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The Endogenous Amine 1‐Methyl‐1,2,3,4‐ Tetrahydroisoquinoline Prevents the Inhibition of Complex I of the Respiratory Chain Produced by MPP +
Author(s) -
Parrado Juan,
Absi Elhadi,
Ayala Antonio,
Castaño Angélica,
Cano Josefina,
Machado Alberto
Publication year - 2000
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.2000.0750065.x
Subject(s) - endogeny , mitochondrion , neurotoxicity , mptp , neurotoxin , striatum , pharmacology , chemistry , monoamine neurotransmitter , tetrahydroisoquinoline , tyrosine hydroxylase , biochemistry , biology , neuroscience , toxicity , dopamine , dopaminergic , enzyme , receptor , serotonin , organic chemistry
: The endogenous monoamine 1‐methyl‐1,2,3,4‐tetrahydroisoquinoline has been shown to prevent the neurotoxic effect of MPP + and other endogenous neurotoxins, which produce a parkinsonian‐like syndrome in humans. We have tested its potential protective effect in vivo by measuring the protection of 1‐methyl‐1,2,3,4‐tetrahydroisoquinoline in the neurotoxicity elicited by MPP + in rat striatum by tyrosine hydroxylase immunocytochemistry. Because we know that cellular damage caused by MPP + is primarily the result of mitochondrial respiratory inhibition at the complex I level, we have extended the study further to understand this protective mechanism. We found that the inhibitory effect on the mitochondrial respiration rate induced by MPP + in isolated rat liver mitochondria and striatal synaptosomes was prevented by addition of 1‐methyl‐1,2,3,4‐tetrahydroisoquinoline. This compound has no antioxidant capacity ; therefore, this property is not involved in its protective effect. Thus, we postulate that the preventive effect that 1‐methyl‐1,2,3,4‐tetrahydroisoquinoline has on mitochondrial inhibition for MPP + could be due to a “shielding effect,” protecting the energetic machinery, thus preventing energetic failure. These results suggest that this endogenous amine may protect against the effect of several parkinsonism‐inducing compounds that are associated with progressive impairment of the mitochondrial function.