氨氮和镉胁迫对芙蓉鲤鲫抗氧化系统和免疫机能的影响

AMMONIA NITROGEN AND CADMIUM STRESS ON ANTIOXIDANT SYSTEM AND IMMUNE FUNCTION OF FURONG CRUCIAN CARP (CYPRINUS CAPIO FURONG.♀×CARASSIUS AURATUS RED VAR.♂)

  • 摘要: 为探究氨氮、镉单一及联合胁迫对鱼类氧化防御系统及非特异性免疫系统的影响, 以芙蓉鲤鲫(Cyprinus capio furong.♀×Carassius auratus red var.♂)为研究对象, 通过静态毒理学实验方法模拟亚急性胁迫, 在胁迫后不同时间点对芙蓉鲤鲫的肝脏进行取样, 并测定其抗氧化指标和非特异性免疫指标。结果显示, 氨氮和镉单一及联合胁迫后肝脏丙二醛(MDA)含量、酸性磷酸酶(ACP)活性和髓过氧化物酶(MPO)活性均出现不同程度的升高, 过氧化氢酶(CAT)活性均呈先下降后升高的趋势。氨氮胁迫后肝脏超氧化物歧化酶(SOD)活性、谷胱甘肽过氧化物酶(GSH-PX)活性、碱性磷酸酶(AKP)活性及谷胱甘肽(GSH)含量均呈先升高后下降的变化趋势。镉胁迫后肝脏SOD和GSH-PX活性在6d时均显著高于对照组, GSH含量在4d时显著低于对照组, AKP活性呈先降低后升高的趋势。氨氮和镉联合胁迫后肝脏SOD和GSH-PX活性在6d和8d时显著增加, AKP活性在8d时显著升高, GSH含量呈先降低后升高的变化趋势。结果表明, 氨氮和镉单一及联合胁迫均可诱导芙蓉鲤鲫产生氧化应激, 激活了鱼体的氧化防御系统和非特异性免疫系统。研究可为深入探讨芙蓉鲤鲫的健康养殖和逆境生理响应机制提供基础资料。

     

    Abstract: It is widely acknowledged that many diverse contaminants coexisting in aquatic ecosystems, which could contribute to single and/or combined adverse effects to aquatic life. Ammonia nitrogen and cadmium are common toxic contaminants in aqueous environment and have multiple impacts on physiological activity, metabolism and body health of fish. Although some studies about the single or combined toxicity to aquatic organisms were carried out, more reports have been concerned about a certain chemical or the similar kinds of chemicals, such as the heavy metals or the organic contaminant. However, the information of the interactive impacts among distinct types of water pollutants remains unclear. To comprehensively assess the effects of ammonia nitrogen and cadmium on antioxidant system and immune function of juvenile Furong crucian carp (Cyprinus capio furong.♀×Carassius auratus red var.♂), we stimulated subacute exposure by static toxicology experiment, and collected liver tissues at 0, 2, 4, 6 and 8 days after exposure, then determined antioxidative indices and non-specific immunity parameters with hepatic histoenzymology. The results showed that malondialdehyde (MDA) content, the activity of acid phosphatase (ACP) and myeloperoxidase (MPO) increased differently in liver after ammonia nitrogen and/or cadmium exposure. Liver catalase (CAT) activity decreased at first and then increased in all treatment groups. Hepatopancreas superoxide dismutase (SOD), glutathion peroxidase (GSH-PX), alkaline phosphatase (AKP) and glutathione (GSH) increased firstly and then declined. The hepatic SOD and GSH-PX activities were higher than that in control group at 6 days post cadmium exposure, while GSH content was lower than that in control group at 4 days post cadmium exposure. The hepatic AKP activities first descended and then raised to the maximum at 8 days post cadmium exposure. After joint exposure of ammonia nitrogen and cadmium, liver SOD and GSH-PX activities rose remarkably at 6 and 8 days for the combination of ammonia nitrogen and cadmium, and hepatic AKP activity increased dramatically at 8 days, while liver GSH content decreased at first and then increased. These results indicated that ammonia nitrogen and cadmium could induce hepatic oxidative stress, activate the oxidative defense system and enhance the nonspecific immunity in Furong crucian carp. This study provides the basis for investigating the response mechanism of stress physiology and healthy culture in Furong crucian carp.

     

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