Experimental Degeneration of the Retina Iii. Inhibitors of Glycolysis and of Respiration as Inducing Agents

Abstract

ONE of the 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. Techniques and Agents UsedThe procedures in injecting the agents, and the ophthalmoscopic and histological techniques employed in assessing results, were essentially the same as in the previous study. The agents and dosages employed are listed in Table I (opposite). The one innovation introduced was electroretinography carried out on the rabbits. The findings will be recorded separately by one of us (A.N.). ResultsOphthalmoscopically and histologically none of the agents produced any changes in the retina in the rat or rabbit. As most of these agents are largely *

TRANSITORY BLINDNESS DURING ETHANOL AND PHENETHYLBIGUANIDE INDUCED LACTIC ACIDOSIS IN A SUBJECT WITH DIABETES MELLITUS A Case Report

“…An inhibition of the oxidative metabolism in the retina as a cause for the blindness in this patient is in harmony with the fact that many retinotoxic substances or conditions interfere with the supply of energy, e. g. anoxia, oubain, iodoacetate, azide (Graymore 1970). Sorsby (1958) tried to induce degeneration of the retina with such agents in sublethal doses, but without impressive results. This was possibly due to the narrow gap which exists between death and retinal affection when such agents are used, as seen in the experimental methanol poisoning (Gilger & Potts 1955).…”

Dicoumarin Compounds in the Treatment of the Pigment Degeneration of the Retina

“…Such was the case with high doses of vitamin A (3,11), although some definite results have been obtained. A number of successes could be also noted by decreasing the internal eye-pressure and simultaneously increasing the general blood-pressure (9,16,17) or by section of the sympathetic supply to the eye (14). Other authors could claim some good results by using tissue therapy in its various forms, hormones, liver extracts, galvanisation etc.…”