<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>9(1)</volume><submitter>Virmani A</submitter><pubmed_abstract>The neurotoxicity induced by the mitochondrial inhibitor 3-nitropropionic acid (3-NPA) is associated with a decrease of ATP synthesis and an increase of free radical production which can lead to apoptosis or necrosis. We have used the PC12, neuron-like rat pheochromocytoma cell line, to study further the mechanism of 3-NPA-evoked neurotoxicity and the effects of acetyl-L-carnitine (ALC) which has neuroprotective actions against various types of mitochondrial inhibitors.Cultured PC 12 cells were exposed to a low dose of 3-NPA 50 (microM) in the presence or absence of 5 mM ALC. The dose of 3-NPA was sub toxic and no changes in pro-apoptotic Bax or anti-apoptotic Bcl-2 gene expression were observed. We followed specific genetic markers to look for changes evoked by 3-NPA toxicity and also cha</pubmed_abstract><journal>Current neuropharmacology</journal><pagination>195-9</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3137180</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Acetyl-L-Carnitine Modulates TP53 and IL10 Gene Expression Induced by 3-NPA Evoked Toxicity in PC12 Cells.</pubmed_title><pmcid>PMC3137180</pmcid><pubmed_authors>Virmani A</pubmed_authors><pubmed_authors>Ali SF</pubmed_authors><pubmed_authors>Binienda ZK</pubmed_authors><pubmed_authors>Koverech A</pubmed_authors></additional><is_claimable>false</is_claimable><name>Acetyl-L-Carnitine Modulates TP53 and IL10 Gene Expression Induced by 3-NPA Evoked Toxicity in PC12 Cells.</name><description>The neurotoxicity induced by the mitochondrial inhibitor 3-nitropropionic acid (3-NPA) is associated with a decrease of ATP synthesis and an increase of free radical production which can lead to apoptosis or necrosis. We have used the PC12, neuron-like rat pheochromocytoma cell line, to study further the mechanism of 3-NPA-evoked neurotoxicity and the effects of acetyl-L-carnitine (ALC) which has neuroprotective actions against various types of mitochondrial inhibitors.Cultured PC 12 cells were exposed to a low dose of 3-NPA 50 (microM) in the presence or absence of 5 mM ALC. The dose of 3-NPA was sub toxic and no changes in pro-apoptotic Bax or anti-apoptotic Bcl-2 gene expression were observed. We followed specific genetic markers to look for changes evoked by 3-NPA toxicity and also cha</description><dates><release>2011-01-01T00:00:00Z</release><publication>2011 Mar</publication><modification>2025-04-19T00:34:29.063Z</modification><creation>2021-02-19T23:52:34Z</creation></dates><accession>S-EPMC3137180</accession><cross_references><pubmed>21886589</pubmed><doi>10.2174/157015911795017182</doi></cross_references></HashMap>