|其他题名: ||Field Studies on the Toxicological Effects from Microcystis Blooms on Fishes and the Cardiac Toxicity of Microcystins in Rat|
|摘要: ||随着人类社会生产力的大幅提高及人口压力的不断增大，全球范围的淡水水体富营养化现象日趋严重，由此引起的蓝藻水华在世界范围内频繁暴发，其伴随产生的毒素与动物及人类健康的关系受到了越来越多的关注。微囊藻毒素（Microcystins, MC）是一类出现频率高、产毒量大、危害严重的蓝藻毒素。鱼类是水生态系统的次级或顶级消费者，直接暴露于微囊藻毒素中，与此相关的鱼类死亡和鱼类中毒事件时有报道。目前，较多的研究证实了在微囊藻毒素急性染毒条件下对各种不同食性鱼类的致毒效应。然而，关于有毒蓝藻水华长时间或者是反复暴露后导致的动物慢性毒性研究还十分匮乏。本文通过野外调查探讨微囊藻水华对不同食性鱼类肝脏和肾脏的生理和生物化学影响，并分析可能原因。
|英文摘要: ||Dense blooms of cyanobacterial (blue–green) algae are one of the consequences of the increasing eutrophication in many waters worldwide. With frequent occurrence of cyanobacterial blooms in recent years, cyanotoxins have become a great threat to aquatic animals, livestock, and human health. Among these toxins, microcystins (MC) are the most common and dangerous hepatotoxins. Fish, one of the main inhabitants in aquatic systems, is usually subjected to MC directly or passively, which consequently causes fish kill or fish poisoning episodes. Till now, most experimental studies documenting the toxicity of MC exposure to fishes have been prone to acute toxicity experiments. Few investigations have been conducted on post-event of wild animal poisonings in which toxic cyanobacteria are suspected, especially when long-term and/or frequent exposure occurs. The main aim of this study was to examine physiological and biochemical responses of fishes with different trophic levels to toxic cyanobacterial blooms in Meiliang Bay, Lake Taihu, with discussion on the possible mechanisms.
Deaths from microcystin toxication have widely been attributed to hypovolemic shock due to hepatic interstitial hemorrhage, while some recent studies suggest that cardiogenic complication is also involved. So far, information on cardiotoxic effects of MC has been rare and the underlying mechanism is still puzzling. We conducted intravenous injection of extracted MC in rats，in order to evaluate the roles of oxidative stress and mitochondrial dysfunction in cardiotoxic effects by MC.
The main results and conclusions were summarized as follows:
1. Physiological and biochemical responses of four fishes with different trophic levels to toxic cyanobacterial blooms were studied in a large net cage in Meiliang Bay, a hypereutrophic region of Lake Taihu. We sampled four fishes: the phytoplanktivorous Hypophthalmichthys molitrix and Aristichthys nobilis, the omnivorous Carassius auratus, and the carnivorous Culter ilishaeformis. Alterations of the antioxidant (GSH) and the major antioxidant enzymes (CAT, SOD, GPx, GST) in livers were monitored monthly, and the ultrastructures of livers were compared between the bloom and the post-bloom periods. During the cyanobacterial blooms, the phytoplanktivorous fishes displayed only slight ultrastructural changes in liver, while both carnivorous and omnivorous fishes presented serious injuries such as swollen endomembrane system and morphologically altered nuclei in hepatocytes. Biochemically, the phytoplanktivorous fishes possessed higher basal GSH concentrations and better correlations between the major antioxidant enzymes in liver, which might be responsible for their powerful resistance to MC.
2. Physiological and biochemical responses in kidneys of fishes with different trophic levels (phytoplanktivorous, omnivorous and carnivorous) to toxic cyanobacterial blooms were studied in a large net cage in Meiliang Bay. Catalase and glutathione S-transferase were significantly higher during blooms than before and after blooms. All fishes showed ultrastructural alterations in kidneys during blooms, which mainly are inosculation of foot processes in epithelial cell of glomeruli. The results suggested that kidney impairment from chronic exposure of toxic cyanobacterial blooms might be the first step, and then followed by hepatic failure. Compared with livers in terms of physiological status, the weaker antioxidant ability of kidney made it more susceptible to chronic MC exposure, besides the effective accumulation of MC metabolites in kidney.
3. To evaluate the impact of toxic cyanobacterial blooms on the planktivorous fish, 12 serum chemistry variables were investigated in silver carp and bighead carp, in a large net cage in Meiliang Bay, a hypereutrophic region of Lake Taihu. The results confirmed adverse effects of cyanobacterial blooms on the two phytoplanktivorous fishes, mainly characterized with potential toxicogenomic effects and metabolism disorders in liver, and kidney dysfunction. In addition, cholestasis was intensively implied by distinct elevation of all four related biomarkers (ALP, GGT, DBIL, TBIL) in bighead carp. Based on a multivariate discriminant analysis, the combination of LDH and AST activities and DBIL and URIC contents for silver carp, and the combination of ALT and ALP activities and TBIL, DBIL and URIC concentrations for bighead carps strongly indicate toxic effects from cyanobacterial blooms.
4. A laboratory experiment was conducted to examine toxic effects of microcystins on heart muscle of rats intravenously injected with extracted MC at two doses, 0.16LD50 (14µg MC-LReq kg-1 body weight) and 1LD50 (87 µg MC-LReq kg-1 body weight). In the dead rats, both TTC staining and maximum elevations of troponin I levels confirmed myocardial infarction after MC exposure, besides a serious interstitial hemorrhage in liver. In the 1LD50 dose group, the coincident falls in heart rate and blood pressure were related to mitochondria dysfunction in heart, while increases in creatine kinase and troponin I levels indicated cardiac cell injury. The corresponding pathological alterations were mainly characterized as loss of adherence between cardiac myocytes and swollen or ruptured mitochondria at the ultrastructural level. MC administration at a dose of 1LD50 not only enhanced activities and up-regulated mRNA transcription levels of antioxidant enzymes, but also increased GSH content. At both doses, level of lipid peroxides increased obviously, suggesting serious oxidative stress in mitochondria. Simultaneously, complex I and III were significantly inhibited, indicating blocks in electron flow along the mitochondrial respiratory chain in heart. In conclusion, the findings of this study implicate a role for MC induced cardiotoxicity as a potential factor that should be considered when evaluating the mechanisms of death associated with microcystin intoxication in Brazil.|
|Appears in Collections:||中科院水生所知识产出（2009年前）_学位论文|
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