Effects of Diltiazem and Lanthanum on Copper Inhibition of Mitochondrial Osub2sub Consumption of Gill of the Oyster, Crassostrea virginica


Meeting Abstract

P2.86  Friday, Jan. 4  Effects of Diltiazem and Lanthanum on Copper Inhibition of Mitochondrial O2 Consumption of Gill of the Oyster, Crassostrea virginica MCCOY, K.*; CARROLL, M.A.; CATAPANE, E.J.; Medgar Evers College; Medgar Evers College; Medgar Evers College margie@mec.cuny.edu

Our lab demonstrated that tissues of the bivalve Crassostrea virginica accumulate from their surroundings copper and other metals in excess of environmental levels. We showed mitochondrial O2 consumption in C. virginica gill and gill mitochondria was inhibited by in vitro copper treatments. This is interesting because many locations where C. virginica inhabit are copper polluted. Now we determined effects of 2 metal transport blockers, diltiazem and lanthanum, on the inhibitory actions of copper on O2 consumption in gill mitochondria of C. virginica. O2 utilization was measured using a YSI Micro-Biological Oxygen Monitor with micro-batch chambers. Addition of CuSO4 (1-20 mM) caused a dose dependent decrease in mitochondrial O2 consumption. Diltiazem (5-10 mM) did not alter mitochondrial O2 utilization and it significantly reduce by over 50% the inhibitory effect of copper on respiration. Lanthanum (5-10 mM) was less effective at protecting against the inhibitory effects of copper and contributed its own inhibitory effect on gill mitochondrial O2 utilization. The study demonstrates under our experimental conditions, diltiazem is effective in blocking copper’s inhibitory effects on gill mitochondrial O2 consumption and may be useful in protecting against the effects of copper uptakes in tissues of other animals as well. The toxic effects of copper on gill mitochondrial could be of physiological significance to the growth and long-term health of oysters and other marine animals living in a copper polluted environment and a copper uptake blocker could be of benefit for preventing diseases caused by high serum copper levels in humans. This work was supported in part by grants 2R25GM06003-05 of the Bridge Program of NIGMS, 0516041071 of NYSDOE, 0622197 of the DUE Program of NSF and 67876-0036 of PSC-CUNY.

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