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Protection of the aged substantia nigra of the rat against oxidative damage by (−)−deprenyl
Author(s) -
Cruz Cristina P.,
Revilla Elisa,
Steffen Vera,
RodríguezGómez Jose A.,
Cano Josefina,
Machado Alberto
Publication year - 1996
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1996.tb15350.x
Subject(s) - substantia nigra , selegiline , medicine , endocrinology , oxidative stress , tyrosine hydroxylase , saline , parkinson's disease , oxidative phosphorylation , oxidative damage , chemistry , biochemistry , dopamine , disease
1 We have studied the effect of (−)−deprenyl on the oxidative damage that the rat substantia nigra suffers during aging. 2 (−)−Deprenyl (2 mg kg −1 , three times a week) administered for two months, beginning at 22 months of age, produced a significant increase in tyrosine hydroxylase (TH) activity (2.67±0.40 and 3.64±0.38 nmol mg −1 protein h −1 in untreated aged rats and treated aged rats respectively, P <0.05) and in TH amount (0.072±0.012 and 0.128±0.38 absorbance 405 nm in untreated aged and treated aged rats respectively, P <0.05). 3 The proteins of aged rat substantia nigra showed a significant decrease of carbonyl groups in treated animals compared with saline‐injected control rats (136.2±21.8 and 71.5±13.2 c.p.m. μg −1 protein in untreated aged and treated aged rats respectively, P <0.05). 4 The carbonyl groups measured in TH enzyme showed a statistically significant decrease (42.3%) after (−)−deprenyl treatment (471.4±73.0 and 271.9±50.00 c.p.m. in untreated aged and treated aged rats respectively, P <0.001). 5 All these results suggest that oxidative damage produced during aging is prevented by (−)−deprenyl treatment and could explain the effect of this drug in Parkinson's disease (PD) and other degenerative diseases such as Alzheimer's disease.

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