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Antitumor activity of hydroxythiamine and methotrexate immobilized on monocarboxycellulose.

The aim of the present study was to examine the antitumor and antivitamin activities of some new combinations of methotrexate (MT) and hydroxythiamine (HT), antagonists of folic acid and thiamine, respectively, immobilized on monocarboxycellulose (MCC). Ehrlich ascites carcinoma and sarcoma 180 were used as test malignant tumors in mice. It has been shown, that the compounds studied decreased significantly the amount of mitotically dividing tumor cells and increased the percentage of dead cells, inhibited the tumor growth (up to 10-30 fold at the early stage of neoplasm development) and elongated the life-span of tumor-bearing animals (by 1.6-3.3-fold) as compared to the control. All MCC-immobilized HT and MT complexes studied demonstrated higher antitumor efficacy compared to the mixture of these drugs or each of the agents applied individually. The specific feature of the newly synthesized substances was strong and prolonged antitumor effect following single administration. The severity of thiamine and folic acid deficiencies essentially depended on the amount of HT and MT in the preparations. A close correlation was found between the inhibition of transketolase in the tumors and the antiblastoma properties of the preparations. It enables us to suggest, that the antithiamine action of these preparations is one of the important factors in the mechanism of their antitumor effect.

Animals↗

[Increased p-homocysteine--a risk factor for thrombosis].

In the healthy population P-homocysteine increases with age and the level is higher in men aged 30-60 years as compared to women of the same age group. Most often, elevated P-homocysteine is caused by genetic defects, vitamin deficiency (folic acid, B6- and B12-vitamin) or renal failure. Based on retrospective as well as prospective studies, it can be concluded that elevated P-homocysteine is a risk factor for arterial as well as venous thrombosis. Severely elevated P-homocysteine is capable of causing premature arteriosclerosis, whereas slightly elevated levels may also be involved. A slightly positive correlation has been found between P-homocysteine on one hand, and smoking, blood pressure and cholesterol on the other, whereas physical activity is slightly negatively correlated to P-homocysteine. Altered function of endothelial cells and coagulation has been demonstrated in relation to elevated P-homocysteine, but the pathogenetic mechanisms have not been fully elucidated. Usually, an elevated P-homocysteine is normalised by folic acid supplementation, although additional treatment with vitamin B6 may be required. Presumably, the risk of thrombosis is thereby reduced, but future controlled studies may reveal whether this holds true.

Adult↗

Malabsorption of vitamin B12 in homozygous beta-thalassemia.

Schilling tests were performed in ten children and 5--12 years suffering from homozygous beta-thalassemia. 57Co labelled vitamin B12 values excreted in the urine have been found much lower than normal and remained low when the same procedure was repeated with the addition of intrinsic factor. The possible factors responsible for this malabsorption of vitamin B12 seemed to be liver damage and folic acid deficiency.

Child↗

[Myelopathy and macrocytic anemia associated with a folate deficiency. Cure by folic acid].

The authors report a case of myelopathy associated with macrotic anemia. The prior inefficacy of treatment with B1, B6 and B12 vitamins, in spite of a normal Schilling test, suggested the possibility of folate deficiency, the concentration of which was found very low in the serum (1.5 mg/ml). The addition of folic acid to the vitamins already administered without success, was followed by rapid recovery of the anemia and a frank neurological improvement maintained after 10 months follow-up. The rare similar cases observed in the world literature are analysed here. The other neurological manifestations, due to folate deficiency, the etiological circumstances and the methods of diagnosis are recalled.

Adult↗

[An adult case of homocystinuria probably due to methylenetetrahydrofolate-reductase deficiency--treatment with folic acid and the course of coagulation-fibrinolysis parameters].

We report a rare male case of homocystinuria probably due to methylenetetrahydrofolate-reductase deficiency. The onset of his disorder was at 19 years of age, and he had no family history. He initially developed gait disturbance, and then generalized seizure in several months, which made him admitted to our hospital. Neurological examinations revealed mental dysfunction, spastic paraplegia, cerebellar ataxia, and sensory disturbance in his feet. MRI showed multiple increased intensities on T2-weighted images in the cerebral white matter. EMG revealed neurogenic changes. These symptoms and signs slowly progressed, and he then developed thrombophlebitis in his lower extremities. Thrombin-antithrombin III complex (TAT) and D-dimer remained high continuously, and plasma homocysteine level was more than ten times higher than the normal range. Plasma cystathionine level was high and methionine level was low. The serum folic acid, vitamin B12, and methylmalonic acid in the urine were normal. Megaloblastic anemia was not seen. Based on these data, he was diagnosed to have homocystinuria probably due to methylenetetrahydrofolate-reductase deficiency. Treatment with high doses of folic acid, pyridoxine and cobalamin normalized plasma cystathionine and methionine levels, and markedly decreased plasma homocysteine, although it remained about three times higher than the normal range. Thereafter, both TAT and D-dimer levels also markedly decreased. The administration of folic acid reduced elevated plasma homocysteine as well as the coagulation--fibrinolysis factors. This implies that they may serve as useful markers for effective treatment of this disease.

Adult↗

Effects of the teratogenic folic acid antagonist, 9-methyl pteroylglutamic acid on uronic acid levels in fetal rat limbs.

Experimental pregnant rats were placed on a transitory folic acid-deficient regimen, i.e. dietary restriction of folic acid plus the teratogen and folic acid antagonist, 9-methyl pteroylglutamic acid; a regimen resulting in multiple congenital skeletal malformations. Controls received a folic acid-supplemented regimen. Accumulation of a primary component of the extracellular matrix, glycosaminoglycans (GAG), was quantitatively evaluated by measuring uronic acid concentrations in fetal limbs. On days 16 and 18 of gestation, fetal limbs were removed, pooled from each litter, and prepared for uronic acid, protein, and DNA quantitation. The treatment results in (1) a decreased rate of protein and DNA accumulation prior to day 16 of gestation, the rate not being affected from day 16 to day 18 of gestation; (2) a trend toward an increased rate of uronic acid accumulation prior to day 16 of gestation, and (3) a decreased rate of uronic acid accumulation from day 16 to day 18 of gestation. Furthermore, our observations confirm our earlier suggestion that there is a decreased rate of accumulation of some nonprotein component(s) in fetal limbs obtained from folic acid-deficient mothers from day 16 to day 18 of gestation.

Animals↗

Folic acid as a cancer-preventing agent.

Higher intakes of folic acid-rich foods such as vegetables, legumes, and whole grains are associated with lower incidence of carcinomas in international comparisons and case-control studies. Deficiency of folic acid in experimental studies causes DNA damage that resembles the DNA damage seen in cancer cells. The requirement for folic acid in DNA synthesis and DNA methylation provides a plausible mechanism for a mutagenic effect of a low-folate diet. It is suggested that cancer can be initiated by DNA damage that results from folic acid deficiency. The relatively low level of folic acid in North American diets might be the underlying reason for high rates of many cancers in North America.

Animals↗

Nutritional factors and oral candidosis.

A variety of nutritional factors including deficiencies of iron, folic acid, vitamins, and diets rich in carbohydrates have been implicated in the pathogenesis of oral candidal infections. The following reviews the growing body of data, from in vivo and in vitro studies, related to each of these implicated factors. Although much disagreement exists as to the specific roles played by these individual factors, there is little doubt that nutritional factors either acting locally or via systemic mechanisms could significantly affect the pathogenesis of oral candidoses. Hence, the role of these less well-characterised predisposing factors should be considered when one is treating patients with intractable oral candidal infections.

Animals↗

Effect of lead acetate on rats fed diets containing low levels of folic acid.

Nutritional factors such as deficiencies of calcium, iron, and protein alter susceptibility to the toxic effects of lead. While the suggestion has been made that vitamins may also influence lead toxicity, possible interactions have not been well documented. The present studies were performed to determine if a dietary deficiency of folic acid enhances the susceptibility to rats of the toxic effects of lead acetate. Lead exposure during the development of folate deficiency resulted in alterations in two of the parameters diagnostic of the individual conditions. Decreases in erythrocyte mean corpuscular volume (MCV) occur during lead poisoning, while increases occur during the development of folate deficiency. In the present study, significant reductions in MCV were observed in both the control + lead and in the low folate + lead groups. The increased MCV characteristic of folate deficiency was prevented by the concomitant lead exposure. Elevations in free erythrocyte protoporphyrin (FEP) levels are characteristic of lead intoxication; in contrast, FEP levels decline during folate deficiency. In the present study, FEP levels were significantly elevated only in the control + lead group. Values in the low folate + lead group were intermediate between those of the control and the control + lead groups, but did not differ significantly from those in the low folate group. The expected lead-induced elevation in FEP levels was diminished by the reduced erythropoiesis characteristic of folate deficiency.

Aminolevulinic Acid↗

Impact of methylenetetrahydrofolate reductase deficiency and low dietary folate on the development of neural tube defects in splotch mice.

BACKGROUND: The etiology of neural tube defects (NTDs) is multifactorial, with environmental and genetic determinants. Folate supplementation prevents the majority of NTDs, and a polymorphism in methylenetetrahydrofolate reductase (MTHFR) has become recognized as a genetic risk factor. The mechanisms by which folate affects NTD development are unclear. The Splotch (Sp) mouse is a well-characterized mouse model for studying spontaneous NTDs. To assess the potential interaction between folate metabolism and the Sp mutant in NTD development, we studied mice with both Sp and Mthfr mutations, as well as the interaction between Sp and low dietary folate. METHODS: Wild-type, single Mthfr+/-mutant, single Sp/+mutant, and double mutant (Mthfr+/-, Sp/+) female mice were mated with males of the same genotype. Embryos were examined for NTDs on gestational day (GD) 13.5. To investigate the effects of folate deficiency on Sp mice, Sp/+female mice were fed a control diet (CD), a moderately folic acid-deficient diet (MFADD), or a severely folic acid-deficient diet (SFADD). They were mated with Sp/+males and the embryos were examined. RESULTS: There were no differences in the incidence or severity of NTDs in embryos from double-mutant mating pairs compared to those from single Sp mutants. Embryos from Mthfr+/-dams did not exhibit NTDs. Diets deficient in folate did not influence the incidence or severity of NTDs in embryos from Sp/+mice. CONCLUSIONS: We did not observe an interaction between Sp and Mthfr mutations, or between the Sp mutation and low dietary folate, in NTD development in Splotch mice.

Animals↗

Reproductive and offspring developmental effects following maternal inhalation exposure to methanol in nonhuman primates.

INTRODUCTION: In an effort to improve air quality and decrease dependence on petroleum, the federal government, industry, and other groups have encouraged development of alternative fuels such as methanol to substitute for gasoline or diesel fuel. Methanol is also a candidate to provide the hydrogen for fuel cells, which are being developed for a variety of power sources (including motor vehicle engines). Before people are exposed to increased concentrations of methanol, the potential health effects of such exposures require study. Methanol, a simple alcohol containing one carbon atom, occurs naturally in plants and animals and participates in human metabolism. People regularly consume low doses of methanol in fruits, vegetables, and fermented beverages as well as soft drinks and foods sweetened with aspartame (which breaks down to methanol in the gastrointestinal tract). Despite its ubiquitous presence, methanol can be highly toxic if sufficient quantities are consumed. Ingestion of methanol (usually in the form of wood alcohol or tainted alcoholic beverages) can result in metabolic acidosis, blindness, and even death. Although the body has the capacity to metabolize the low doses of methanol to which people are regularly exposed, it cannot handle high doses because too much methanol overwhelms the body's ability to remove a toxic metabolite (formate). When formate accumulates, methanol poisoning occurs. One factor that regulates the rate at which formate is removed is the liver level of a derivative of the vitamin folic acid. People who are deficient in folic acid (including 15% to 30% of pregnant women) may be particularly susceptible to the toxic effects of methanol. If methanol were to be widely adopted as a fuel, environmental exposures would increase through ingestion of contaminated drinking water, inhalation of vapors from evaporative and other emissions, and dermal contact. Current concentrations of methanol in ambient air are very low, 1 to 30 parts per billion (ppb). If all motor vehicles in the United States were converted to 100% methanol fuel, methanol levels in ambient air are estimated to increase approximately 1,000-fold (to 1 to 10 ppm in cities) and in a worst-case situation could occasionally reach concentrations as high as 200 ppm in enclosed spaces (HEI 1987). Inhaling these concentrations of methanol for short periods of time is not predicted to affect formate production and thus should not present a health risk. However, little is known about the consequences of long-term inhalation of methanol vapors, especially in susceptible populations of pregnant women and developing fetuses. HEI, therefore, developed a research program to address this information gap. APPROACH: Dr. Thomas Burbacher and colleagues of the University of Washington studied the effects of long-term exposure to methanol vapors on metabolism and reproduction in adult female monkeys (Macaca fascicularis) and developmental effects in their offspring, who were exposed prenatally to methanol. The investigators exposed adult female monkeys (11 to 12 animals/group) to one of four concentrations of methanol vapors (0, 200, 600, and 1,800 ppm) for 2.5 hours a day, seven days a week during the following periods: (1) before breeding, (2) during breeding, and (3) during pregnancy. They collected blood from the adults at regular intervals to monitor methanol levels (which served as a marker of internal dose) and formate concentrations. They also conducted pharmacokinetic studies to determine whether methanol disposition (which includes absorption, distribution, metabolism, and excretion) was altered as a result of repeated methanol exposures and to assess pregnancy-related changes. Because high doses of methanol damage the central nervous system, the infants (8 to 9 animals/group) were examined at regular intervals during the first nine months of life to assess their growth and neurobehavioral development. RESULTS: Exposure to methanol vapors did n

Animals↗

Prevalence of micronutrient deficiency particularly of iron, zinc and folic acid in pregnant women in South East Asia.

Micronutrient deficiency, whether clinical or subclinical, may affect growth, cognition and reproductive performance. In pregnant women moderate to severe deficiencies of iron, zinc and folic acid have been shown to increase risk of low birth weight, pregnancy complications and birth defects. Any attempt to introduce a micronutrient supplementation programme during pregnancy must be based on adequate data on the prevalence of micronutrient deficiencies, their adverse effects and the potential for reversing these through supplementation. This paper reviews parameters for assessment of iron, zinc and folic acid deficiencies in pregnancy and the available data on prevalence of these in pregnant women in South Asia. Iron deficiency and anemia affect 50 % or more of pregnant women, the prevalence of folic acid deficiency may be up to 30-50 % and there is evidence to suggest that zinc deficiency is likely to be widespread but supportive data are scarce.

Anemia, Iron-Deficiency↗

Alterations in nucleotide pools in rats fed diets deficient in choline, methionine and/or folic acid.

The fidelity of DNA synthesis is critically dependent on the correct balance and availability of the deoxynucleoside triphosphate (dNTP) precursors for the polymerases involved in replication and repair. Since folate-derived one-carbon groups are essential for the de novo synthesis of both purines and pyrimidines, the purpose of the present investigation was to determine whether diet-induced depletion of folates would alter intracellular dNTP pools. Fischer 344 rats were fed one of four semi-purified diets for a period of 8 weeks: (i) supplemented control; (ii) deficient in folic acid; (iii) deficient in methionine and choline; and (iv) deficient in methionine, choline and folic acid. In contrast to natural diets, semi-purified diets are nucleotide-free and consequently lack substrates for salvage pathway synthesis. This omission may place unusual stress on folate-dependent de novo nucleotide synthesis especially under conditions of dietary methyl-donor deficiency. Reversed-phase HPLC analysis of dNTP in spleen cell extracts indicated that both the thymidylate monophosphate and thymidylate triphosphate pools were decreased in spleen cells from the deficient rats consistent with a decrease in folate-dependent de novo synthesis. In addition, purine biosynthesis appeared to be negatively affect by methyl-donor deficiency as evidenced by a reduction in dGTP and dATP pools. These data indicate that deoxynucleotide pool imbalance, well known to produce cytogenetic and mutagenic events in vitro, can also be induced in this in vivo model of diet-induced carcinogenesis.

Animals↗