Meeting Abstract

P2.103  Wednesday, Jan. 5  The Effects of Manganese on Mitochondrial Aconitase and Cytochrome c Oxidase in the Gill of the Bivalve Crassostrea virginica HUANG, K.*; HUANG, H.; NICHOLAS, Z.; HUTCHINSON, A.; DESROCHES, R.; CATAPANE, E.J.; CARROLL, M.A.; Medgar Evers; Medgar Evers; Kingsborough; Medgar Evers; Medgar Evers; Medgar Evers; Medgar Evers catapane@mec.cuny.edu

Manganese (Mn) is an essential trace metal but excessive exposure can lead to Mn toxicity. In humans Mn is neurotoxic and can lead to Manganism, a Parkinsons-like disorder. It is hypothesized that Mn toxicity causes mitochondrial dysfunction. Mitochondrial dysfunction is recognized as a factor in aging and many neurodegenerative diseases including Alzheimer’s and Parkinson’s disease. Being a redox-active element, excess Mn can increase mitochondrial oxidative stress and impair activities involved in energy homeostasis. Previously we showed Mn accumulates in gill and other tissues of the bivalve, Crassostrea virginica and Mn treatments selectively disrupt the dopaminergic system controlling lateral cilia in gill. We also showed it impairs gill mitochondrial respiration. In this study we examined effects of Mn treatments on two mitochondrial enzymes: aconitase, a Kreb Cycle enzyme and cytochrome c oxidas, complex IV of the respiratory chain. Gill mitochondria were prepared from adult C. virginica and aliquots of mitochondrial suspension were exposed to various concentration of Mn. Mitochondrial aconitase and cytochrome c oxidase activities were determined spectrophotometrically. Mn (up to 50 Mn) was found to inhibit aconitase, but not cytochrome c oxidase activity. The results corroborate our previous findings that Mn disrupts mitochondrial function in oyster gill and further demonstrates a mechanism by which Mn can disrupt energy homeostasis by impairing aconitase, an oxidative stress-sensitive enzyme of the Kreb Cycle.