A Study of Acute and Long Term Additions of Copper on Glutathione S-Transferase Activity in Gill Tissue of the American Oyster, Crassostrea virginica


Meeting Abstract

P3.120  Jan. 6  A Study of Acute and Long Term Additions of Copper on Glutathione S-Transferase Activity in Gill Tissue of the American Oyster, Crassostrea virginica DOCTEUR, Nympha*; FLORES, Liz; CARROLL, Margaret A.; CATAPANE, Edward J.; Medgar Evers College; Medgar Evers College; Medgar Evers College; Medgar Evers College margie@mec.cuny.edu

Copper is a common aquatic pollutant. While bivalve mollusks are used for monitoring and bioaccumulation kinetics studies, little is known about their biochemical responses to metal accumulation. Metal accumulation can increase oxidative stress by various means including depletion of cellular antioxidants such as reduced glutathione (GSH). Glutathione S-Transferase (GST) is a ubiquitous group of Phase II detoxification enzymes that catalyze the conjugation of electrophilic substrates, such as organic xenobiotics, to GSH. While studies have been done on GST in mammals and other vertebrates, less is known in invertebrates. To study the effects of Cu+2 we incubated C. virginica with increasing concentrations of Cu+2 (up to 400 µM) for 3 days by removing 1 shell from the animals and maintaining them in individual, aerated containers of artificial sea water at 18�C. Other oysters were treated short-term with Cu+2 (up to 600 µM) for 4 hours. Controls were similarly treated without Cu+2. Gill tissue was removed and processed to obtain the post-mitochondrial supernatant. GST activity in this fraction was measured spectrophotometrically using 1-chloro-2,4 dinitrobenzene and GSH as substrates, and calculated using the conjugate’s molar extinction coefficient of 0.0096µM-1cm-1. In this study we found that exposing the animals to Cu+2 reduced GST activity by up to 61% in the 3-day experiments, and by up to 67% in the short-term experiments. This study is important because it will help us gain further insight into role of toxic metal exposures on oxidative stress and the cellular mechanism that defend against oxidative stress. This work was supported by grants 1R25GM62003 of NIGMS, 0516061071 of NYSDOE, and 66288-0036 of PSC-CUNY. We thank Frank M. Flower & Sons, Inc., Oyster Bay, NY for supplying oysters.

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