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Titolo:
VITAMIN-E PREVENTS APOPTOSIS IN CORTICAL-NEURONS DURING HYPOXIA AND OXYGEN REPERFUSION
Autore:
TAGAMI M; YAMAGATA K; IKEDA K; NARA Y; FUJINO H; KUBOTA A; NUMANO F; YAMORI Y;
Indirizzi:
SANRAKU HOSP,DEPT INTERNAL MED,CHIYODA KU TOKYO 101 JAPAN TOA UNIV,DEPT FOOD IND SCI YAMAGUCHI JAPAN TOKYO MED & DENT UNIV,DEPT INTERNAL MED 3 TOKYO 113 JAPAN KYOTO UNIV,GRAD SCH HUMAN & ENVIRONM STUDIES KYOTO 606 JAPAN
Titolo Testata:
Laboratory investigation
fascicolo: 11, volume: 78, anno: 1998,
pagine: 1415 - 1429
SICI:
0023-6837(1998)78:11<1415:VPAICD>2.0.ZU;2-D
Fonte:
ISI
Lingua:
ENG
Soggetto:
SPONTANEOUSLY HYPERTENSIVE RATS; FREE-RADICALS; NITRIC-OXIDE; ALZHEIMERS-DISEASE; ALPHA-TOCOPHEROL; CYTO-TOXICITY; CELL-DEATH; INJURY; SUPEROXIDE; BCL-2;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
45
Recensione:
Indirizzi per estratti:
Citazione:
M. Tagami et al., "VITAMIN-E PREVENTS APOPTOSIS IN CORTICAL-NEURONS DURING HYPOXIA AND OXYGEN REPERFUSION", Laboratory investigation, 78(11), 1998, pp. 1415-1429

Abstract

Cerebral ischemia followed by oxygen reperfusion induces apoptosis inhippocampal neurons in stroke-prone spontaneously hypertensive rats (SHRSP) but not in Wistar Kyoto rats (WKY). The overproduction of oxygen-free radicals that occurs in the tissues of SHRSP is implicated in reoxygenation injury after hypoxia. Antioxidants inhibit reoxygenation injury in hippocampal slices, and temporal cortices in Alzheimer's disease increase sensitivity to oxygen-free radicals. Because this sensitivity may contribute to the development of the disease, we have studied hypoxia and oxygen reperfusion using cortical neurons isolated from WKY and SHRSP (at 15 days of gestation). We have tried to determine whether cortical neurons are damaged under these conditions, and whetherneurons from SHRSP are more vulnerable than those from WKY. We have tried also to verify whether neuronal damage is minimized by vitamin E using the following techniques: (a) Trypan blue staining, (b) in situ staining of apoptosis, (c) ultrastructural examination, and (d) measurement of lactic dehydrogenase (LDH) activity in the bathing medium. Furthermore, we have examined the mechanisms involved in the developmentof neuronal damage and have studied ways of minimizing it. We demonstrated that 36 hours of hypoxia significantly increased the rate of cell death in SHRSP (p < 0.01), although 12 to 24 hours of hypoxia did not increase cell death in either WKY or SHRSP. in addition, 6 to 36 hours of hypoxia and 1.5 to 5 hours of oxygen reperfusion heavily damagedcells of both WKY and SHRSP, and most became apoptotic or necrotic. In contrast, cells incubated with 50 to 300 mu g/ml of vitamin E remained intact, although 10 to 20 mu g/ml of vitamin E did not totally preserve the cells. Moreover, vitamin E protected the neurons from high concentrations of sodium nitroprusside (nitric oxide donor) in a dose-dependent manner. Vitamin E, when added to the cells, increased in concentration in a time-dependent manner over a 24-hour period and in a dose-dependent manner below 200 mu g/ml, and it was detected mostly in the mitochondria. We also demonstrated that serial treatments with allopurinol (a xanthine oxidase inhibitor) or superoxide dismutase preserved neurons during hypoxia and oxygen reperfusion. These data indicate that SHRSP neurons are weaker than WKY neurons in long-term hypoxia; oxygen radical generation occurs in the early minutes after reperfusion,and then the oxygen-free radicals cause heavy damage to the cells; and antioxidants including vitamin E react with the radicals, thereby preventing apoptosis and necrosis. Therefore, antioxidants appear to be the most important agents in lowering oxygen-free radical damage in cortical neurons.

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Documento generato il 13/07/20 alle ore 14:31:06