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    不同养殖水温对大口黑鲈幼鱼生长性能、脂肪代谢和肝脏抗氧化性能的影响

    DIFFERENT REARING WATER TEMPERATURES ON GROWTH PERFORMANCE, LIPID METABOLISM, AND HEPATIC ANTIOXIDANT CAPACITY OF JUVENILE LARGEMOUTH BASS (MICROPTERUS SALMOIDES)

    • 摘要: 为探究养殖水温对大口黑鲈(Micropterus salmoides)幼鱼生长性能、脂肪代谢和抗氧化性能的影响。以初始均重为(15.00±0.91) g的大口黑鲈幼鱼为研究对象, 设置18℃、21℃、24℃、27℃和30℃共5个水温梯度, 养殖周期为30d。在养殖实验结束后, 利用剩余实验鱼进行204h的氨氮胁迫实验, 每桶加入氯化铵母液(200 mg/mL)使水体总氨氮达64 mg/L (pH 7.5), 各温度处理组水中非离子氨浓度呈逐步增加趋势, 分别为0.770、0.957、1.184、1.457和1.784 mg/L。实验结果显示: 大口黑鲈的终末均重、增重率、特定生长率和肥满度随水温升高呈先升后降趋势, 在27℃组达到最高且显著高于其余各组(P<0.05), 18℃组饲料系数显著高于其余各组(P<0.05)。基于的回归分析得出, 最适生长水温为25.46℃。18℃组肠道胰蛋白酶和脂肪酶活性显著高于其他组(P<0.05), 各水温组间淀粉酶活性无显著差异(P>0.05)。在抗氧化方面, 肝脏总超氧化物歧化酶(T-SOD)活性随水温升高显著下降(P<0.05); 而谷胱甘肽过氧化物酶(GPx)和谷胱甘肽转移酶(GST)活性在30℃组显著升高(P<0.05)。肝脏甘油三酯、总胆固醇含量及脂滴面积在21℃组达到最高, 伴随脂肪酸合成基因(acc)和脂肪酸摄取基因(fatp1)表达显著上调(P<0.05); 24℃和27℃组内源性脂肪组装分泌入血的核心载脂蛋白基因(apob)表达上调; 30℃组血清和肝脏甘油三酯、总胆固醇含量均最低。脂质分解代谢基因(lplcpt1)表达在各组间无显著差异(P>0.05)。18℃组肝脏甘油三酯含量显著低于其他组(P<0.05)。在氨氮胁迫下, 30℃组于胁迫后12h即出现死亡, 而18℃和21℃组至48h才发生死亡, 高温与氨氮呈现协同毒性效应。综上结果表明, 大口黑鲈幼鱼的最适生长水温为25.46℃, 而低温抑制生长并诱发肝脏脂质异常代谢, 高温会抑制生长、诱导氧化应激、降低脂质积累并加剧氨氮胁迫毒性。

       

      Abstract: This study was conducted to investigate the effects of rearing water temperatures on growth performance, lipid metabolism, and antioxidant capacity of juvenile largemouth bass (Micropterus salmoides). Juvenile fish initial mean body weight: (15.00±0.91) g were randomly allocated to five temperature treatments (18, 21, 24, 27, and 30℃) for 30 days, after which an ammonia nitrogen stress test was conducted for 204h. Ammonium chloride stock solution (200 mg/mL) was added to each tank to achieve a total ammonia nitrogen concentration of 64 mg/L at pH 7.5, yielding un-ionized ammonia concentrations of 0.770, 0.957, 1.184, 1.457, and 1.784 mg/L for the respective temperature groups. The results showed that final mean body weight, weight gain rate, specific growth rate, and condition factor increased initially and then decreased with increasing water temperature, peaking at 27℃ and significantly higher than those in other groups (P<0.05). Feed conversion ratio in the 18℃ group was significantly higher compared with other temperature groups (P<0.05). Regression analysis based on weight gain rate indicated that the optimal rearing water temperatures for growth was 25.46℃. Intestine trypsin and lipase activities in the 18℃ group were obviously higher compared with all other temperature groups (P<0.05), whereas no significant differences were observed in intestine amylase activity among groups (P>0.05). Regarding antioxidant capacity, hepatic total superoxide dismutase (T-SOD) activity decreased with increasing water temperature (P<0.05), whereas the activities of glutathione peroxidase (GPx) and glutathione S-transferase (GST) were significantly elevated in the 30℃ group (P<0.05). Hepatic triglyceride content, total cholesterol content, and percentage of Oil Red O staining area were significantly elevated in the 21℃ group, accompanied by significant upregulation of the fatty acid synthesis gene (acc) and fatty acid uptake gene (fatp1) (P<0.05). The 18℃ group exhibited significantly lower hepatic triglyceride content compared with the other groups (P<0.05). The 24℃ and 27℃ groups exhibited elevated expression of apob, a core apolipoprotein gene involved in the assembly and secretion into the blood. The 30℃ group exhibited the lowest triglyceride (TG) and total cholesterol (TC) contents in both serum and liver. No significant differences were observed in the expression of lipid catabolism genes (lpl and cpt1) among groups (P>0.05). Under ammonia nitrogen stress, mortality occurred within 12h after exposure in the 30℃ group, whereas fish in the 18℃ and 21℃ groups survived until 48h, indicating a synergistic toxic effect between elevated temperature and ammonia. Collectively, these results indicate that the optimal growth temperature for juvenile largemouth bass is 25.46℃. Low temperature impairs growth and leads to aberrant hepatic lipid metabolism, whereas high temperature inhibits growth, causes oxidative stress, reduces lipid deposition, and exacerbates the toxicity of ammonia nitrogen stress.

       

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