سال انتشار: ۱۳۸۵

محل انتشار: دومین سمپوزیوم بین المللی تکنولوژی و بیولوژی زعفران

تعداد صفحات: ۱۰

نویسنده(ها):

D.S Del-Angel – Laboratorio de Neuroquímica Instituto Nacional de Pediatría S.S.A. México D.F. 04530 México
N.L.H Martínez – Laboratorio de Neuroquímica Instituto Nacional de Pediatría S.S.A. México D.F. 04530 México
M.E.G Cruz – Laboratorio de Neuroquímica Instituto Nacional de Pediatría S.S.A. México D.F. 04530 México
E.C Urrutia – Laboratorio de Oncología Experimental Instituto Nacional de Pediatría S.S.A. México D.F. 04530 México

چکیده:

Given its widely reported antioxidant properties, the effects of saffron extract (SE) were tested in striatal synaptosomes isolated from the brain of rats exposed to the mitochondrial toxin 3-nitropropionic acid (3-NPA). The assays of thiobarbituric acid-reactive substances (TBARS) formation and 3-(3,5-dimethylthiazol-2-yl)2,5-diphenyltetrazolium bromite (MTT) reduction were used as current markers of lipid peroxidation (LP) and synaptosomal viability, respectively. Our results show that 3-NPA alone (20 mg/kg/day, i.p.), given to rats for 3 days, produced a significant increase in LP and decreased the mitochondrial function in synaptosomal fractions when compared with control. In contrast, striatal synaptosomes from those animals receiving SE (1 mg/kg/day, i.p.) for 5 days (administration schedule starting 1 day before and finishing 1 day after 3-NPA), exhibited levels of LP similar to control, while preserved their mitochondrial function. Another index of LP, the formation of lipid fluorescent products, was tested in brain homogenates incubated with 3-NPA and/or SE. 3-NPA significantly increased LP by 90 %, while SE decreased this marker. Altogether, these data suggest that protective actions of SE produced in the 3-NPA model may be related with its antioxidant properties, as saffron is rich in antioxidant carotenoids. Our data also open a research field on the potential neuroprotective properties of saffron compounds against neurodegenerative disorders with energy impairment and excitotoxic components.