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Estudo do papel do estresse oxidativo em córtex cerebral de ratos submetidos ao modelo experimental de hiperprolinemia tipo II
| Content Provider | Semantic Scholar |
|---|---|
| Author | Delwing, Daniela |
| Copyright Year | 2003 |
| Abstract | Hyperprolinemia type II is an autosomal recessive disorder caused by the severe deficiency of ∆ – pyrroline-5-carboxylate dehydrogenase activity, resulting mainly in tissue accumulation of proline. Most patients detected so far show neurological manifestations including epilepsy and mental retardation. Although neurological dysfunction is commonly found in a considerable number of hyperprolinemic patients, the mechanisms by which this occurs are poorly understood. Oxidative stress is an important event that has been related to the pathogenesis of some conditions affecting the central nervous system (CNS) such as neurodegenerative disorders, epilepsy and dementia. This is understandable since the CNS is highly sensitive to oxidative stress due to its high oxygen consumption, its high iron and lipid contents, especially polyunsaturated fatty acids, and the low activity of antioxidant defenses. Considering that: a) very little is known about the role of high sustained levels of proline in CNS, b) proline activates NMDA receptor and is epileptogenic and c) the oxidative stress is associated with diseases that affect the CNS, in the present study we determined the in vivo and in vitro effects of proline on some parameters of oxidative stress, such as chemiluminescence, total radical-trapping antioxidant potential (TRAP) and the activities of the antioxidant enzymes catalase (CAT), glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) in Wistar rat cerebral cortex. |
| File Format | PDF HTM / HTML |
| Alternate Webpage(s) | https://lume.ufrgs.br/bitstream/handle/10183/4156/000408208.pdf;sequence=1 |
| Language | English |
| Access Restriction | Open |
| Content Type | Text |
| Resource Type | Article |
