低氧胁迫对鲻幼鱼生长、能量代谢和氧化应激的影响

为研究低氧胁迫对鲻幼鱼生长、能量代谢和氧化应激的影响,实验将其放在溶解氧(DO,mean±SE)含量分别控制在(1.66±0.41)、(4.35±0.53)、(7.03±0.36)mg/L的条件下养殖10 d,然后恢复至接近饱和溶解氧含量7.0 mg/L的条件下养殖30 d,研究其特定生长率、排氨率、耗氧率、氧氮比和血浆、肌肉、肝脏及鳃组织的总抗氧化能力(T-AOC)、过氧化物歧化酶(SOD)活力、抗超氧阴离子活力(ASOR)、丙二醛(MDA)含量、乳酸(LD)含量、总谷胱甘肽(T-GSH)、还原型谷胱甘肽(GSH)和氧化型谷胱甘肽(GSSG)含量。结果表明:低氧胁迫对鲻幼鱼的生长、能量代谢影响显著,较严重缺氧组鲻的体质量、特定生长率(SGR)、耗氧率和排氨率显著低于其他处理,不具有补偿生长的能力;而轻微缺氧组获得完全补偿生长。低氧胁迫对鲻氧化应激指标影响显著,胁迫结束时鲻通过提高某些抗氧化酶的活力来增强抗氧化能力,以提高其应对恢复正常溶解氧环境可能带来的氧化应激的能力,同时在恢复溶氧后鲻氧化应激反应也较强烈。在恢复溶解氧阶段,肝脏中GSH显著增加,说明鲻体内的保护机制被激活。肝脏和鳃中MDA的含量在低氧胁迫后与溶解氧含量呈明显的负相关性,在复氧30 d后仍然高于对照组,表明低氧胁迫加强鲻肝脏和鳃组织脂质过氧化反应。

Effect of hypoxia on growth performance, energy metabolism and oxidative stress of Mugil cephalus

To investigate the effects of hypoxia exposure and subsequent normoxic recovery on growth performance, energy metabolism and oxidative stress of juvenile Mugil cephalus, the dissolved oxygen content (DO, mean±SE) of the aquarium was controlled at hypoxia (1.66±0.41), moderate hypoxia (4.35±0.53), saturation (7.03±0.36) mg/L, respectively, for 10 days and then recovery to normoxic state 7.0 mg/L for 30 days. Specific growth rate, oxygen consumption rate, ammonia excretion rate, O:N ratios and oxidative stress indicators, including the content of T-AOC,SOD, ASOR, MDA, LD,T-GSH, GSSG, and GSH in the plasma, muscle, liver and gill were measured. The results showed that hypoxia exposure for 10 days generally decreased the levels of body weight, specific growth rate, oxygen consumption and ammonia excretion rate of juvenile fish. Fish experienced moderate hypoxia would achieve completely compensatory growth in a short period with normal dissolved oxygen content. But fish under hypoxia conditions had non-compensatory growth. Hypoxia and recovery had a great influence on the oxidative stress indicators. Hypoxia stimulated increases in the activities of lactic acid (LD) levels in blood, activities of superoxide dismutase (SOD) in muscle and liver, activities of anti-superoxide anion (ASOR) in gill, which supported the idea that anticipatory preparation takes place in order to deal with the oxidative stress that will occur during reoxygenation. Meanwhile the SOD activity in blood, muscle, liver and activities of ASOR in muscle, liver increased at different phases during reoxygenation, indicating that the oxidative stress during normoxic recovery was intense. GSH level in liver was elevated under recovery which appears to trigger the protection mechanism. Hypoxia and reoxygenation also significantly increased MDA level in liver and gill, and it seems that hypoxia may cause lipid peroxidation damage in liver and gill.