首页|期刊导航|中国水产科学|基于多组学揭示臭氧胁迫对草鱼鳃抗氧化能力和能量代谢的影响

基于多组学揭示臭氧胁迫对草鱼鳃抗氧化能力和能量代谢的影响OA

Integrated metabolomic and transcriptomic analysis reveals the effects of ozone exposure on antioxidant capacity and energy metabolism in the gills of Ctenopharyngodon idella

中文摘要英文摘要

为探究臭氧胁迫对草鱼(Ctenopharyngodon idella)鳃生理功能的影响及其分子机制,本研究将草鱼随机暴露于 0(对照)、0.1、0.2 和 0.3 mg/L臭氧中 24 h.暴露结束后,测定鳃组织的抗氧化指标、离子含量,并进行代谢组和转录组测序分析.研究结果显示,臭氧暴露导致超氧化物歧化酶(SOD)活性、丙二醛(MDA)及 8-羟基脱氧鸟苷(8-OHdG)含量降低,而总抗氧化能力(T-AOC)和谷胱甘肽(GSH)含量升高.离子稳态分析表明,臭氧暴露显著升高了鳃组织中 K+浓度,但降低了 Ca2+浓度.代谢组分析共鉴定出 519种差异代谢物(DEMs),其中 230种上调,289种下调,主要富集于甘油磷脂代谢、甘油酯代谢、亚油酸代谢和花生四烯酸代谢等通路.转录组分析共获得5159个差异表达基因(DEGs),包括2177个上调和2982个下调基因.KEGG富集分析显示,DEGs显著富集于花生四烯酸代谢、谷胱甘肽代谢、糖酵解/糖异生及铁死亡等通路.其中,糖酵解途径的关键限速酶己糖激酶(hk)、磷酸果糖激酶(pfk)和丙酮酸激酶(pk)基因表达显著上调,提示臭氧胁迫诱导了能量代谢重编程以适应不利环境.同时,铁死亡通路中的铁蛋白重链 1(ferritin)、转铁蛋白受体 1(tfr1)、血红素加氧酶 1(ho-1)及溶质载体家族 7成员 11(slc7a11)基因表达显著上调,表明铁死亡途径被激活.综上,臭氧胁迫可通过诱发氧化应激、干扰离子与能量代谢稳态以及激活铁死亡信号通路,进而损害草鱼鳃组织的生理功能.本研究为解析臭氧对鱼类鳃的毒性机制提供了数据支持,并为相关研究的技术规范与风险评估提供了理论依据.

To investigate the effects of ozone exposure on physiological functions and the underlying molecular mechanisms in the gills of grass carp(Ctenopharyngodon idella),the fish were randomly divided into four groups and exposed to ozone concentrations of 0(control),0.1,0.2,and 0.3 mg/L for 24 h.Following exposure,antioxidant parameters and ion contents in gill tissues were measured,and metabolomic and transcriptomic analyses were performed.The results showed that ozone exposure significantly decreased superoxide dismutase(SOD)activity and the contents of malondialdehyde(MDA)and 8-hydroxydeoxyguanosine(8-OHdG),while increasing total antioxidant capacity(T-AOC)and glutathione(GSH)levels.Ion homeostasis analysis revealed a significant elevation in K+content and a marked reduction in Ca2+content in the gills.Metabolomic profiling identified 519 differentially expressed metabolites(DEMs),including 230 up-regulated and 289 down-regulated metabolites.These DEMs were primarily enriched in glycerophospholipid metabolism,glycerolipid metabolism,linoleic acid metabolism,and arachidonic acid metabolism.Furthermore,transcriptomic analysis identified 5159 differentially expressed genes(DEGs),including 2177 up-regulated and 2982 down-regulated genes.KEGG enrichment analysis indicated that these DEGs were significantly enriched in pathways such as arachidonic acid metabolism,glutathione metabolism,glycolysis/gluconeogenesis,and ferroptosis.Notably,the expression of genes encoding key rate-limiting enzymes in the glycolysis pathway,including hexokinase(hk),phosphofructokinase(pfk),and pyruvate kinase(pk),was significantly up-regulated,suggesting that ozone stress induced reprogramming of energy metabolism to cope with the adverse environment.Meanwhile,the significant up-regulation of genes in the ferroptosis pathway,including ferritin heavy chain 1(ferritin),transferrin receptor 1(tfr1),heme oxygenase 1(ho-1),and solute carrier family 7 member 11(slc7a11),indicated activation of ferroptosis.In conclusion,ozone exposure impaired the physiological functions of grass carp gills by inducing oxidative stress,disrupting ion and energy metabolic homeostasis,and activating the ferroptosis signaling pathway.This study provides crucial data for elucidating the toxicological mechanisms of ozone on fish gills and offers a theoretical basis for risk assessment and the establishment of technical guidelines in related fields.

丁庄孜炜;贾睿;侯诒然;周琳珺;张成锋;朱健;李冰

南京农业大学无锡渔业学院,江苏 无锡 214128南京农业大学无锡渔业学院,江苏 无锡 214128||中国水产科学研究院淡水渔业研究中心,农业农村部稻渔综合种养生态重点实验室,江苏 无锡 214081中国水产科学研究院淡水渔业研究中心,农业农村部稻渔综合种养生态重点实验室,江苏 无锡 214081中国水产科学研究院淡水渔业研究中心,农业农村部稻渔综合种养生态重点实验室,江苏 无锡 214081中国水产科学研究院淡水渔业研究中心,农业农村部稻渔综合种养生态重点实验室,江苏 无锡 214081南京农业大学无锡渔业学院,江苏 无锡 214128||中国水产科学研究院淡水渔业研究中心,农业农村部稻渔综合种养生态重点实验室,江苏 无锡 214081南京农业大学无锡渔业学院,江苏 无锡 214128||中国水产科学研究院淡水渔业研究中心,农业农村部稻渔综合种养生态重点实验室,江苏 无锡 214081

农业科技

草鱼鳃臭氧代谢抗氧化铁死亡

Ctenopharyngodon idellagillsozonemetabolismantioxidantferroptosis

《中国水产科学》 2026 (8)

19-33,15

中央级公益性科研院所基本科研业务费专项资金项目(2025JBFR082023TD64).

10.12264/JFSC2026-0344

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