Toxic Effects of Manganese on Mitochondrial Catalase and Cytochrome C Oxidase in Gills of the Bivalve Crassostrea virginica


Meeting Abstract

P3.54  Wednesday, Jan. 6  Toxic Effects of Manganese on Mitochondrial Catalase and Cytochrome C Oxidase in Gills of the Bivalve Crassostrea virginica KELLY, K.*; BROWN, K.; SAINT-DIC, R.; CATAPANE, E.J.; CARROLL, M.A.; Medgar Evers College, Brooklyn catapane@mec.cuny.edu

Manganese (Mn) is an essential trace nutrient but overexposure causes Manganism in people. The mechanism of Mn toxicity remains unknown. Mn accumulates in mitochondria and toxicity may be associated with organelle dysfunction disrupting energy homeostasis and raising levels of reactive oxygen species. Previously we showed Mn accumulates in gill of Crassostrea virginica, disrupts the dopaminergic innervation of lateral cilia in gill, and impairs gill mitochondrial respiration. We examined effects of Mn on 2 mitochondrial enzymes, cytochrome c oxidase (COX) and catalase (CAT). COX is the principle terminal oxidase of high affinity oxygen in aerobic respiration. We prepared mitochondria from gill treated with Mn. COX activity was determined spectrophotometrically by observing the decreased absorbance at 550 nm as Fe+2cytochrome c is oxidized to Fe+3cytochrome c. We found exposure to Mn (5-40 mM) caused up to a 40% loss in cytochronme c oxidase activity. CAT protects against oxidative stress by degrading H2O2. Present primarily in cytosol or peroxisomes of aerobic cells, little has been reported on mitochondrial CAT, especially in bivalves. We removed right shells of oysters and placed them in containers of ASW with or without Mn for 3 days. Gill mitochondria were prepared and CAT activity determined. We found CAT in gill mitochondria and 3 day treatments with 1 mM Mn caused a 50% loss in CAT. The results corroborate our previous findings Mn disrupts mitochondrial function in oyster gill and demonstrate a mechanism by which Mn increases oxidative stress by impairing complex IV of the respiratory chain and inhibiting the activity of mitochondrial CAT. The work was supported by grants 0622197 of NSF, 2R25GM06003-05 of NIGMS, 0516041071 of NYSDOE, and P382A080040 of the USDE.

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