,the neurobehavioral activities of zebrafish were significantly inhibited,in addition,changes in ROS levels were detected,as well as changes in the activities of a series of antioxidant enzymes and acetylcholinesterase.Taking these findings together,it is deduced that NPF may induce neurobehavioral toxicities by initiating oxidative stress,the underlying m echanisms require further investigations at the genetic level.These results may provide insights into further evaluations of neurotoxicity and health risk assessment of NPF.
作者
胡玲
俞雄飞
章跃龙
刘鹏
刘汉伟
HU Ling;YU Xiongfei;ZHANG Yuelong;LIU Peng;LIU Hanwei(Ningbo Academy of Inspection and Quarantine,Ningbo 315000,China;Ningbo Customs District Technology Center,Ningbo 315000,China;Ningbo Joysun Product Testing Co.Ltd.,Ningbo 315000,China)
出处
《生态毒理学报》
北大核心
2025年第6期376-383,共8页
Asian Journal of Ecotoxicology
基金
国家自然科学基金资助项目(32101233)。
