4.6 Article

Multixenobiotic Resistance Mechanism in Gills of Reared vs. Wild Mediterranean Mussel Mytilus galloprovincialis (Lamarck, 1819)

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WATER AIR AND SOIL POLLUTION
卷 225, 期 8, 页码 -

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SPRINGER
DOI: 10.1007/s11270-014-2073-z

关键词

Apoptosis; Multixenobiotic resistance (MXR) mechanism; Metals; Gill tissue; Mytilus galloprovincialis

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  1. Croatian Ministry of Science, Education and Sport [001-0000000-3633, 058-0582261-2246]

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Mussel (Mytilus galloprovincialis (Lamarck, 1819)) is directly exposed to sea water contamination that elicits significant physiological and cellular response, although its extent mounted in aquaculturereared in comparison to wild bivalve populations is scarcely known. Therefore, we have compared contamination biomarkers in mussels from reared (Marina farm) and wild, anthropogenically affected site (Vranjic Bay). While predictably, the levels of metals (Cu, Cd, Pb, Zn, Fe, and Hg) in whole bivalve tissues determined by atomic absorption spectrophotometry resulted in significantly higher concentrations in wild mussels, accompanied by elevated number of apoptotic cells in gills, the activity of multixenobiotic resistance defense mechanism (MXR), measured as the accumulation rate of model substrate rhodamine B (RB) gave contrasting results. The functional RB assay evidenced a lower MXR efflux activity in the gill tissue of wild mussels, indicating two possible scenarios that will need further focus: (1) persisting sea water pollution increased cell damage of bivalve gill cells and consequently led to leakage of the RB into cytoplasm and dysfunctional MXR efflux in wild mussels; or/and (2) a mixture of different toxic compounds present in Vranjic Bay sea water induced oversaturation of MXR efflux, inducing elevated accumulation of the dye. Consequently, it seems that an efficient physiological functioning of MXR in wild mussels is strongly hampered by existence of an unknown quantity of sea water pollutants that may endanger intrinsic organismal defense system and lead toward the enhancement of toxicity.

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