1940
DOI: 10.1042/bj0340563
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Glycolysis in retinal extracts

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Cited by 24 publications
(6 citation statements)
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“…10 g.) taken orally are fatal from acute gastro-intestinal, hepatic, renal, and central-nervous-system damage (Lidbeck et al, 1943). Protracted intake of about 14 parts per million of water over many years may result in calcium fluoride being deposited in bone, tendons, and periosteum (Singh et al, 1962).…”
mentioning
confidence: 99%
See 1 more Smart Citation
“…10 g.) taken orally are fatal from acute gastro-intestinal, hepatic, renal, and central-nervous-system damage (Lidbeck et al, 1943). Protracted intake of about 14 parts per million of water over many years may result in calcium fluoride being deposited in bone, tendons, and periosteum (Singh et al, 1962).…”
mentioning
confidence: 99%
“…Sorsby and Harding (1960), however, described retinal oedema followed by degenerative changes in 17 out of 94 rabbits within five days of giving sodium fluoride; and De Berardinis and others have produced retinal degeneration in rabbits by intracarotid injection of 150 mg. of sodium fluoride (Babel and Avanza, 1961 ;De Berardinis et al, 1962). Fluoride is a powerful inhibitor of glycolysis and has been shown by Holmes (1940) and Kerly and Bourne (1940) to inhibit lactic-acid formation and phosphorylation in retinal extracts. Although it cannot be definitely established that the eye lesion in our patient was caused by sodium fluoride, there was no evidence for any other cause of toxic optic neuritis or retinal oedema, such as methyl-alcohol poisoning or disseminated sclerosis.…”
mentioning
confidence: 99%
“…Normal rats (140-240 grams) and rabbits (2)(3)(4)(5) in the fed state were utilized. Dog eyes were obtained from animals used in other experiments.…”
Section: Methodsmentioning
confidence: 99%
“…Also, he showed that retinal glycolytic activity even exceeded that of many tumors. It has since been indicated (2,3) that the breakdown of glucose to pyruvic acid in the retina is accomplished through the Embden-Meyerhof pathway, and that the citric acid cycle is probably a further step in its degradation (4). As late as 1961 Rahman and Kerly ( 5 ) concluded, from studies with specifically labelled glucose (214, that the Hexose Monophosphate shunt was responsible for about 25 O / o of retinal glucose metabolism.…”
Section: Introductionmentioning
confidence: 99%
“…G 1-P was not phosphorylated by the extracts and its presence did not interfere with the utilization of glucose. Kleinzeller (1942) found that ITP could replace ATP as a phosphate donator for yeast hexokinase; this was tested with both retinal and partly purified yeast extracts, but glucose was not phosphorylated in the presence of either extract by ITP. The reason for the difference from Kleinzeller's results is not apparent.…”
Section: Hexokinawementioning
confidence: 99%