کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
4351206 | 1615197 | 2006 | 4 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Mitochondrial damage induced by fetal hyperphenylalaninemia in the rat brain and liver: Its prevention by melatonin, Vitamin E, and Vitamin C
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
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چکیده انگلیسی
Abnormal oxidative stress was observed in hyperphenylalaninemia and other inborn errors of intermediary metabolism, owing to the accumulation of toxic metabolites, free radical production and increased LPO products. In our model of maternal hyperphenylalaninemia, pregnant rats were injected with 300Â mg/kg BW l-phenylalanine (PHE) and 50Â mg/kg BW p-chlorophenylalanine (PCPA) dissolved in saline. In this research study, we measured LPO-by-products, i.e., malonaldehyde (MDA) and 4-hydroxynonenal (4-HNE) and we demonstrated that maternal hyperphenylalaninemia increased both markers of oxidative stress in the brain and liver mitochondria of the pups. We also demonstrated that administration of melatonin, Vitamin E, and Vitamin C, in this order of potency, prevented the oxidative damage to the mitochondria, especially in the brain. We therefore conclude that maternal hyperphenylalaninemia induces a clear state of oxidative stress that is somehow directly involved in brain and liver impairment, which can be prevented by melatonin, Vitamin E, and Vitamin C.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience Letters - Volume 392, Issues 1â2, 9 January 2006, Pages 1-4
Journal: Neuroscience Letters - Volume 392, Issues 1â2, 9 January 2006, Pages 1-4
نویسندگان
Francisco MartÃnez-Cruz, Carmen Osuna, Juan M. Guerrero,