Volume 27 Issue 5
Feb.  2014
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LI Xiao-Yu, LIU Yong-Ding, SONG Li-Rong, QIAO Zhi-Gang. RESPONSES OF ANTIOXIDANT SYSTEMS IN THE HEPATOCYTES OF COMMON CARP (CYPRINUS CARPIO L.) TO THE TOXICITY OF MICROCYSTIN-LR[J]. ACTA HYDROBIOLOGICA SINICA, 2003, 27(5): 472-475.
Citation: LI Xiao-Yu, LIU Yong-Ding, SONG Li-Rong, QIAO Zhi-Gang. RESPONSES OF ANTIOXIDANT SYSTEMS IN THE HEPATOCYTES OF COMMON CARP (CYPRINUS CARPIO L.) TO THE TOXICITY OF MICROCYSTIN-LR[J]. ACTA HYDROBIOLOGICA SINICA, 2003, 27(5): 472-475.
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RESPONSES OF ANTIOXIDANT SYSTEMS IN THE HEPATOCYTES OF COMMON CARP (CYPRINUS CARPIO L.) TO THE TOXICITY OF MICROCYSTIN-LR

  • College of Life Science, Henan Normal University, Xinxiang, 453002;
    2. Institue of Hydrobiology, The Chinese Academy of Sciences, Wuhan, 430072

  • Received Date: October 26, 2002
  • Rev Recd Date: November 24, 2002
  • Published Date: September 24, 2003
    Graphical Abstract
    • Abstract
  • The freshwater, bloom-forming cyanobacterium (blue-green alga) Microcystis aeruginosa produces a peptide hepatotoxin (microcystins, MC), which causes the damage of animal liver. Recently, toxic Microcystis blooms frequently occur in the eutrophic lake and have caused many troubles to the environment in China. Microcystins remained in water supply also become the severe threat to people health. Microcystin-LR from Microcystiswas isolated and purified with high performance liquid chromatography (HPLC) and its toxicity to mouse and fish liver were partly studied (Li et al., 2001). In this study, six indexes (Reactive oxygen species, Glutathione, Superoxide dismutase, Catalase, Glutathione peroxide and Glutathione S-transferase) in common carp hepatocytes were determined with the kits supplied by the Nanjing Bioengineering Institute when the cells were exposed to 10μg/L microcystin-LR. The results showed that Reactive oxygen species (ROS) contents increased obviously after 6h exposure to the toxin. In contrast, Glutathione (GSH) levels in the hepatocytes exposed to microcystin-LR decreased by 47% compared with the control. The activities of Superoxide dismutase (SOD), Catalase (CAT) and Glutathione peroxide (GSH-Px) increased after 6h exposure to microcystin-LR, but Glutathione S-transferase (GST) activity showed no difference with the control. These results suggested that the toxicity of microcystin-LR caused the increase of ROS contents and the depletion of GSH in hepatocytes exposed to the toxin and these changes led to oxidant shock in hepatocytes. Activities increases of SOD, CAT and GSH-Px revealed that these three kinds of antioxidant enzymes might play important roles in eliminating the excessive ROS. From the present study, we could infer the possible toxicity mechanism of microcystin-LR on the common carp hepatocytes. MC can potently inhibit protein phosphatase type-1 and 2A after the toxin were transported to cytoplasm by the bile acid transporter in the cell membrane of hepatocytes and the inhibition may disturb the cellular phosphorylation balance, cause the marked increase of ROS contents and the depletion of GSH in hepatocytes. As a result, these changes would lead to oxidant shock in the hepatocytes. Although antioxidant enzymes (SOD, CAT and GSH-Px) had played their roles in eliminating cytosolic ROS and regenerating GSH, they could not prevail over the oxidant stress induced by the toxin. Therefore, these effects caused the damages of hepatocytes, leading to apoptosis and even necrosis of cells.
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  • [1]
    Carmichael W W. The toxins of cyanobacteria [J]. Sci. Am., 1994, 270:64-72[2] Xu L H, Zhang Y Y. Recent developments in the study of the molecular intoxication mechanism of microcystins. [J]. Acta Hydrobiologica Sinica., 1993,17(4):365-374. [徐立红,张NB040元.微囊藻毒素分子致毒机理研究进展[J]. 水生生物学报,1993,17(4):365-374][3] Hallegreff G M. A review of harmful algal bloom and their apparent global increase [J]. Phycologia,1993,32(2):79[4] Dawson R M. The toxicology of microcystins [J]. Toxicon, 1998,36(7):953-962[5] Codd G A, Bell S G, Knya K, et al. Cyanobacterial toxin, exposure routes and human health [J]. Eur. J. Phrcol., 1999,34:405[6] Falconer I R, Beresford A, Runnear M T C. Evidence of liver damage in a human population exposed to toxin from a bloom of the blue-green alga Microcystis aeruginosa in a drinking water supply reservoirs [J]. Med. J. Aust., 1983,1:511[7] Yu S Z. Drinking water and primary liver cancer [M]. Beijing:Academic Press,1989[8] Bell S G, Codd G A. Cyanobacterial toxin and human health [J]. Rev. Med. Microbiol.,1994,5:256-264[9] Takenaka S, Otsu R. Effects of L-cysteine and reduced glutathione on the toxicity of microcystin-LR:the effect for acute liver failure and inhibition of protein phosphatase 2A activity [J]. Aquatic Toxicology, 1999,48:65-68

    Carmichael W W. The toxins of cyanobacteria [J]. Sci. Am., 1994, 270:64-72[2] Xu L H, Zhang Y Y. Recent developments in the study of the molecular intoxication mechanism of microcystins. [J]. Acta Hydrobiologica Sinica., 1993,17(4):365-374. [徐立红,张NB040元.微囊藻毒素分子致毒机理研究进展[J]. 水生生物学报,1993,17(4):365-374][3] Hallegreff G M. A review of harmful algal bloom and their apparent global increase [J]. Phycologia,1993,32(2):79[4] Dawson R M. The toxicology of microcystins [J]. Toxicon, 1998,36(7):953-962[5] Codd G A, Bell S G, Knya K, et al. Cyanobacterial toxin, exposure routes and human health [J]. Eur. J. Phrcol., 1999,34:405[6] Falconer I R, Beresford A, Runnear M T C. Evidence of liver damage in a human population exposed to toxin from a bloom of the blue-green alga Microcystis aeruginosa in a drinking water supply reservoirs [J]. Med. J. Aust., 1983,1:511[7] Yu S Z. Drinking water and primary liver cancer [M]. Beijing:Academic Press,1989[8] Bell S G, Codd G A. Cyanobacterial toxin and human health [J]. Rev. Med. Microbiol.,1994,5:256-264[9] Takenaka S, Otsu R. Effects of L-cysteine and reduced glutathione on the toxicity of microcystin-LR:the effect for acute liver failure and inhibition of protein phosphatase 2A activity [J]. Aquatic Toxicology, 1999,48:65-68
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