The aim of this study was to observe the effect of folate and antioxidants alone on homocysteine levels and oxidative stress markers, and to evaluate whether their co-administration promotes their effects. One hundred patients with hyperhomocysteinemia were randomized into four equal groups, which were then treated with folate, antioxidants or folate plus antioxidants for 2 months; group IV was a control group. Serum homocysteine, folate and oxidative stress markers were measured before the study, at the end of folate and/or antioxidants administration and 3 months later. Folate caused a significant decrease in homocysteine concentration. Antioxidants did not influence homocysteine concentration, but they improved the antioxidative defense (plasma antioxidant capacity and intraerythrocyte glutathione were increased) and partially prevented lipid peroxidation (malondialdehyde level was slightly decreased). Supplementation with folate had a similar effect on intracellular glutathione and plasma malondialdehyde. Simultaneous administration of folate and antioxidants did not show any additive effect with the exception of a slower decrease of folate concentration after its supplementation had been discontinued. Folate may be considered as an effective antioxidant in patients with hyperhomocysteinemia; this can be a result of decreased production of free radicals due to a reduced level of homocysteine. Its antioxidative effect cannot be promoted by co-administration of antioxidants.
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http://dx.doi.org/10.33549/physiolres.930520 | DOI Listing |
Nutrients
January 2025
National Institute for Nutrition and Health, Chinese Center for Disease Control and Prevention, Beijing 100050, China.
Objective: This study aims to identify whether the development of insulin resistance (IR) induced by high selenium (Se) is related to serine deficiency via the inhibition of the de novo serine synthesis pathway (SSP) by the administrations of 3-phosphoglycerate dehydrogenase (PHGDH) inhibitor (NCT503) or exogenous serine in mice.
Method: forty-eight male C57BL/6J mice were randomly divided into four groups: adequate-Se (0.1 mgSe/kg), high-Se (0.
Toxics
January 2025
School of Chemical and Environmental Engineering, Shanghai Institute of Technology, Shanghai 201418, China.
2,6-Dichloro-1,4-benzoquinone (2,6-DCBQ) is an emerging chlorinated disinfection byproduct (DBP) in bodies of water. However, this compound poses an unknown toxic effect on cyanobacteria. In this study, the toxicological mechanisms of 2,6-DCBQ in () were investigated through physiological and nontargeted metabolomic assessments.
View Article and Find Full Text PDFJ Physiol Sci
January 2025
Department of Medical Physiology, Faculty of Medicine, Ain Shams University, Cairo, Egypt.
Folic acid (FA), with its anti-inflammatory and antioxidant properties, may offer protection against ischemia-reperfusion (IR) injury. This study investigated whether FA safeguards rat kidneys from IR by targeting high mobility group box-1 (HMGB1), a key inflammatory mediator. Fifty adult male Wistar rats were randomly allocated into four groups: control, IR, IR + FA pretreatment, and FA alone.
View Article and Find Full Text PDFGenes Nutr
January 2025
Department of Nutrition, University of Oslo (UiO), Oslo, Norway.
Background: One-carbon metabolism links folate and methionine metabolism and this is essential for nucleotide synthesis in the cells. Alterations in one-carbon metabolism are associated with cardiovascular disease (CVD), type 2 diabetes and cancer. Our aim was to investigate whether SNPs in antioxidant-enzyme genes impact the concentrations of folate in serum (s-folate), plasma total homocysteine (p-tHcy) and total glutathione in plasma (p-tGSH) in healthy subjects after supplementation with folic acid.
View Article and Find Full Text PDFJ Hum Nutr Diet
February 2025
Department of Biostatistics and Medical Informatics, University College of Medical Sciences, Delhi, India.
The progression of Alzheimer's disease (AD) is intricately tied to the impairment of neurons, crucial for neurological functions. Despite extensive research, the precise mechanism underlying AD development remains elusive due to its multifaceted aetiology. Vitamin deficiency has emerged as a notable contributor to AD onset and progression, exerting a significant influence on brain function.
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