D-serine treatment induces oxidative stress in rat brain
Autor: | Guliz Armagan, Lutfiye Kanit, Ayfer Yalcin |
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Rok vydání: | 2011 |
Předmět: |
GPX1
Health Toxicology and Mutagenesis Excitotoxicity Biology Pharmacology Cell Fractionation Toxicology GPX4 medicine.disease_cause Neuroprotection Rats Sprague-Dawley Lipid peroxidation chemistry.chemical_compound Malondialdehyde Serine medicine Animals chemistry.chemical_classification Chemical Health and Safety Dose-Response Relationship Drug Glutathione peroxidase Public Health Environmental and Occupational Health Brain DNA General Medicine Glutathione Oxidants Mitochondria Rats Oxidative Stress chemistry Biochemistry Lipid Peroxidation Oxidoreductases Oxidative stress DNA Damage Synaptosomes |
Zdroj: | Drug and Chemical Toxicology. 34:129-138 |
ISSN: | 1525-6014 0148-0545 |
Popis: | D-serine plays a significant role in neuronal activity, including learning, memory, neuronal migration at developmental stages, and cell-death signaling. It has been also suggested that D-serine can potantiate the neurotoxicity induced by N-methyl-D-aspartate (NMDA) receptor activation due to its coagonist function. However, little is known about the role of D-serine in oxidative stress mechanisms. The aim of this study was to determine the possible neurotoxic or oxidative effects of the dose- (50-200 mg/kg) and time-dependent (2 or 6 hours) D-serine administration on lipid, protein, DNA, mitochondrial integrity (i.e., function), levels of antioxidant enzyme activities (e.g., catalase, glutathione peroxidase, and superoxide dismutase), and glutathione (GSH) in the rat brain. Our results showed that D-serine significantly increases the levels of lipid peroxidation, protein carbonyls, and DNA damage. In addition, D-serine treatment changes cellular antioxidant status due to the decreased levels of antioxidant enzymes, GSH, and mitochondrial function. Therefore, it is concluded that the regulation of D-serine levels in the brain may be an important target for the development of neuroprotective strategies against neurodegenerative processes where excitotoxicity is involved. |
Databáze: | OpenAIRE |
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