Acute toxicity and responses of antioxidant systems to 1-methyl-3-octylimidazolium bromide at different developmental stages of goldfish
Glutathione Peroxidase
Superoxide Dismutase
Imidazoles
Ionic Liquids
Catalase
Kidney
Glutathione
01 natural sciences
Antioxidants
Intestines
Oxidative Stress
Liver
Goldfish
Malondialdehyde
Toxicity Tests, Acute
Animals
Lipid Peroxidation
14. Life underwater
0105 earth and related environmental sciences
DOI:
10.1007/s10646-011-0785-z
Publication Date:
2011-09-12T16:03:02Z
AUTHORS (5)
ABSTRACT
Acute toxicity of 1-methyl-3-octylimidazolium bromide ([C(8)mim]Br) to goldfish at different developmental stages and responses of the antioxidant system in adult goldfish were evaluated in the present study. The results indicate that post-embryonic developmental toxicity of [C(8)mim]Br on goldfish is developmental-stage dependent. The juvenile and larva goldfish are more sensitive to [C(8)mim]Br-toxicity than the adult fish. Histological observations in adult goldfish reveal that acute [C(8)mim]Br exposure damages the hepatopancreas, intestines, and kidneys, indicating that these are possible target organs of [C(8)mim]Br toxicity in goldfish. Subsequent biochemical assays in adult goldfish show that [C(8)mim]Br also induces changes in the activities of the superoxide dismutase, catalase, glutathione peroxidase, and glutathione content of fish hepatopancreas. These results suggest that [C(8)mim]Br exposure may induce oxidant stress and lipid peroxidation in hepatopancreas of adult goldfish. In addition, we also find that [C(8)mim]Br causes a remarkable increase in malondialdehyde (MDA) levels in the hepatopancreas of adult goldfish, and thus we think that the MDA level change can be a biomarker of [C(8)mim]Br toxicity in goldfish. The present study indicates that ionic liquids can be a threat to the survival, growth, and development of the fish population once they are accidentally leaked into aquatic ecosystems.
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