Effects of cysteamine on oxidative status in cerebral cortex of rats.

Abstract:

:Cystinosis is a systemic genetic disease caused by a lysosomal transport deficiency accumulating cystine in most tissues. Tissue damage depends on cystine accumulation, but the mechanisms of this damage are still obscure. Cysteamine administration depletes cystine accumulated, increasing survive of affected patients. Studies performed in fibroblasts of cystinotic patients suggest that apoptosis is enhanced in this disease. Considering that oxidative stress is a known apoptosis inducer, our main objective was to investigate a possible antioxidant effect of cysteamine on several parameters of oxidative stress in the brain of young rats. Animals received three subcutaneous injections at 3-h intervals of a buffered solution (pH 7.4) of 10 mg/kg body weight cysteamine and were sacrificed 1 h after the last injection. Cysteamine decreased lipoperoxidation and glutathione peroxidase activity, and increased the carbonyl content of proteins and catalase activity. In vitro studies showed that cysteamine reduced lipoperoxidation, 2',7'-dihydrodichlorofluorescein oxidation, carbonyl content of proteins and catalase activity, and increased glutathione peroxidase activity. These results suggest that cysteamine may act as a scavenger of superoxide free radicals and hydrogen peroxide. Therefore, it is possible that cysteamine may extend life of cystinotic patients acting not only as a cystine depleting drug, but also as a free radical scavenger, reducing cell damage by apoptosis.

journal_name

Metab Brain Dis

journal_title

Metabolic brain disease

authors

Kessler A,Biasibetti M,Feksa LR,Rech VC,Melo DA,Wajner M,Dutra-Filho CS,Wyse AT,Wannmacher CM

doi

10.1007/s11011-007-9078-x

subject

Has Abstract

pub_date

2008-03-01 00:00:00

pages

81-93

issue

1

eissn

0885-7490

issn

1573-7365

journal_volume

23

pub_type

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