Effects of Taurine on Manganese Accumulations in Gill of the Eastern Oyster, Crassostrea virginica

Abstract

Taurine (TAU) is an amino acid present in the diet and is a byproduct of cysteine metabolism. TAU is a neuroprotective agent against some neurodegenerative diseases including Alzheimer's, Parkinson's and Huntington's. Manganese (Mn) is a neurotoxin causing Manganism in people which often is confused with Parkinson's disease, an idiopathic neurodegenerative condition causing death of dopamine neurons. Our lab uses the oyster, Crassostrea virginica, as a test model to study toxic effects of metals on animal physiology. C. virginica, has a well‐studied serotonin and dopamine (DA) system controling gill lateral cell (GLC) cilia beating. Our previous work showed Mn disrupts the DA, but not serotonin control of GLC cilia. Our recent work shows TAU protects against the toxic effects of Mn on DA control of GLC cilia. We hypothesize TAU would be beneficial against Mn toxicity in C. virginica by reducing Mn accumulations in gill or by enhancing Mn removal from Mn exposed gill. Gills were treated 2 days in artificial salt water (ASW), ASW with TAU, ASW with Mn, or ASW with TAU and Mn (500 μM each). Gills were rinsed, dried, weighed, and digested in HNO3 in a CEM SP‐D Microwave Digester. Aliquots of digested gill were analyzed for Mn by electrothermal vaporization with deuterium lamp background correction in a Perkin Elmer AAnalyst 800 Atomic Absorption Spectrophotometer with a THGA Graphite Furnace. Results show Mn treatments caused significantly higher Mn accumulations compared to endogenous Mn of ASW controls or TAU (alone) treatment. Samples co‐treated with TAU and Mn had no significant difference in Mn accumulations compared to treatments of Mn alone suggesting TAU does not block Mn accumulation into gill. To determine if TAU could remove Mn from gill, in other experiments gills were treated 2 days with Mn (500 μM), rinsed with ASW, then treated 2 days in either ASW, ASW with TAU, or ASW with EDTA (0.5 to 2.5 mM each). Results showed the highest levels of EDTA (2.5 mM) were the most effective at removing Mn from gill by up to 80% compared to ASW controls. TAU treatments were effective to a lesser degree, removing only about 25% compared to ASW controls. The study shows while TAU did not prevent Mn from accumulating in gill, it did have some beneficial effects in removing Mn, similar to the way chelating agents have long been used in treatment of various pathologies of metal toxicity. Considering TAU is a natural biological component of cells and metabolism and has shown some success as a protective agent in other neurodegenerative diseases, more studies are needed to determine if TAU can be used as an effective, and safer, therapeutic agent in the clinical treatment of Manganism.Support or Funding InformationGrant 2R25GM06003 of the Bridge Program of NIGMS and a Carnegie Foundation award.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.