Cadmium affects nitric oxide metabolism during normoxia and intermittent anoxia in eastern oysters Crassostrea virginica


Meeting Abstract

P3.55  Wednesday, Jan. 6  Cadmium affects nitric oxide metabolism during normoxia and intermittent anoxia in eastern oysters Crassostrea virginica SOKOLOVA, I.M.*; IVANINA, A.; EILERS, S.; KUROCHKIN , I.; SOKOLOV, E.P.; University of North Carolina at Charlotte, Charlotte, NC; University of North Carolina at Charlotte, Charlotte, NC; University of North Carolina at Charlotte, Charlotte, NC; University of North Carolina at Charlotte, Charlotte, NC; Carolinas Medical Center, Charlotte, NC isokolov@uncc.edu

Nitric oxide (NO) is an intracellular signaling molecule involved in regulation of many cellular functions including mitochondrial metabolism and bioenergetics; however, its role in invertebrates is not well understood. We determined sensitivity of mitochondrial and cellular respiration to NO and the effects of Cd and intermittent anoxia on NO metabolism in oysters, Crassostrea virginica. NOS activity was strongly suppressed by exposure to 50 µg L-1 Cd for 30 days, and further decreased during anoxic exposure in Cd-exposed oysters but not in their control counterparts. Nitrate/nitrite content (indicative of NO levels) decreased during anoxic exposure to less than 10% of the normoxic values, and recovered within 1 h of re-oxygenation in control oysters. In Cd-exposed oysters the recovery of steady-state NO levels lagged behind reflecting their lower NOS activity. Oyster mitochondrial respiration was inhibited by exogenous NO, with sensitivity on a par with mammalian mitochondria, and ADP-stimulated mitochondrial respiration was significantly more sensitive to NO than resting respiration. In isolated gill cells, manipulations of endogenous NOS activity had no effect on respiration, likely due to the fact that mitochondria in the resting state are relatively NO-insensitive. Likewise, Cd-induced stimulation of cellular respiration did not correlate with decreased NOS activity in isolated gill cells. These data suggest that regulation of bioenergetics is an evolutionarily conserved function of NO. Supported by NSF.

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