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Background: In Oman, ischemic heart disease (IHD) is the most common type of cardiovascular disease, and there are multifactorial causes, including nutritional deficiencies of B vitamins (folate and B12) and health illiteracy. Objective: This study aimed to characterize the health literacy, nutrition literacy, and B-vitamin (folate and B12) status of patients with recurrent episodes of IHD. Methods: This cross-sectional study was conducted over a period of 5 months from February to June 2022. The enrolled study participants had an angiographically proven recurrence of IHD, and they were interviewed using a study questionnaire to identify their sociodemographic data, health status, and nutrition status. Folate and B12 were measured in the sera of the study participants. Results: Most participants were in their middle age (62%), and the frequency of the IHD recurrence was noticed among men, married, and unemployed. The serum values of folate and vitamin B12 were within the normal range among the IHD patients. Health literacy categories were affected by the employment status (χ21 = 6.05, P = 0.01), and the binary logistic regression confirmed the statistical significance between employment status and health literacy (odds ratio; 1.7, P = 0.005). Nutrition literacy had a significant difference regarding the education variable (χ21 = 8.34, P = 0.004), and the sociodemographic variables were not associated with nutrition literacy. Conclusion: The investigated health and nutrition literacy measures might be used for assessing IHD patients' literacy and detecting any deficits that needed to be improved. [ABSTRACT FROM AUTHOR]

Folate and vitamin B12 deficiency is associated with depletion of the major intracellular antioxidant glutathione, and oxidative stress is emerging as an etiological mechanism for colon cancer. Azoxymethane (AOM), a potent carcinogen, induces colon cancer in rats by causing pathophysiological changes and oxidative stress. We investigated the synergistic effect of folate and vitamin B12 supplementation against AOM-induced carcinogenesis and oxidative stress in rat colon. Adult male rats were distributed into four groups: 1) Basal diet only; 2) AOM injection (15 mg/kg once per week in weeks 5 and 6); 3) Folate and vitamin B12 supplemented diet; 4) Folate and B12 diet with AOM injection. After 16 weeks, rats were sacrificed, colon tissue dissected, indicators of oxidative stress were measured, and immunohistochemical and ultrastructural changes were evaluated. AOM-injected rats showed oxidative stress, evident by glutathione depletion, oxidation of cellular proteins, and DNA oxidative damage. AOM increased mucosal levels of antiapoptotic and proapoptotic proteins Bcl2 and Bax and caused ultrastructure changes in colonic cell organelles. Folate and vitamin B12 supplementation decreased the level of oxidative stress and ameliorated the cytotoxic effects of AOM. In this in vivo experimental model of colon cancer, folate and vitamin B12 supplementation combats carcinogen-induced oxidative stress. [ABSTRACT FROM AUTHOR]

Objective: Arab populations lack data related to nutritional assessment in children with autism spectrum disorders (ASDs), especially micronutrient deficiencies such as folate and vitamin B12. Methods: To assess the dietary and serum folate and vitamin B12 statuses, a hospital-based case-control study was conducted in 80 Omani children (40 children with ASDs versus 40 controls). Results: The ASD cases showed significantly lower levels of folate, vitamin B12, and related parameters in dietary intake and serum levels. Conclusion: These data showed that Omani children with ASDs exhibit significant deficiencies in folate and vitamin B12 and call for increasing efforts to ensure sufficient intakes of essential nutrients by children with ASDs to minimize or reverse any ongoing impact of nutrient deficiencies. [ABSTRACT FROM AUTHOR]

Aim: This case-control study was aimed to evaluate the folate and vitamin B12 status among patients recently diagnosed with colorectal cancer (CRC), in Jordan. Materials and Methods: The study involved 220 recently diagnosed Jordanian CRC patients and 220 age- and gender-matched healthy controls. The dietary intake and biochemical assessment of folate and vitamin B12 were determined for all the study participants. Results: The CRC patients had lower daily intake and serum levels of both folate (189.28 ± 11.78 µg/day and 6.6 ± 1.3 µg/l, respectively) and vitamin B12 (1.09 ± 0.4 µg/day and 233.7 ± 17.9 pg/ml, respectively) as compared to their matched control groups (212.58 ± 13.18 µg/day and 16.2 ± 2.8 µg/l, respectively, for folate) and (2.49 ± 1.3 µg/day and 458.9 ± 30.9 pg/ml, respectively, for vitamin B12). Conclusion: The CRC Jordanian patients who participated in this study had a low status of folate and vitamin B12, and a well-established etiological factor for CRC. [ABSTRACT FROM AUTHOR]

Methionine synthase (MS) is a ubiquitous enzyme that requires vitamin B12 (cobalamin) and 5-methyl-tetrahydrofolate for the methylation of homocysteine to methionine. Previous studies have shown that acute or chronic ethanol (ETOH) administration results in the inhibition of MS and depletion of glutathione (GSH), and it has been proposed that GSH is required for the synthesis of methylcobalamin (MeCbl). We measured GSH levels and investigated the ability of different cobalamin cofactors [cyano- (CNCbl), glutathionyl- (GSCbl), hydroxo- (OHCbl), and MeCbl] to support MS activity in liver and brain cortex from control and ETOH-treated rats. In control animals, MS activity was higher in liver than in cortex for all cobalamins and MeCbl-based activity was higher than for other cofactors. S-adenosylmethionine (SAM) was required for OHCbl, CNCbl, and GSCbl-based activity, but not for MeCbl. Feeding an ETOH-containing diet for four weeks caused a significant decrease in liver MS activity, in a cobalamin-dependent manner (OHCbl ≥ CNCbl > GSCbl > MeCbl). In brain cortex, OHCbl, CNCbl, and GSCbl-based activity was reduced by ETOH treatment, but MeCbl-based activity was unaffected. GSH levels were reduced by ETOH treatment in both liver and cortex homogenates, and addition of GSH restored OHCbl-based MS activity to control levels. Betaine administration had no significant effect on GSH levels or MS activity in either control or ETOH-fed groups. The ETOH-induced decrease in OHCbl-based MS activity is secondary to decreased GSH levels and a decreased ability to synthesize MeCbl. The ability of MeCbl to completely offset ETOH inhibition in brain cortex, but not liver, suggests tissue-specific differences in the GSH-dependent regulation of MS activity. [ABSTRACT FROM AUTHOR]

Vitamin B12 is an essential cofactor for normal activity of the ubiquitous enzyme methionine synthase (MS), which methylates homocysteine as part of the methionine cycle. Studies have shown that chronic ethanol (ETOH) exposure in rats results in inhibition of MS and depletion of glutathione (GSH), the major intracellular antioxidant. We investigated the ability of either hydroxocobalamin (OHCbl) or methylcobalamin (MeCbl) to support MS activity. OHCbl is converted to MeCbl via a GSH-dependent mechanism. In liver and cortex of the control animals, MeCbl-based MS activity was higher than OHCbl-based MS activity. ETOH treatment reduced both MeCbl and OHCbl-based MS activity in liver, however, in cortex ETOH reduced OHCbl-based MS activity, but not MeCbl-based activity. ETOH lowered liver and cortex GSH levels by 30%. Our results indicate that ethanol inhibits MS activity in both liver and cortex in conjunction with depleted intracellular GSH levels, but only in cortex was a unique protective effect for MeCbl observed against the ETOH-mediated inhibition of MS activity. Thus intracellular oxidative stress may be responsible for the ETOH-induced decrease in MS activity, and MeCbl administration could represent a strategy to overcome this inhibitory effect. [ABSTRACT FROM AUTHOR]

Abstract: Objective: The purpose of this study was to examine the status of folate and vitamin B12 (B12) in relation to serum homocysteine (HCY) and oxidative stress indices in patients with type 2 diabetes (T2DM). Methods: This case–control study involved 100 Omani adults (50 patients newly diagnosed with T2DM and 50 age- and gender-matched healthy controls). Several parameters were investigated, including dietary intake and biochemical assessments of folate, B12, HCY, oxidative stress markers (glutathione and total antioxidant status), and antioxidant enzymes (superoxide dismutase, glutathione peroxidase, and catalase). Results: Low serum levels of folate, B12, and hyperhomocysteinemia were prevalent in patients with T2DM compared with controls. Oxidative stress was evident in patients with T2DM as indicated by low serum levels of glutathione, total antioxidant status, and impaired antioxidant enzymatic activities (superoxide dismutase, glutathione peroxidase, and catalase). Conclusion: The low intake of folate and B12 is associated with low serum levels of these two nutrients and hyperhomocysteinemia in Omani adults with T2DM. [Copyright &y& Elsevier]

Abstract: Recently higher rates of autism diagnosis suggest involvement of environmental factors in causing this developmental disorder, in concert with genetic risk factors. Autistic children exhibit evidence of oxidative stress and impaired methylation, which may reflect effects of toxic exposure on sulfur metabolism. We review the metabolic relationship between oxidative stress and methylation, with particular emphasis on adaptive responses that limit activity of cobalamin and folate-dependent methionine synthase. Methionine synthase activity is required for dopamine-stimulated phospholipid methylation, a unique membrane-delimited signaling process mediated by the D4 dopamine receptor that promotes neuronal synchronization and attention, and synchrony is impaired in autism. Genetic polymorphisms adversely affecting sulfur metabolism, methylation, detoxification, dopamine signaling and the formation of neuronal networks occur more frequently in autistic subjects. On the basis of these observations, a “redox/methylation hypothesis of autism” is described, in which oxidative stress, initiated by environment factors in genetically vulnerable individuals, leads to impaired methylation and neurological deficits secondary to reductions in the capacity for synchronizing neural networks. [Copyright &y& Elsevier]