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Zinc binding to the gills of rainbow trout: the effect of long‐term exposure to sublethal zinc
Author(s) -
Galvez F.,
Webb N.,
Hogstrand C.,
Wood C. M.
Publication year - 1998
Publication title -
journal of fish biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.672
H-Index - 115
eISSN - 1095-8649
pISSN - 0022-1112
DOI - 10.1111/j.1095-8649.1998.tb00957.x
Subject(s) - rainbow trout , gill , biology , zinc , kinetics , binding site , trout , in vivo , environmental chemistry , biophysics , fish <actinopterygii> , zoology , biochemistry , chemistry , fishery , physics , organic chemistry , quantum mechanics , microbiology and biotechnology
The effects of sublethal waterborne Zn (2·28 μmol l −1 ) on Zn binding kinetics to the apical gill surface were studied in juvenile rainbow trout ( Oncorhynchus mykiss ). Two separate radiotracer techniques were employed to ascertain this information. First, in vitro binding kinetic experiments were performed at extremely elevated zinc concentrations (up to 20 mmol l −1 ) to measure relatively low‐affinity binding sites at the gill epithelium. There were no differences in Zn binding parameters ( K m and B max ) for fish sublethally exposed to Zn for 21 days and their simultaneous controls. Nevertheless, Ca did have an increased inhibitory effect on Zn binding in Zn‐exposed fish suggesting that the anionic groups on the gill epithelium of these fish had been altered in some manner. Additionally, in vivo Zn binding kinetics were investigated using environmentally relevant waterborne Zn concentrations (low μmol l −1 range) to isolate high‐affinity Zn binding sites (Ca transporters). No appreciable alterations in the Km and B max values for Zn binding were seen between the Zn‐exposed group and its simultaneous control following 15 days of exposure. Furthermore, no significant differences in CC morphometry were observed between treatments. Despite these lack of treatment effects, there were temporal alterations in K m , B max and CC fractional surface area in both groups. It is proposed that these fluctuations are controlled by hormonal factors (such as stanniocalcin), believed to play a role in Ca influx.