Mechanism of Hypoxia-Induced Cytotoxicity in Cultured Rat Retinal Neurons
Journal of the Korean Ophthalmological Society
;
: 1975-1986, 1997.
Artigo
em Coreano
| WPRIM
| ID: wpr-55064
ABSTRACT
Retinal neurons are highly vulnerable to hypoxia/ischemia. Excitotoxicity and free radical injury have been proposed as the major mechanisms of ischemic retinal injury have been proposed as the major mechanisms of ischemic retinal neuronal death. In the present study, we examined these possibilities in retinal cultures. Exposure of these cultures to hypoxia for 48 hr induced selective death of neurons. Addition of an antioxidiant trolox markedly attenuated hypoxiainduced retinal neuronal death, whereas addition of glutamate antagonists, MK-801 or CNQX,did not. Morphologically, hypoxic neuronal death in cultures was accompanied by cell body swelling, a feature of necrosis, yet simultaneously exhibited some features of apoptosis such as TUNEL positivity and protection by cycloheximide. However, unlike in classical programmed cell death, adding buthionine sulfoximine, a potent inhibitor of glutathione synthesis, completely reversed the protective effect of cycloheximide. The results have demonstrated that free radical injury is the main mechanism of neuronal death in the present retinal culture, and suggest an intriguing possibility that free redical injury may become a prominent mechanism, when excitotoxic injury is masked.
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Retinaldeído
/
Maleato de Dizocilpina
/
Morte Celular
/
Apoptose
/
Antagonistas de Aminoácidos Excitatórios
/
Butionina Sulfoximina
/
Marcação In Situ das Extremidades Cortadas
/
Cicloeximida
/
Neurônios Retinianos
/
Glutationa
Limite:
Animais
Idioma:
Coreano
Revista:
Journal of the Korean Ophthalmological Society
Ano de publicação:
1997
Tipo de documento:
Artigo
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