Mitochondrial Deletions in Normal and Degenerating Rat Retina

摘要: Photoreceptor death by apoptosis is the central pathology of most forms retinal degeneration. Mitochondria play key roles in apoptosis, releasing both signals which induce (cytochrome c, caspases) and inhibit (Bc1-2). Because mitochondria are site oxidative metabolism they also a major formation toxic oxygen intermediates form as recruited into phosphorylation pathway. Previous studies have shown that deletions mtDNA accumulate postmitotic tissues (central nervous, muscle) their accumulation accelerated stress (such hypoxia) (Takeda et al. 1996;Lee 1994; Merril 1996; Englander 1999). It seems possible therefore at induces neurones. This study investigates rat retina, normal (non-degenerative) degenerative strains. Deletions were undetectable Sprague-Dawley albino rats (24 months) but detected 15 months rapidly degenerating RCS strain. The appearance strain, tension known to rise degeneration progresses, gives support ideas factor deletions, progress late stages