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Factors affecting manganese accumulations in gill mitochondria of Crassostrea virginica (996.1)
Author(s) -
Shoneye Temitope,
Nuhar Ahmed,
Catapane Edward,
Carroll Margaret
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.996.1
Subject(s) - mitochondrion , uniporter , ruthenium red , chemistry , biophysics , calcium , cytosol , biology , biochemistry , enzyme , organic chemistry
Manganese (Mn) is a neurotoxin causing Manganism in people exposed to high environmental levels. Oxidative stress is implicated as a factor of Mn toxicity. The mechanisms is attributed to toxic levels of free radicals inducing mitochondrial dysfunction. Reports indicate Mn accumulates in mitochondria, however controversy exists to the extent of Mn accumulation in mitochondria and whether this contributes to the cause of Manganism. We have been using the oyster, Crassostrea virginica , to study Mn neurotoxicty. We found Mn disrupts the animals’ dopaminergic system and mitochondrial respiration. Mn is believed to use the mitochondrial Ca 2+ uniporter and H + or Na + /Ca 2+ exchanger for movements in and out of mitochondria. We hypothesize Ca 2+ channel blockers will alter mitochondrial Mn accumulations. We prepared mitochondrial fractions from gills. Mitochondria were treated with Ca 2+ channel blockers prior to Mn exposure, pelleted and washed, then digested in HNO 3 and analyzed in an AA. Mitochondria treated with Mn (1 ‐ 5 mM) exhibited a dose dependent accumulation of up to 1000% compared to controls. The channels blockers, LaCl 3, diltiazem, verapamil and ruthenium red (0.25 ‐ 2 mM) reduced accumulations. LaCl 3 was the most effective. The study shows mitochondria accumulate Mn and the mechanism of influx and efflux can be affected by drugs that interact with mitochondrial Ca 2+ uniporter and H + or Na +/ Ca 2+ exchanger. Grant Funding Source : NYSED‐ 0516041171, NSF‐0622197