Studies in the Pteridine Series

Blair, John A (1958) Studies in the Pteridine Series. PhD thesis, University of Glasgow.

Abstract

It has been found that the green colour of certain snakes is caused by a structural blue colour together with two yellow pigments. One of these yellow pigments has been identified as riboflavin. Other colourless fluorescent compounds were also isolated. In one species these were isoxanthopterin and 2-amino-4-hydroxypteridine-6-carboxylic acid and in two other species the previous two compounds and 2-amino-4-hydroxypteridine. A metabolic scheme linking these substances and giving a possible origin for them has been suggested (see facing page). Further evidence has been obtained for this scheme. There were indications from the literature that folic acid was oxidisable by xanthine oxidase. It has been found that xanthine oxidase is without effect on pteroyl-L-monoglutamic acid but that in the presence of methylene blue and xanthine oxidase pteroyl-L-monoglutamic acid is oxidised to 2-amino-4-hydroxy pteridine-6-cerboxylic acid. Isoxanthopterin but not 2-amino-4-hydroxypteridine-6-carboxylic acid has been isolated from normal human urine. It Is now suggested that folic acid is catabolised in the mammalian body to the inert end-product isoxanthopterin. Recent work by other investigators has supported the existence of a catabolic pathway for folic acid. Albert has suggested that pteridines (e.g. xanthopterin) would be found in higher concentration in tissues undergoing excessive rate of growth than in normal ones. To test this hypothesis normal hamster kidneys and tumours arising from them (primary and transplanted) were analysed for their pterin content. No xanthopterin could be found. It was found that a blue fluorescent substance, tentatively identified as 2-amino-4-hydroxypteridine-6-carboxylic acid was present in normal kidney tissue in much higher concentration than in the neoplastic issue. Previous surveys of neoplastic tissues have shown that their folio acid content is the same or higher than normal tissues. The reduced content of 2-amino-4-hydroxy pteridine-6-carboxylic acid would therefore suggest that the neoplastic cells degraded folio acid to a much lesser extent than did normal cells. The failure of neoplastic cells to degrade folic acid might explain why neoplasms have a greater growth rate than their normal tissue of origin. It is known that if golden hamsters are injected with certain pteridines and a variety of other substances their kidneys hypertrophy. When the hypertrophied kidneys were analysed for pterin content neither xanthopterin nor 2-amino-4-hydroxy pteridine-6-carboxylic acid could be isolated. This would suggest that an increased rate of cell division is accompanied by the failure of the cell to degrade folic acid. It is now suggested that the catabolism of folic acid is a means of controlling cell division; normal cell hyperplasia being due to a local high concentration of folic acid caused by a temporary inhibition of folic acid catabolism; neoplasia being accompanied by a permanent inhibition of folic acid catabolism.

• Item Type: Thesis (PhD)
• Qualification Level: Doctoral
• Keywords: Organic chemistry
• Date of Award: 1958
• Depositing User: Enlighten Team
• Unique ID: glathesis:1958-79285
• Copyright: Copyright of this thesis is held by the author.
• Date Deposited: 05 Mar 2020 11:06
• Last Modified: 05 Mar 2020 11:06
• URI: https://theses.gla.ac.uk/id/eprint/79285