Abstract:The metabolism of [2-14C]+[3', 5', 7, 9-3H] folic acid and [214C]+[3', 5', 7, 9-3H] 10-formylfolate was studied in hospital inpatients. Metabolites detected in the urine after folic acid feeding included the unchanged compound, other folates and a number of breakdown products, such as p-acetamidobenzoyl-L-glutamate and p-acetamidobenzoate. This confirms the existence of a folate catabolic pathway in man. Patients with malignant disease excreted less of the dose in urine, incorporated more into the reduced fola… Show more
“…The metabolic and nutritional significance of this phenomenon is uncertain at present. Large doses of 10formyl-FA (5 mg) in humans have been reported to be excreted intact and not metabolized, as well as to retard the metabolism of accompanying small doses (60 gg) of folic acid (Saleh et al, 1982). The results of the present (Tables II and III) and previous studies (Connor and Blair, 1979;Pheasant et al, 1981), which indicate that low doses of 10-formyl-FA are effectively utilized in mammalian (rat) and avian species, suggest the need for further evaluation of the role of 10-formyl-FA in human nutrition.…”
Section: Discussionmentioning
confidence: 99%
“…In a manner similar to that of 5-methyl-THF, 10formyl-THF is resistant to cleavage of the C9-N10 bond but is converted to 10-formylfolic acid (10-formyl-FA) under oxidative conditions (Maruyama et al, 1978; Lewis and Rowe, 1979). 10-Formyl-FA has been shown to be a potent inhibitor of dihydrofolate reductase, which is a key enzyme in folate metabolism (Bertino et al, 1965;d'-Urso-Scott et al, 1974), although the in vivo folacin activity is unclear in view of conflicting published data (Beavon and Blair, 1975; Connor and Blair, 1979; Pheasant et al, 1981;Saleh et al, 1982).…”
The biological activity of 10-formylfolic acid (10-formyl-FA) and 5-methyl-5,6-dihydrofolic acid (5methyl-DHF) was examined to determine the potential contribution of these oxidized folates to the folacin activity of foods. Both compounds exhibited high folacin activity for Lactobacillus casei in microbiological assays under standard conditions in the presence of ascorbate. Chick bioassays with plasma folacin as the indicator of biological activity revealed approximately 100% activity for 10formyl-FA and 80% activity for the natural l isomer of 5-methyl-DHF, respectively, relative to folic acid. Tritiated forms of these compounds were synthesized and compared with tritiated folic acid for their incorporation into the liver folacin pools of rats after oral dosing. Fractionation of conjugase-treated liver extracts by HPLC indicated that 10-formyl-FA and 5-methyl-DHF were absorbed and metabolized in a manner that was qualitatively and quantitatively similar to that of tritiated folic acid. These results suggest that the formation of 10-formyl-FA and 5-methyl-DHF in foods by oxidation of reduced folates would not yield important losses of folacin activity.
“…The metabolic and nutritional significance of this phenomenon is uncertain at present. Large doses of 10formyl-FA (5 mg) in humans have been reported to be excreted intact and not metabolized, as well as to retard the metabolism of accompanying small doses (60 gg) of folic acid (Saleh et al, 1982). The results of the present (Tables II and III) and previous studies (Connor and Blair, 1979;Pheasant et al, 1981), which indicate that low doses of 10-formyl-FA are effectively utilized in mammalian (rat) and avian species, suggest the need for further evaluation of the role of 10-formyl-FA in human nutrition.…”
Section: Discussionmentioning
confidence: 99%
“…In a manner similar to that of 5-methyl-THF, 10formyl-THF is resistant to cleavage of the C9-N10 bond but is converted to 10-formylfolic acid (10-formyl-FA) under oxidative conditions (Maruyama et al, 1978; Lewis and Rowe, 1979). 10-Formyl-FA has been shown to be a potent inhibitor of dihydrofolate reductase, which is a key enzyme in folate metabolism (Bertino et al, 1965;d'-Urso-Scott et al, 1974), although the in vivo folacin activity is unclear in view of conflicting published data (Beavon and Blair, 1975; Connor and Blair, 1979; Pheasant et al, 1981;Saleh et al, 1982).…”
The biological activity of 10-formylfolic acid (10-formyl-FA) and 5-methyl-5,6-dihydrofolic acid (5methyl-DHF) was examined to determine the potential contribution of these oxidized folates to the folacin activity of foods. Both compounds exhibited high folacin activity for Lactobacillus casei in microbiological assays under standard conditions in the presence of ascorbate. Chick bioassays with plasma folacin as the indicator of biological activity revealed approximately 100% activity for 10formyl-FA and 80% activity for the natural l isomer of 5-methyl-DHF, respectively, relative to folic acid. Tritiated forms of these compounds were synthesized and compared with tritiated folic acid for their incorporation into the liver folacin pools of rats after oral dosing. Fractionation of conjugase-treated liver extracts by HPLC indicated that 10-formyl-FA and 5-methyl-DHF were absorbed and metabolized in a manner that was qualitatively and quantitatively similar to that of tritiated folic acid. These results suggest that the formation of 10-formyl-FA and 5-methyl-DHF in foods by oxidation of reduced folates would not yield important losses of folacin activity.
“…As a consequence, 1-5 mg folic acid is prescribed as a treatment to avoid malnutrition as well as MTX-related side effects involving mouth ulcers and gastrointestinal discomfort [19], [20]. In the absence of elevated consumption, malignancy is a catabolic condition synonymous with lower serum folate rates [21], [22].…”
BACKGROUND: Cancers are an abnormal irregular growth of cells. There is an interaction between cancer cells, immune cells, and neurotransmitters with nutritional elements and vitamins. With the administration of chemotherapeutic agents, many studies have highlighted the importance of these interactions and the role of chemotherapeutic drugs in augmenting or ameliorating such changes. Therefore, early detection of vitamins level changes is vital to improve patients’ short-term outcome and quality of life.
AIM: The aim was assessment of serum vitamins level changes in patients with cancer pre- and post-chemotherapy.
MATERIALS AND METHODS: A cohort study was carried out on newly diagnosed patients with cancer in Al-Amal National Radiation Oncology Hospital/Baghdad/Iraq during the period from January 2019 to July 2019. Assessments of the studied samples were conducted as a baseline before receiving chemotherapy and after the third cycle of chemotherapy. Weight, height and body mass index (BMI) were measured for each subject enrolled in the study. Serum level of the following vitamins: A, B1, B2, B3, B6, B12, folic acid, D, and E was measured using ELISA technique.
RESULTS: One Hundred patients who were diagnosed with different types of cancer were enrolled in this study. Seventy seven (77%) females and twenty three (23%) males. Mean age was 50.15 years ranged between (18-75) years old, BMI range (16-42). Serum vitamin levels that have shown a significant decrease post chemotherapy as compared with baseline were: A (0.64 ± 0.23 vs 0.64 ± 0.23, P=0.0003), E (19.47 ± 4.714 vs 14.70 ± 5.354, P<0.0001), B12 (366.0 ± 95.94 vs 291.1 ± 102.6, P<0.001), B9 (16.13 ± 4.13 vs 16.13 ± 4.13, P<0.0001) whereas vitamins B6 and D which showed lower than normal baseline level underwent significant increase after chemotherapy yet remained below normal (vitamin B6 4.19 ± 1.94 vs 8.22 ± 5.39; vitamin D 21.11 ± 7.21 vs 26.55 ± 15.22).
CONCLUSION: Our findings highlight the importance of updating and tailoring our regimens to suit the changes of the nutritional elements and parameters of performance status of cancer patients in terms of outcome and patient satisfaction.
“…Folate deficiency has been associated with malignancy [156,157], and abnormalities in its metabolism have been linked to acute and chronic leukaemias, disseminated lymphomas [158], and various metastatic carcinomas [159]. Catabolism of folate is reduced in the presence of malignancy [160], at least in the rat, which suggests that the low folate levels are the result of sequestration by tumour tissues [160[, reflecting an increased requirement for folatc in malignant disease due to the presence of additional cell mass. Thus, the specific interaction between the drug methotrexate (a folate antagonist) and folate can be used to inhibit tumour growth, although a folate 'rescue' is essential following a period of drug action.…”
Protein-energy malnutrition (PEM) is common in cancer patients and may develop into the syndrome known as 'cancer cachexia'. This is characterised by complex disturbances in carbohydrate, lipid, protein, and electrolyte metabolism. The aetiology is equally complex, with host and therapeutic factors contributing to the reduced food intake and effects on host tissues. Anorexia is of prime importance, differing in its cause from one patient to another and often presenting a barrier to successful nutritional support. Further research is necessary to elucidate the interaction of central and peripheral factors that may be involved in the aetiology of anorexia. Because of the interplay of biochemical, physiological, and psychological consequences of cancer, the nutritional support of the patient presents a considerable challenge to the caring professions.
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