1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced complex I inhibition is reversed by disulfide reductant, dithiothreitol in mouse brain
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Acknowledgements
We are grateful to Eisai Pharmaceutical (Japan) for providing ubiquinone 1. This research was funded by a grant from the US-India fund for Cultural, Educational and Scientific Cooperation.
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2019, Progress in NeurobiologyCitation Excerpt :It should be noted that PD affects men more than women, thus the neuroprotective effects of estrogens might be better in women (Dluzen and McDermott, 2000; Jurado-Coronel et al., 2017; Saunders-Pullman, 2003). For instance, exposure of male mice to 1-methyl-4-phenyl-1, 2, 3, 6, tetrahydro-pyridine (MPTP) (a neurotoxin that has inhibitory actions on MRC C–I activity) led to defective mitochondria and loss of dopaminergic neurons in some brain parts, whereas female mice showed no changes (Annepu and Ravindranath, 2000). The oxidation of critical thiol groups by MPTP causes disruptions in the MRC C–I (Drose et al., 2014; Dröse et al., 2016).
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2018, Food and Chemical ToxicologyCitation Excerpt :In the same context, rotenone, the specific inhibitor of mitochondrial complex I, has been shown to induce dopaminergic neurotoxicity, and has been successfully used as a PD model in vitro and in vivo (Camilleri and Vassallo, 2014; Xiong et al., 2012). In addition, other dopaminergic neurotoxins, such as 6-OHDA, MPTP, MA and paraquat, have also been reported to inhibit mitochondrial complex I activity and induce mitochondrial dysfunction in the nigrostriatal area of the brain (Annepu and Ravindranath, 2000; Dixit et al., 2013; Kupsch et al., 2014; Smith et al., 1994; Thrash et al., 2010; Thrash-Williams et al., 2013). Compelling evidence has indicated that PKCδ and its mitochondrial translocation contribute to mitochondrial dysfunction in dopaminergic neurotoxicity (Hanrott et al., 2006; Latchoumycandane et al., 2011; Nam et al., 2015; Nguyen et al., 2015; Shin et al., 2014; Sun et al., 2008).
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2014, Analytical BiochemistryConstitutive expression and functional characterization of mitochondrial glutaredoxin (Grx2) in mouse and human brain
2007, Brain ResearchCitation Excerpt :Complex I contains several cysteine residues in its active site (Dupuis et al., 1991), and the facile glutathionylation of thiol groups in the enzyme by reactive oxygen species can potentially result in inhibition of the enzyme. Our earlier studies show that the complex I inhibition caused by MPTP can be reversed by dithiothreitol, further confirming that protein thiol oxidation is a primary cause for complex I inhibition (Annepu and Ravindranath, 2000). Therefore, maintenance of protein thiol homeostasis is critical for preserving the functional activity of complex I.
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