Meeting Abstract
P1.114 Thursday, Jan. 3 Manganese Disruption of Mitochondrial Respiration in the Bivalve Crassostrea virginica and its Protection by p-Aminosalicylic Acid DAVIS, K.*; SADDLER, C.; CARROLL, M.A.; CATAPANE, E.J.; Medgar Evers College; Kingsborough Community College; Medgar Evers College; Medgar Evers College catapane@mec.cuny.edu
Manganese is an essential metal that at excessive levels in the brain produces extrapyramidal symptoms called Manganism which is similar to Parkinsons disease. The mechanism of action of manganese is not completely understood but is thought to be due to factors including decreased brain dopamine levels, altered dopamine receptor activity and/or oxidative stress in mitochondria. p-Aminosalicylic acid (PAS) is a drug which recently is being shown to alleviate symptoms of Manganism. We studied the effects of manganese and PAS on mitochondrial respiration in gill of the bivalve mollusc, Crassostrea viginica. C. viginica gill is a tissue which is innervated by dopaminergic neurons. Mitochondrial respiration was measured using a YSI Micro-Biological Oxygen Monitor with a micro-batch chamber. Additions of manganese (0.1 – 10 mM) caused dose dependent decreases in mitochondrial O2 consumption. Adding PAS (0.1, 1 mM) prior to manganese additions protected the mitochondria. The study demonstrates that manganese does adversely affect mitochondrial respiration and that the protective actions of PAS may in part be due to its ability to shield mitochondria from manganese induced oxidative stress. 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.
