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Changes in the brain mitochondrial proteome of male Sprague-Dawley rats treated with manganese chloride.

Authors: Zhang, Surong  Fu, Juanling  Zhou, Zongcan 
Citation: Zhang S, etal., Toxicol Appl Pharmacol. 2005 Jan 1;202(1):13-7.
Pubmed: (View Article at PubMed) PMID:15589972
DOI: Full-text: DOI:10.1016/j.taap.2004.06.001

To probe the mitochondrial involvement in Mn intoxicity, aliquots of brain mitochondria samples from control and treated (30 mg/kg manganese chloride, ip) male Sprague-Dawley rats were separated by two-dimensional polyacrylamide gel electrophoresis (2D-PAGE) and searched for protein abundance changes induced by Mn exposure. The electrophoretic separation resolved over 300 distinct spots as visualized by colloidal Coomassie blue (CCB), of which three spots were induced and three spots were inhibited after Mn exposure in all the five brain mitochondria preparations. Analysis by matrix-assisted laser desorption/ionization time of flight (MALDI-TOF) indicated that these spots are calcium-transporting ATPase type 2C (ATP-dependent Ca(2+) pump PMR1); 60-kDa heat shock protein; Mitochondrial transmembrane GTPase FZO1B; ATP-binding cassette, sub-family b; Long-chain-fatty-acid-CoA ligase; ATP Synthase Beta Chain; and Succinate dehydrogenase flavoprotein subunit. The changes of the mitochondrial ATP synthase beta-subunit and Succinate dehydrogenase flavoprotein subunit indicate an effected level of mitochondrial ATP content and/or ATP-producing capacity. This result provides suggestion that respiratory chain complexes were implicated in the mitochondrial dysfunction induced by Mn intoxicity. And the changes of 60-kDa heat shock protein and ATP-dependent Ca(2+) pump PMR1 expression indicate that the Ca homeostasis and stress effect were involved in Mn intoxicity.

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CRRD Object Information
CRRD ID: 13204841
Created: 2017-07-21
Species: All species
Last Modified: 2017-07-21
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.