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Between the 30th and 36th week of gestation 30 patients were treated with ferrum in combination with folic acid. Every 14 days in both groups the erythrocytes, the hemoglobin and the folic acid were evaluated. There was a high significance between the two groups after the therapy. No intestinal side effects must be registered in the "verum" group.
The authors made a study on 90 patients affected by various degrees of uterine cervix dysplasia searching for folic acid plasmatic concentrations. The team members affected by CIN have been compared with a test team consisting of women with normal pap-test and vaginoscopy. The study proved that the average levels of folic acids have significantly decreased in cases of dysplasia compared with the test team. These results allow stating that low folic acid plasmatic concentrations may be associated with cervix neoplasms development.
High serum total homocysteine (tHcy) is gaining scrutiny as a risk factor for cardiovascular disease in the general population. The relationship between tHcy and mortality and cardiovascular events in patients with end-stage renal disease (ESRD) is unsettled. This randomized trial evaluates the efficacy of high-dose folic acid in preventing events in ESRD. A total of 510 patients on chronic dialysis were randomized to 1, 5, or 15 mg of folic acid contained in a renal multivitamin with a median follow-up of 24 mo. Mortality, cardiovascular events, and homocysteine levels were assessed. There were 189 deaths, and 121 patients experienced at least one cardiovascular event. Composite rates of mortality and cardiovascular events among the folic acid groups did not differ (at 24 mo: 43.7% in 1 mg group, 38.6% in 5 mg group, 47.1% in 15 mg group; log-rank P = 0.47). Unexpectedly, high baseline tHcy was associated with lower event rates. From lowest to highest quartile, event rates at 24 mo were 54.5% for Q1, 41.8% for Q2, 41.2% for Q3, and 34.7% for Q4 (log-rank P = 0.033). In contrast to some studies describing tHcy as a risk factor for mortality and cardiovascular events, this study found a reverse relationship between tHcy and events in ESRD patients. Administration of high-dose folic acid did not affect event rates.
Rat embryos (9.5-day-old) were cultured for 48 hours in serum from diet-induced folic-acid-deficient rats. Resultant embryos were frequently abnormal; many were growth retarded and exhibited a defect in the turning mechanism that inverts the embryo from ventrally to dorsally convex. Affected embryos displayed abnormal twisting or kinking of the neural tube. Gross anaemia was also frequently observed, and the protein content of the embryos was markedly less than that of embryos grown in normal rat serum. Supplementation of the deficient serum with folic acid improved growth and greatly reduced the occurrence of deformities. It virtually eliminated the incidence of gross anaemia but only partially restored the protein content of the embryos to the level observed in those grown in normal rat serum. The effects of the folate deficiency could be eliminated by supplementation with normal rat serum. The data indicate that embryos have a requirement for adequate folate in order for normal growth and differentiation to take place; they also suggest that some of the embryopathic effects of maternal folate deficiency are mediated by secondary effects on maternal metabolism. This may take the form of a disturbance in the production of maternally synthesised growth factors necessary for normal embryonic development.
A double-blind, crossover study of a 10 mg folic acid per day (vs. placebo) treatment was carried out in 25 fra(X) males (ages 1-31 years). Each treatment period lasted 6 months. Before, during and after the study, the patients were assessed blindly with psychological, language and behavioral evaluations, and parent or caretaker reports were collected. Standardized testing did not show statistically significant changes in the group as a whole; psychological testing demonstrated a statistically significant improvement on folic acid in the prepubertal males. After uncoding, caretaker or parent reports also demonstrated behavioral improvements in the prepubertal males while being treated with folic acid.
We present the results achieved with vitamin (pyridoxine and folic acid) and betaine (trimethyl-glycine) treatment of three patients with homocystinuria. Cases 1 and 2 were detected by having clinical findings suggestive of the disease (ocular and orthopedic alterations) and case 3 was diagnosed after a family metabolic screening was done. All presented a positive Brand's test and an abnormal elevation of plasma and urine homocysteine, as well as high methionine and low cystine levels in the plasma. Initially, when pyridoxine (600 mg/d) and folic acid (10 mg/d) were given for one month, a partial fall in the homocysteine levels was observed in cases 2 and 3, but not in case 1. When betaine was added (6 g/d), homocysteine disappeared from the plasma after the first month in cases 2 and 3, but only after the third month in case 1. Case 1 also showed a moderate clinical improvement in behavior and school performance. The treatment was maintained for two years in case 1, and for one year in cases 2 and 3. After betaine therapy, no disturbances were observed in the hepatic, renal and bone marrow functions, nor were there any clinically relevant ill-effects. These findings show that betaine offers a therapeutic alternative in the treatment of this disease, independent of the patient's response to pyridoxine.
OBJECTIVES: We investigated whether reducing post-methionine homocysteine concentrations via various treatments other than folic acid affects vascular function, as measured through flow-mediated dilation (FMD) of the brachial artery. High fasting and post-methionine homocysteine concentrations are associated with cardiovascular disease risk, but homocysteine might be a surrogate marker for low folate status. DESIGN: This was a randomized, placebo-controlled, double-blind, crossover study. SETTING: The study took place at Wageningen University in Wageningen in the Netherlands. PARTICIPANTS: Participants were 39 apparently healthy men and women, aged 50-70 y. INTERVENTIONS: Participants ingested 10 mg of folic acid, 3 g of betaine, 5 g of serine, and placebo together with an oral methionine load. Each supplement was tested on two different days. OUTCOME MEASURES: On each of the eight treatment days, plasma homocysteine concentrations and FMD were measured before (t = 0 h, fasting) and 6 h (t = 6 h) after methionine loading. RESULTS: The mean (+/- SD) fasting homocysteine concentrations averaged over the eight test days were 9.6 +/- 2.1 micromol/l. Mean fasting FMD was 3.1 +/- 2.4 FMD%. A methionine load with placebo increased homocysteine concentrations by 17.2 +/- 9.3 micromol/l at 6 h after loading, similar to the increase following methionine loading with folic acid. A methionine load together with betaine and with serine increased homocysteine by 10.4 +/- 2.8 micromol/l (p < 0.001 relative to placebo) and by 12.1 +/- 8.2 micromol/l (p < 0.001 relative to placebo), respectively. Methionine loading with placebo did not affect FMD, and neither did methionine loading with folic acid, betaine, or serine; differences relative to placebo were +0.7 FMD% (95%CI, -0.6; 1.9), +0.2 FMD% (-1.0; 1.3), and +0.3 FMD% (-0.8; 1.4), respectively. CONCLUSIONS: Experimentally induced acute changes in homocysteine concentrations did not affect FMD in healthy volunteers. This implies that potential adverse effects of high homocysteine concentrations on the cardiovascular system are not mediated through vascular function. However, homocysteine or folate may affect cardiovascular disease risk through other mechanisms.
Apoptosis is a complex process involving a variety of mechanisms and it has been shown to be a response of cells to various chemical agents including chemotherapeutic ones. We aimed to induce DNA breaks and apoptosis in cultured endometrial stromal cells by mitomycin C (MMC), a chemotherapeutic agent, and also we aimed to observe the effects of beta-carotene and folic acid on MMC-induced apoptosis. Cultured endometrial stromal cells were exposed to MMC for 48 and 72 hours and in order to reverse MMC effects, we added beta-carotene and folic acid to the cultures. DNA fragmentation was observed in all cells. Apoptotic cell ratios and caspase-3 activity were observed to be dependent on exposure time. Ultrastructural examinations revealed positive effects of beta-carotene and folic acid, however they were not sufficient enough to prevent apoptosis in all cells. Beta-carotene profoundy reduced caspase-3 activity whereas folic acid did not seem to have a similar effect. As apoptosis involves several mechanisms, in a cell in which all these mechanisms are triggered, we think that antioxidants and DNA repair agents alone are not enough to reverse all of them.
BACKGROUND: Serum homocysteine levels are a risk factor in cardiovascular disease. Knowledge on how dietary factors might affect these levels is therefore of interest. OBJECTIVE: To evaluate serum homocysteine levels in a group of elderly people and analyse the effect of pyridoxine, vitamin B12 and folic acid intakes on these levels. DESIGN: The study subjects were 130 independently-living elderly people over the age of 65. A dietetic study was performed using a 7-day food record. Serum homocysteine levels were determined by HPLC. RESULTS: Mean pyridoxine, vitamin B12 and folate intakes were 67.2+/-16.8%, 392.8+/-549.2% and 84.5+/-28.3% of recommended values respectively. With regard to sex, differences were seen only for vitamin B12 intake (9.1+/-12.7 microg/day in men, and 6.5+/-8.8 microg/day in women). Some 93.6% of subjects showed pyridoxine intakes below those recommended, as did 17.6% with respect to vitamin B12 and 72.8% with respect to folic acid. Homocysteine levels were 12.4 micromol/l (12.6+/-3.7 micromol/l in men and 12.2+/-7.9 micromol/l in women) (P<0.05). No significant differences were seen in homocysteine levels between subjects with lower than recommended intakes of pyridoxine or vitamin B12 and those with better intakes. However, subjects with folic acid intakes below 200 microg/day showed higher homocysteine levels (13.0+/-6.7 micromol/l) than did subjects with more adequate intakes (10.9+/-4.1 micromol/l) (P<0.05). CONCLUSION: The diet of the study subjects might be improved, especially with respect to pyridoxine and folic acid. Raising the intake of the latter might be especially useful in controlling homocysteine levels and the risk of cardiovascular disease.
OBJECTIVE: To evaluate the effects of postmenopausal hormone therapy (HT) with or without the addition of folic acid (FA) on serum homocysteine levels in a randomized, placebo-controlled design. Additionally, a non-randomized control group with no treatment was included. METHODS: Forty non-hysterectomized healthy postmenopausal women were randomly allocated to receive either oral continuous combined HT (0.625 mg conjugated equine estrogen with 2.5 mg medroxyprogesterone acetate daily) and oral folic acid (5 mg/day, n = 20) or HT and placebo (n = 20) for 3 months. A control group (n = 15) did not receive any study medication and was followed in the same manner. The fasting total serum homocysteine level was measured by fluorescence polarization immunoassay with a sensitivity of < 0.5 micromol/l. Serum levels of folate, estrogen and lipid profile were also followed. RESULTS: The mean age of the postmenopausal women was 52 +/- 6 years. Baseline homocysteine level was the highest in the HT + FA group (9.96 +/- 2.82 micromol/l), compared to HT + placebo (9.64 +/- 1.89 micromol/l) and control groups (9.01 +/- 1.83 micromol/l) (ANCOVA, p = 0.022). Low baseline folate and vitamin B12 levels contributed significantly to the high level of baseline homocysteine in the HT + FA group. The addition of FA to HT led to a significant decrease in the serum homocysteine level from the baseline level of 9.96 +/- 2.82 micromol/l to the final level of 8.92 +/- 2.53 micromol/l (p = 0.023). On the other hand, HT alone (HT + placebo group) significantly increased the serum homocysteine level from 9.64 +/- 1.89 micromol/l to 10.22 +/- 1.77 micromol/l without a decline in serum folate level (p = 0.045). The serum homocysteine level in the control group did not change significantly (from 9.01 +/- 1.83 micromol/l to 9.58 +/- 2.05 micromol/l, p = 0.29). CONCLUSIONS: Three months of oral continuous combined HT increased the fasting total serum homocysteine level without affecting the serum folate level. Lowering the homocysteine level in postmenopausal woman on HT is achievable by folic acid supplementation.
Peripheral blood lymphocyte sister chromatid exchange(SCE) frequencies, serum folic acid(FA) levels were examined in 15 epileptic patients treated with carbamazepine(CBZ), and another 15 epileptic patients treated with CBZ and folic acid(FA). The untreated epileptic patients and the healthy subjects served as control. The results showed that SCE frequencies were significantly higher in CBZ Group, compared with CBZ plus FA Group and control(P < 0.01). Serum FA levels were lower in CBZ Group compared with healthy control(P < 0.01). It suggests that CBZ can induce the increase of SCE frequencies. Supplementation with FA may effectively prevent chromosome DNA damage induced by CBZ.
5-Fluorouracil (5-FU) has been the foundation of advanced colorectal cancer treatment for over 40 years. The Apc(Min/+) mouse, which is genetically predisposed to intestinal neoplasia, was used to examine the effects of 5-FU in this system and the impact of dietary folic acid on those effects. 5-FU treatment resulted in a 60-80% reduction in tumor number. Clinically relevant toxicities, including myelosuppression and mucositis, are a part of this response. Tumor numbers rebounded completely following termination of 5-FU therapy, indicating that the drug inhibits tumor growth but does not eradicate them. In mice that were fed with a defined diet containing no folic acid (0 ppm), 5-FU not only induced regression of pre-existing tumors, but also inhibited tumor recovery following drug withdrawal. Our data indicate that a dietary folic acid deficiency, in promoting tumor regression and inhibiting tumor recovery, may enhance the therapeutic effects of 5-FU.
Folic acid was used for the complex treatment of patients with multiple sclerosis. The doses employed were 200-300 mcg daily. It was established that folic acid improved the reparative processes in the gastric mucosa and produced a pronounced therapeutic effect on the neurological status of the patients, favoured improvement of their general condition.
This study was designed to determine the folate status of an adolescent population and to demonstrate the effect of folic acid supplementation on subjects with low folate status. In phase one, folate status was evaluated in a biracial sample of 164 adolescents 12 to 15 years old. Socioeconomic, demographic, anthropometric, and 7-day food record data were collected, and serum and erythrocyte folate levels were determined. Thirty-five adolescents considered to have had low folate status 6 months earlier participated in phase two, a 2-month supplementation period and reevaluation. No racial differences were observed in folate status, as indicated by amount of folate in the blood and diet. Boys had significantly (p less than .05) higher folate levels in serum and erythrocytes than did girls. Thirteen percent of the boys and 40% of the girls were folate deficient as judged by amount of erythrocyte folate less than 317 nmol/L (140 ng/mL). The folate-deficient subjects had significantly (p less than .05) lower values of hemoglobin than did the normal subjects. Seventeen percent of the boys and 42% of the girls had folate intakes below the recommended dietary allowance for folate. Supplementation of 400 micrograms folic acid daily for 2 months resulted in significant (P less than .05) increases in serum folate, erythrocyte folate, and hemoglobin values and a decrease in mean corpuscular volume. Evidence of high prevalence of low folate status, positive relationship between erythrocyte folate and hemoglobin, and responses of hemoglobin and mean corpuscular volume to the supplement indicated that folate consumption may not be optimal in some groups of adolescents, especially in girls.
We have validated the analysis of nucleoplasmic bridges (NPBs) and nuclear buds as biomarkers of genomic instability within the cytokinesis-block micronucleus assay in long-term lymphocyte cultures. Lymphocytes from 20 subjects were cultured in medium containing 12-120 nM folic acid for 9 days. Binucleate cells were scored for micronuclei (MN), NPBs and nuclear budding on day nine after 24h incubation in the presence of the cytokinesis inhibitor cytochalasin-B. Folic acid concentration was correlated significantly (P<0.0001) and negatively (r=-0.63 to -0.74) with all these markers of chromosome damage. Chromosome damage was minimised at 60-120 nM folic acid, which is greater than the concentration of folate normally observed in plasma (<30 nM). Current evidence suggests that (a) NPBs originate from dicentric chromosomes in which the centromeres have been pulled to the opposite poles of the cell at anaphase and are therefore, indicative of chromosome rearrangement and (b) that the nuclear budding process is the mechanism by which cells remove amplified DNA and is therefore a marker of gene amplification. The strong correlation between micronucleus formation, nuclear budding and NPBs (r=0.75-0.77, P<0.001) is supportive of the hypothesis that folic acid deficiency causes genomic instability and gene amplification by the initiation of breakage-fusion-bridge (BFB) cycles. These results also suggest that the CBMN assay may be a useful model for the study of the BFB cycle which may be one of the key mechanisms for the hypermutability phenotype required for the rapid evolution of cancer cells.
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