Experimental degeneration of the retina. III. Inhibitors of glycolysis and of respiration as inducing agents.

ONE ofthe grounds on which disturbance of glycolysis has been assumed to be responsible for experimentally induced degeneration of the retina is the observation recorded by Noell (1951) that injection of sodium iodoacetate abolishes the electric response of the retina much more markedly in mammals than in other species. This finding is suggestive in view of the fact that the mammalian retina is much more dependent on glycolysis than the retina of the lower vertebrates. Furthermore, the high glycolytic activity of the retina raises the possibility that retinal degeneration might arise from interference with this activity; indeed, the action of sodium iodoacetate in inducing experimental degeneration has been ascribed to its possible effect on glycolysis. Since iodoacetate is an outstanding thiol reactor, other such reactors were studied and their effects have been recorded previously (Sorsby, Newhouse, and Lucas, 1957; Lucas, Newhouse, and Davey, 1957). With one exception, none of the thiol reactors used produced any experimental lesions in the rat or rabbit, the exception being bromoacetate, an analogue of iodoacetate, and this gave only a mild lesion in the rabbit and none at all in the rat. The present study was undertaken to test whether inhibitors of glycolysis and respiration-other than thiol reactors-produce retinal damage in the experimental animal in vivo. The literature contains several tentative negative results. Thus Karli (1954) failed to obtain degeneration of the retina in the rabbit by the use of sodium fluoride and of phloridzin, and Babel and Ziv (1956) also failed to obtain any results-ophthalmoscopic, electroretinographic, or histological-from the use of fluoride and glyceraldehyde. In the present investigation, a representative series of inhibitors of glycolysis and of respiration was tried in the rat and the rabbit.