期刊
AQUATIC TOXICOLOGY
卷 70, 期 3, 页码 169-178出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.aquatox.2004.06.010
关键词
cyanobacterial toxin; glutathione; microcystin-LR
Cyanobacterial roxins have been shown to have adverse effects on mammals, birds and fish and are therefore being increasingly recognised as a potent stress and health hazard factor in aquatic ecosystems. Microcystins, which are cyclic heptapeptides and a main group of the cyanotoxins, are mainly retained within the producer-cells during cyanobacterial bloom development. However, these toxins are released into the surrounding medium by senescence and lysis of the blooms. The released toxins could then come into contact with a wide range of aquatic organisms including invertebrates, fish and aquatic plants. In many organisms, biotransformation of the toxins will take place via several glutathione-related conjugate. During the biotransformation process in which the toxin and the toxin conjugate are broken down, the formation of reactive oxygen species might occur. These reactive oxygen species activate several antioxidant enzymes such as superoxide dismutase, catalase, ascorbate peroxidase and also influence the glutathione-ascorbate cycle. Aim of this study was to investigate formation of the glutathione-conjugate, activation of glutathione S-transferases and the elevation of several antioxidant enzymes giving evidence for the promotion of oxidative stress by microcystins. During exposure of Ceratophyllum demersum to the cyanobacterial toxin rnicrocystin-LR in an concentration of 5.0 mug/L, an elevation of rnicrosomal and cytosolic glutathione S-transferase was measured, showing the beginning formation of the glutathione-toxin conjugate. The superoxide dismutase as well as in parallel the hydrogen peroxide level increased giving evidence for oxidative stress in the aquatic plant. Other reactive oxygen detoxifiying enzymes were also elevated and the glutathione pool, expressed in reduced glutathione and glutathione disulfide concentration was changed accordingly. (C) 2004 Elsevier B.V. All rights reserved.
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