食物中多氯联苯PCB 126对南方鲇的致死效应及代谢胁迫的研究
LETHAL EFFECT AND METABOLIC STRESS OF DIETARY PCB126 ON THE SOUTHERN CATFISH,SILURUS MERIDIONALIS CHEN
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摘要: 于2007年10-12月,为探讨食物中多氯联苯126(3,3′,4,4′,5-pentachlorobiphenyl,PCB 126)对南方鲇(Silurus meridionalis Chen)的致死效应及代谢胁迫作用,将72尾南方鲇幼鱼分为6个实验组,配制PCB126含量分别为0、50、100、200、400和800μg/kg的6组饲料,采用室内养殖系统,在(27.5±0.2)℃水温条件下以3%BW/d的日粮水平单尾喂养8周。观测结果表明:PCB126含量为0、50和100μg/kg的饲料组在实验期间无实验鱼死亡,至实验结束时的PCB126总摄入量分别为0、30.56和66.66μg/kg;而200、400和800μg/kg的饲料组有实验鱼死亡,半致死时间(Medianlethaltime,LT50)分别为34d、16d和11d,与饲料中PCB126水平呈负相关,至半致死时PCB126总摄入量分别为90.18、92.05和94.11μg/kg,三者间无显著差异,但均显著高于无实验鱼死亡饲料组的PCB126总摄入量(p0.05);肝指数(Hepatosomatic index,HSI)及静止代谢率随饲料中PCB126水平的增加而升高;在无实验鱼死亡的饲料组,肝线粒体代谢耗氧率和细胞色素c氧化酶(Cytochrome c oxidase,CCO)活性随饲料中PCB126水平的增加而升高,而在有实验鱼死亡的饲料组,肝线粒体代谢耗氧率和CCO活性则随饲料中PCB126水平的增加而呈下降趋势。本研究提出,PCB126对南方鲇的致死临界累计摄入量在92μg/kg左右;PCB126对南方鲇在整体水平表现为使静止代谢增强的胁迫效应,但在肝线粒体水平表现为低浓度使其代谢耗氧率增强,这应当是该种鱼应对多氯联苯类污染物的一种生理调节结果,而高浓度的PCB126则使肝脏功能受到不可耐受的损害,不能对胁迫做出进一步的代谢调节。
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关键词:
- 南方鲇 /
- 多氯联苯PCB 126 /
- 半致死时间 /
- 静止代谢率 /
- 细胞色素c氧化酶
Abstract: 3,3',4,4',5-pentachlorobiphenyl (PCB 126), a kind of typical persistent organic pollutant, is one of the poly-chlorinated biphenyls (PCBs) congeners with high bioaccumulation and strong toxicity. It has been considered to have detrimental effects on the health of the human and animals as well as on ecosystems for being difficult to be decomposed or be transformed in both environment and organisms. In order to test the lethal effect and metabolic stress of dietary PCB 126 on the southern catfish, Silurus meridionalis Chen, from October to December, 2007, 72 one-year-old juvenile south-era catfish acclimated with control diet for 2 weeks prior to study initiation were randomly divided into 6 experimental groups (12 fish in each group) for different dietary PCB 126 treatments. Six iso-nitrogenous (45% crude protein), iso-li-pidic (12% crude lipid) and iso-carbohydrate (15% crude carbohydrate) experimental diets with different levels of PCB 126 were formulated, the dietary concentrations of PC B 126 were 0(as control), 50, l O0,200,400 and 800 μg/kg, re-spectively. In each group, the southern catfish were individually fed with each experimental diet in an indoor rearing sys-tem at 3% BW per day ration level for 8 weeks at (27.5±0.2)℃. The median lethal time (LT50), the total amounts of PCB 126 intake during the experiment, hepatosomatic index (HSI), the resting metabolic rate (RMR) as well as the rate of oxygen consumption and activity of cytochrome c oxidase (CCO) of the liver mitochondria in southern catfish were deter-mined and calculated. The results showed that no mortality of the experimental fish occurred during the experiment in groups fed with the diets in the PCB 126 concentrations of 0, 50 and 100 μg/kg, and the total amounts of PCB 126 intake were 0, 30.56 and 66.66μg/kg body weight at the termination of the experiment, respectively, whereas, the mortality was observed in fish fed with the diets containing PCB 126 of 200, 400 and 800 μg/kg, and the LT50 was 34d, 16d and 11d, respectively, which were negatively correlated to dietary levels of PCB 126. The accumulative amounts of PCB 126 intake at the median lethal time in these three groups were 90.18, 92.05 and 94.11μg/kg body weight, respectively, and there was no significant difference among them, but all of them were significantly higher than those in the other three groups (p<0.05). HSI and RMR increased with the increasing dietary level of PCB 126. The rate of oxygen consumptionand activity of CCO of the liver mitochondria increased with the increasing dietary level of PCB 126 in the groups without mortalities, while decreased with the further increasing dietary level of PCB 126 in the groups with mortalities. The present study suggested that the accumulative lethal critical amounts of PCB 126 intake for the southern catfish were approximately 92 μg/kg body weight and the lethal time was concentration-dependent. The stress effects of dietary PCB 126 on the me-tabolism of the southern catfish caused an increase in the resting metabolic rate of individual fish. At the mitochondrial level of the liver, the stress effects of dietary PCB 126 on the metabolism exhibited that the metabolic rates were increased at a lower level of concentration, there was more energetic expenditure needed by the fish to resist the contaminants, and an increase in capacity of supplying metabolic energy by the liver mitochondria, which should be a physiologically regula-tive mechanism for this fish species to cope with persistent organic pollutants such as PCBs. However, the higher concen-trations of dietary PCB 126 may cause an intolerable functional impairment of mitochondria, so that, it was unable to have a further regulation of the metabolism to the stress of PCB 126. -
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