Carbonic anhydrase 2-like and Na^sup +^-K^sup +^-ATPase [alpha] gene expression in medaka (Oryzias latipes) under carbonate alkalinity stress
High carbonate alkalinity is one of the major stress factors for living organisms in saline-alkaline water areas. Acute and chronic effects of carbonate alkalinity on expression of two genes, carbonic anhydrase 2-like (CA2-like) and Na^sup +^-K^sup +^-ATPase [alpha] subunit (NKA-[alpha]) mRNA in med...
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Veröffentlicht in: | Fish physiology and biochemistry 2015-12, Vol.41 (6), p.1491 |
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Sprache: | eng |
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Zusammenfassung: | High carbonate alkalinity is one of the major stress factors for living organisms in saline-alkaline water areas. Acute and chronic effects of carbonate alkalinity on expression of two genes, carbonic anhydrase 2-like (CA2-like) and Na^sup +^-K^sup +^-ATPase [alpha] subunit (NKA-[alpha]) mRNA in medaka (Oryzias latipes) were evaluated to better understand the responses important for coping with a carbonate alkalinity stress. In the acute exposure experiment, the expression of CA2-like and NKA-[alpha] mRNA in the gill and kidney of medaka were examined from 0 h to 7 days exposed to 30.4 mM carbonate alkalinity water. Exposure to high carbonate alkalinity resulted in a transitory alkalosis, followed by a transient increase in gill and kidney CA2-like and NKA-[alpha] mRNA expression. In the chronic exposure experiment, the expression of these two genes was examined in the gill and kidney at 50 days post-exposure to six different carbonate alkalinity concentrations ranging from 1.5 to 30.4 mM. Gill and kidney CA2-like mRNA levels in 30.4 mM were approximately 10 and 30 times higher than that of the control (1.5 mM), respectively. Less differences were found in NKA-[alpha] expression in the 50-days exposure. The results indicate that when transferred to high carbonate alkalinity water, a transitory alkalosis may occur in medaka, followed by compensatory acid-base and ion regulatory responses. Thus, CA2-like and NKA-[alpha] are at least two of the important factors that contribute to the regulation of alkalinity stress. |
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ISSN: | 0920-1742 1573-5168 |
DOI: | 10.1007/s10695-015-0101-6 |