Title of article :
Effect ofin VitroExposure to Tributyltin on Generation of Oxygen Metabolites by Oyster Hemocytes
Author/Authors :
Robert S. Anderson، نويسنده , , Lisa L. Brubacher، نويسنده , , Lisa M. Ragone Calvo، نويسنده , , Eugene M. Burreson، نويسنده , , Michael A. Unger، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 1997
Pages :
7
From page :
84
To page :
90
Abstract :
Mollusks depend chiefly on hemocyte-mediated cytotoxic mechanisms such as reactive oxygen species (ROS) to defend against pathogenic microorganisms. The effect ofin vitrotributyltin chloride (TBT) exposure on ROS generation by oyster (Crassostrea virginica) blood phagocytes is quantified in this study. Luminol-augmented chemiluminescence (LCL) was used to measure ROS activity of resting and zymosan-stimulated cells after 1 or 20 hr TBT exposure. LCL is thought to measure primarily the activity of the myeloperoxidase/hydrogen peroxide/halide antimicrobial pathway. Hemocytes in TBT-free medium (controls) produced low level LCL, which was markedly stimulated by the addition of zymosan particles. Both resting and zymosan-stimulated LCL values were significantly inhibited by ≥80 ppb TBT after either 1 or 20 hr of exposure. Exposure to ≤2 ppb TBT concentrations for 20 hr produced slightly enhanced LCL activity, suggesting a hormesis-like effect. Partial reversibility of TBT suppression of LCL took place when previously exposed cells were put in TBT-free medium. The TBT concentrations used in these studies were not cytolethalin vitroand were considerably less than oyster tissue levels recorded after chronic, sublethalin vitroexposures. The data suggest that the common aquatic contaminant TBT can interact rapidly withC. virginicahemocytes to produce a partially reversible immunotoxicological lesion. Xenobiotic-induced suppression of ROS production by hemocytes may increase host susceptibility to infectious diseases.
Journal title :
Environmental Research
Serial Year :
1997
Journal title :
Environmental Research
Record number :
727460
Link To Document :
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