Meeting Abstract

P1.174  Friday, Jan. 4  Manganese Accumulations in Gill Mitochondria of Crassostrea viginica? NUHAR, A.*; BOISETTE, B.; CARROLL, M.A.; CATAPANE, E.J.; Medgar Evers College; Medgar Evers College; Medgar Evers College; Medgar Evers College catapane@mec.cuny.edu

Manganese (Mn) is a neurotoxin causing Manganism in people chronically exposed to elevated levels in their environment. Mn targets dopamine (DA) neurons in basal ganglia. Oxidative stress has been implicated as a factor of Mn toxicity and DA dysfunction. Mitochondria play a role as cause and target of oxidative stress damage. The mechanisms of damage is attributed to Mn’s capacity to produce toxic levels of free radicals and induce mitochondrial dysfunction. Others report Mn accumulates in mitochondria and represent the 1̊ pool of Mn in cells. Controversy exists to the extent of Mn accumulation in mitochondria. Others report Mn accumulates within nuclei and cytoplasm, but not mitochondria. Our lab is using the oyster, Crassostrea virginica, as a test animal to study Mn neurotoxicty. We found Mn disrupts the DA system as well as mitochondrial respiration. To study if Mn accumulates within mitochondrial of gill cells of C. virginica we used differential centrifugation and atomic absorption spectrometry. Gills were homogenized and centrifuged to isolate nuclear, mitochondrial and post-mitochondrial fractions. Each fraction was analyzed for Mn. To determine if isolated mitochondria accumulate Mn we prepared treated mitochondrial suspensions with up to 300 mM Mn. Results show a dose dependent accumulation of Mn in mitochondria of up to 5000%. Two day treatments of animals with 500 and 1000 μM Mn increased Mn (μg/gdw) in gill from a baseline of 5.8 to 41.6 and 133.8, respectively, and centrifugation revealed Mn accumulations were primarily in nuclear and mitochondrial fractions. The study shows mitochondria accumulate Mn. In vivo treatments reveal accumulations with both the nuclear and mitochondrial fractions.