Taurine Reduces the Toxic Effects of Manganese on Mitochondrial Membrane Potential
Authors: Florestan Christina , Gazca Kelly , Carroll Margaret A. , Catapane Edward J. 
Published: June 2021

Manganese (Mn) is an essential metal that at excessive levels in brain produces extrapyramidal symptoms called Manganism that is similar to Parkinson's disease. The toxic mechanism of Mn is not completely understood. Currently there is no effective treatment. One proposed mechanism suggests Mn causes cellular oxidative stress causing damage to the brain's dopamine system. Previously we showed Mn reduced O2 consumption and depolarized mitochondrial membrane potential in gill mitochondria of Crassostrea virginica. We also showed the deleterious effects of Mn on gill mitochondria were reduced by EDTA and p‐aminosalicylic acid (PAS), two drugs used therapeutically for patients with Manganism. Our recent work with C. virginica is showing taurine, a drug that alleviates symptoms in a number of other neurodegenerative diseases, reduced the deleterious effects of Mn on the cilio‐inhibitory effect of dopamine innervation of gill lateral cell (GLC) cilia. We hypothesize taurine can prevent neurotoxic effects of Mn on GLC mitochondrial membrane potential. We tested this using the mitochondrial fluorescent probe TMRM to study effects of taurine in protecting mitochondrial membrane potential in Mn treated GLC. C. virginica gill sections were placed on modified microscope slides holding 2 ml of ASW (artificial sea water) with 2.5μM TMRM, and exposed to Mn alone, taurine alone, co‐treated with Mn and taurine (125 μM each), or control gill sections without Mn or taurine. Sections were viewed on a Leica fluorescence microscope with epilume illumination using a 50 watt HBO mercury excitation lamp fitted with Texas Red filters (Ex 560 nm, Em 630 nm). Photomicrographs were taken with a Leica DFC400 camera at 100 and 200X at 0, 10 and 20 min. All sections were photographed with the same camera settings. Fluorescence intensity of GLC mitochondria was measured using ImageJ from NIH. We found control cells, not treated with Mn or taurine, were brightly fluorescing indicating a strong mitochondrial membrane potential. Taurine treated cells had fluorescence intensity similar to controls. Mn treated cells had a 40% reduction in fluorescence over the 20 minute period. Cells co‐treated with Mn and taurine had reduced fluorescence compared to controls, but the loss of fluorescence was only 20% that of cells treated with Mn and no taurine. These differences were statistically significant (ANOVA). The study showed taurine has protective effects against Mn toxicity on mitochondrial membrane potential and support our physiology studies demonstrating the neuro‐protective effect of taurine against the toxic actions of Mn on the dopamine cilio‐inhibitory innervation of GLC in C. virginica. These finding should be of interest to those exploring possible therapeutic treatments for Manganism.

Support or Funding Information

2R25GM06003 of the Bridge Program of NIGMS.

This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.