Abstract
CHOLINE-OXIDASE converts choline to betaine through an intermediary step of betaine aldehyde formation1. Betaine, which is a trimethylglycine, initiates the transfer of methyl groups in stages, with the formation of dimethyl and monomethyl glycine2. Since in tumours there is a rapid turnover of nucleic acids3, it was thought that all the processes, including transmethylation, leading to precursor formation, may also be accelerated. It was thus anticipated that choline-oxidase activity might be higher in the host tissues of tumour-bearing animals. Miller4 has shown that the overall choline-oxidase activity requires diphosphopyridine nucleotide as an activator, but whether the choline-dehydrogenase or the betaine aldehyde dehydrogenase requires it has not been established5. During the course of our studies on tumour–host relationships it was observed that the diphosphopyridine nucleotide-levels in host tissues were considerably diminished6. One would anticipate from this a lowering of choline-oxidase activity in host tissues deficient in diphosphopyridine nucleotide. In view of these mutually exclusive and apparently contradictory possibilities it was considered necessary to study the influence of tumour on the levels of choline-oxidase in host tissues.
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NARURKAR, M., KUMTA, U. & SAHASRABUDHE, M. Choline-Oxidase Activity of Host-Livers of Tumour-bearing Animals. Nature 180, 1128–1129 (1957). https://doi.org/10.1038/1801128a0
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DOI: https://doi.org/10.1038/1801128a0
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