Increase in levels of total free fatty acids in rat brain regions following 3-nitropropionic acid administration
Section snippets
Acknowledgements
This study was supported by FDA/NCTR/CFSAN funds. Rebecca P. Danam and Ivan A. Ross are acknowledged for their help in this project.
References (24)
- et al.
Lipid peroxidation in rats intoxicated with 3-nitropropionic acid
Toxicon
(1995) - et al.
Consistent striatal damage in rats induced by 3-nitropropionic acid and cultures of Anthrinium fungus
Neurotoxicol. Teratol.
(1995) - et al.
Brain enzyme and clinical alterations induced in rats and mice by nitroaliphatic toxicants
Toxicol. Lett.
(1985) Overview of enzyme systems involved in bioreduction of drug and in redox cycling
Biochem. Pharmacol.
(1986)- et al.
3-Nitropropionic acid produces striatum selective lesions accompanied by iNOS expression
J. Chem. Neuroanat.
(1996) - et al.
Glutamate becomes neurotoxic via the N-methyl-d-aspartate receptor when intracellular energy levels are reduced
Brain Res.
(1988) - et al.
Protective actions of l-carnitine and acetyl-l-carnitine on the neurotoxicity evoked by mitochondrial uncoupling or inhibitors
Pharmacol. Res.
(1995) - et al.
3-Nitropropionate, the toxic substance of indigofera, is a suicide inactivator of succinate dehydrogenase
Proc. Natl. Acad. Sci. USA
(1977) - et al.
Neurochemical and histologic characterization of striatal excitotoxic lesions produced by the mitochondrial toxin 3-nitropropionic acid
J. Neurosci.
(1993) - et al.
The effects of perinatal hypoxia on the behavioral, neurochemical, and neurohistological toxicity of the metabolic inhibitor 3-nitropropionic acid
Metab. Brain Dis.
(1995)
Age-dependent vulnerability of the striatum to the mitochondrial toxin 3-nitropropionic acid
J. Neurochem.
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The H <inf>2</inf>O <inf>2</inf> scavenger ebselen decreases ethanol-induced locomotor stimulation in mice
2012, Drug and Alcohol DependenceCitation Excerpt :Manrique et al. (2006) showed that administration of 3-nitropropionic acid (3-NPA), an H2O2 generator, boosts ethanol-induced locomotion in mice. However, this compound was also able to increase the activity of catalase per se (Binienda and Kim, 1997; Binienda et al., 1998; Manrique et al., 2006). Therefore, it is possible that the increment in the locomotor stimulating effects produced by ethanol after administration of 3-NPA could be due to a higher activity of catalase, to an increment in H2O2 levels or to both.
Acute administration of 3-nitropropionic acid, a reactive oxygen species generator, boosts ethanol-induced locomotor stimulation. New support for the role of brain catalase in the behavioural effects of ethanol
2006, NeuropharmacologyCitation Excerpt :Therefore, the effect of 3-NPA on locomotion cannot be explained by changes in the ethanol levels reaching the brain. In accordance with Binienda and Kim (1997) and Binienda et al. (1998), in our study we observed that a pre-treatment with 3-NPA increased the activity of catalase in the brain homogenates as compared to control homogenates. Moreover, our data also showed that l-carnitine prevented the effects of 3-NPA on brain catalase activity, an effect that was reported by Binienda and Ali (2001).