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Generalized skin pigmentation in five African women with megaloblastic anaemia in the postnatal period was associated with low serum folate levels, as distinct from vitamin B(12) deficiency. It is suggested that the occurrence of pigmentation in both folate and vitamin B(12) deficiency may reflect a common abnormality of metabolism.
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Six experiments have been completed on day-old male cross-bred chicks for periods of up to 2 and 4 weeks to learn more about the role of pyridoxine in the etiology of gizzard erosion. At the end of each experiment, chicks were sacrificed and their gizzards removed and scored for the severity and incidence of erosion. The results of these experiments confirm the previous finding that the severity and incidence of gizzard erosion is increased by B6 deficiency. They further show that taurocholic acid, at 1% of the diet, had a protective effect against this erosion. Feeding B6-adequate rations to chicks that previously had been fed a B6-deficient diet led to partial healing of gizzard erosions. Results also indicate that the feeding of purified diets to growing chickens produces a higher incidence of erosion than that of practical-type diets. Texture of the diet did nt influence the incidence of the erosion, because grinding a practical diet to the same fineness as a purified diet did not increase gizzard erosion. Pair-feeding experiments showed that gizzard erosion in partially starved chicks was not a specific result of anorexia but of deficiencies in certain nutrients, one of which is vitamin B6.
Six Patas monkeys were fed a protein-free diet while 16 animals of the same species receoved a standard monkey diet. The protein-depleted monkeys showed reduced absorption of folic acid but not Dxylose, and 5 out of 6 exhibited depressed exocrine pancreatic function. When challenged with Vibrio cholerae, animals with reduced folic acid absorption and pancreatic enzyme production excreted the micro-organisms for a longer time.
Lometrexol (5,10-dideazatetrahydrofolic acid) is a new antifolate that is highly selective in inhibiting the key enzyme of purine synthesis glycinamide ribonucleotide formyltransferase. The most promising preclinical features of lometrexol in animal models were its significant activity against a broad panel of solid tumors, the schedule dependency of its antitumor activity, and the availability of a rescue regimen with folinic or folic acid. In the present study, lometrexol was first given daily for 3 consecutive days, repeated every 4 weeks (part I). The occurrence of delayed myelotoxicity prompted the development of a rescue regimen with lometrexol given in a single dose on day 1, followed by oral folinic acid, 15 mg four times a day, from day 3 to day 5 (part II). Longer time intervals between administration of lometrexol and start of rescue were then evaluated (part III), and in the last part of the study (part IV), the maximum tolerated dose of single intermittent doses of lometrexol with folinic acid given from day 7 to day 9 was established. Sixty adult patients entered the study. In part I, the highest daily dose that could be safely given was 4 mg/m2, for a total dose of 12 mg/m2. Cumulative early stomatitis and delayed thrombocytopenia were dose limiting. The use of oral folinic acid made it possible to escalate the dose up to 60 mg/m2, and the maximum tolerated dose was reached at this dose when folinic was given from day 7 to day 9, with anemia being the dose-limiting toxicity. A shorter time interval between lometrexol and folinic acid administrations (from day 5 to day 7) is recommended for Phase II evaluations to optimize the antitumor effect. Anemia was normochromic and macrocytic, possibly due to a deficiency of folic acid. One partial response of 8 months' duration was reported in a patient with epithelial cancer of the ovary, relapsing after cisplatin and alkylating agents. The use of folic acid as rescue, proposed on the basis of experimental data and pharmacological considerations, has also allowed the repeated administration of lometrexol at doses higher than in the previous studies. The advantages of rescue with folinic acid over supplementation with folic acid, however, are difficult to define.
"Natural" phenomena allow conclusions that maternal dietary deficiencies or excesses can affect development of the human embryo and fetus adversely. The most important finding in recent years has been the relationship between maternal folic acid status and neural tube defects.
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Previous studies have suggested that the metabolism of methyl groups is an important factor in the function of the exocrine pancreas. Ethionine, an inhibitor of cellular methylation reactions, produces hemorrhagic pancreatitis when administered to mice fed a choline-deficient diet. Glycine N-methyltransferase, an enzyme which regulates the ratio of S-adenosylmethionine to S-adenosylhomocysteine, is particularly abundant in the exocrine pancreas. Since de novo synthesis of methyl groups requires the participation of folate coenzymes, we investigated the effect of folate deficiency on pancreatic exocrine function. Rats were fed an amino acid-defined folate-deficient diet or the same diet supplemented with folate ad libitum. A third group received the folate supplemented diet pair-fed to the deficient group. After 3 and 5 wk, pancreatic amylase secretion was measured in perfused duodenal segments of anesthetized animals before and after cholecystokinin injection. Pancreatic secretion was significantly reduced in the deficient group compared with the pair-fed control group after 5 wk. These results indicate that severe folate deficiency impairs pancreatic exocrine function.