Guangxi Key Laboratory of Beibu Gulf Marine Biodiversity Conservation, Ocean College, Qinzhou University, Qinzhou, China; Institute of Hydrobiology and Water Environment, School of Life Sciences, Southwest University, Chongqing, China.
Institute of Hydrobiology and Water Environment, School of Life Sciences, Southwest University, Chongqing, China.
Comp Biochem Physiol C Toxicol Pharmacol. 2018 Dec;214:17-22. doi: 10.1016/j.cbpc.2018.08.003. Epub 2018 Aug 24.
We investigated the standard metabolic rate and liver mitochondria metabolism of the southern catfish when exposed to waterborne cadmium. Juvenile southern catfish were exposed to waterborne cadmium concentrations (0, 62.5, 125, 250 and 500 μg/L, respectively) for 8 weeks, and the final body mass, the standard metabolic rate, the state III respiration rate, the activity of cytochrome C oxidase (CCO) of liver mitochondria, and the hepatosomatic index (HSI) were determined. The results showed that the 62.5 μg/L, 125 μg/L, and 250 μg/L experiment groups had a significantly higher standard metabolic rate than that of the control group. Standard metabolic rate in the 500 μg/L experiment group did not differ from the control group. State III respiration rate of liver mitochondria decreased with an increase in cadmium concentration. The 125 μg/L, 250 μg/L, and 500 μg/L experiment groups had a significantly lower state III respiration rate than that of the control group. The activity of CCO in the 500 μg/L experiment group was significantly lower than that of the control group. These results suggest that at low cadmium concentrations, the southern catfish could continuously improve the standard metabolism to provide extra energy in response to the cadmium stress. Cadmium exposures caused damage to the structure and function of liver mitochondria and decreased the activity of mitochondria enzymes, which results in a decrease in the energy of the liver metabolism. The adjustment of the metabolism of liver mitochondria in southern catfish was inconsistent with the adjustment of individual standard metabolism.
我们研究了南方鲶鱼在暴露于水基镉时的标准代谢率和肝线粒体代谢。将幼年南方鲶鱼暴露于水基镉浓度(分别为 0、62.5、125、250 和 500μg/L)8 周后,测定最终体质量、标准代谢率、III 期呼吸率、肝线粒体细胞色素 C 氧化酶(CCO)活性和肝体比(HSI)。结果表明,62.5μg/L、125μg/L 和 250μg/L 实验组的标准代谢率明显高于对照组。500μg/L 实验组的标准代谢率与对照组无差异。肝线粒体 III 期呼吸率随镉浓度的增加而降低。125μg/L、250μg/L 和 500μg/L 实验组的 III 期呼吸率明显低于对照组。500μg/L 实验组的 CCO 活性明显低于对照组。这些结果表明,在低镉浓度下,南方鲶鱼可以通过持续提高标准代谢率来提供额外的能量,以应对镉胁迫。镉暴露对肝线粒体的结构和功能造成损害,降低了线粒体酶的活性,导致肝代谢能量减少。南方鲶鱼肝线粒体代谢的调节与个体标准代谢的调节不一致。