Effects of Calcium Disodium EDTA on the Neurotoxicity of Manganese on Biogenic Amines in the Nervous System and Innervated Organs of Crassostrea virginica


Meeting Abstract

P1.131  Sunday, Jan. 4  Effects of Calcium Disodium EDTA on the Neurotoxicity of Manganese on Biogenic Amines in the Nervous System and Innervated Organs of Crassostrea virginica LAGARES, E.*; DAHNIEL, S.; CARROLL, M.A.; CATAPANE, E.J.; Medgar Evers College elagares28@yahoo.com

Manganese (Mn) is a neurotoxin which induces Manganism, a Parkinson-like disease, in individuals exposed to high airborne levels. Exposure to high levels of Mn for long periods may cause mental and emotional disturbances, and slow and clumsy body movements. Manganism occurs because Mn injures dopamine neurons in the brain involved in control of body movements. Recently, p-aminosalicylic acid (PAS) has been shown to alleviate symptoms of Manganism in humans, but its mechanism of action is unknown. The oyster, Crassostrea virginica, possesses a dopaminergic system innervating the gill and regulating lateral ciliary activity. Previously we showed PAS protected dopamine neurons against the neurotoxic effects of Mn. PAS has anti-inflammatory and chelating ability. The ability of PAS to ameliorate symptoms of Manganism is postulated to be related to its chelating actions. To test this, we treated C. virginica with Mn and calcium disodium EDTA (EDTAca), a chelating agent. C. virginica were exposed to 500 µM of Mn with and without 50 or 500 µM of EDTAca for 3 days. Controls were similarly treated without Mn or EDTAca. Biogenic amines were measured by HPLC techniques with fluorescence detection. Cerebral ganglia, visceral ganglia and gill were dissected, weighed, homogenized, centrifuged, filtered and injected into a Beckman HPLC system with a Phenomenex Gemini µ C18 column and a Jasco FP 2020 Spectrofluorometer with a 50 mM acetate buffer mobile phase. EDTAca treatments protected the ganglia and gill against the effects of Mn. These findings may provide insights into the actions of Mn and PAS in treatments of Manganism. 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 0420359 of the MRI Program of NSF.

the Society for
Integrative &
Comparative
Biology