An endogenous substance of the brain, tetrahydroisoquinoline, produces parkinsonism in primates with decreased dopamine, tyrosine hydroxylase and biopterin in the nigrostriatal regions
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Dopaminergic neurotoxic effects of 3-TFMPP derivatives
2018, Life SciencesCitation Excerpt :The initial increase in the release of dopamine can lead to increased dopamine metabolism and autoxidation, resulting in the generation of reactive oxygen species, which leads to oxidative stress, mitochondrial dysfunction, apoptosis and neuroinflammation [63–66]. Furthermore, the dopaminergic neurotoxins also inhibit the rate limiting enzyme in the synthesis of dopamine, tyrosine hydroxylase [67,68]. Based on the current literature on various dopaminergic neurotoxins, increased generation of reactive oxygen species, mitochondrial Complex-I inhibition, and augmented caspase-3 activity play an imperative role in dopaminergic neurotoxicity.
Current Status, Gaps, and Weaknesses of the Mechanism of Selective Dopaminergic Toxicity of MPTP/MPP<sup>+</sup>
2017, Advances in Molecular ToxicologyCitation Excerpt :In the brain, TIQs are convert to the corresponding fully aromatized cationic toxic forms [NMe-IQs (10)] through N-methylation by catecholamine N-methyltransferases [to generate N-Me-TIQs (9)] followed by the MAO or nonspecific amine oxidases catalyzed oxidation parallel to the bioactivation of MPTP (Scheme 3.5) [117]. Similar to MPTP, the chronic treatment of primates with TIQs produces parkinsonian symptoms and the reduction of DA levels and TH activity in the nigrostriatal region of the brain [129,130]. In primate and mouse models, TIQs reduce the number of TH positive neurons in the substantia nigra [131].