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• W2081350263 abstract "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 300 mg/kg BW l-phenylalanine (PHE) and 50 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." @default.
• W2081350263 created "2016-06-24" @default.
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• W2081350263 date "2006-01-01" @default.
• W2081350263 modified "2023-10-02" @default.
• W2081350263 title "Mitochondrial damage induced by fetal hyperphenylalaninemia in the rat brain and liver: Its prevention by melatonin, Vitamin E, and Vitamin C" @default.
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• W2081350263 doi "https://doi.org/10.1016/j.neulet.2005.02.073" @default.
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