Vitamin B6 suppresses apoptosis of NM-1 bovine endothelial cells induced by homocysteine and copper

Endo, Naruki; Nishiyama, Kazuo; Okabe, Masaru; Matsumoto, Mitsuharu; Kanouchi, Hiroaki; Oka, Tatsuzo

doi:10.1016/j.bbagen.2006.11.009

Cited by 27 publications

(20 citation statements)

References 25 publications

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“…Our results suggest that B 12 may either directly or indirectly act as an antioxidant. This effect has also been reported for vitamin B 6 in bone and atherosclerosis diseases where antioxidants may play a role in preventing bone and endothelial losses [Byun et al, 2005;Endo et al, 2007]. Thus, vitamin B 12 might function not only as cofactor of cobalamin-dependent enzymes, but also apparently as possible scavenger of ROS.…”

Section: Discussionmentioning

confidence: 61%

Genetic and cellular studies of oxidative stress in methylmalonic aciduria (MMA) cobalamin deficiency type C (cblC) with homocystinuria (MMACHC)

Richard¹,

Jorge‐Finnigan²,

García‐Villoria³

et al. 2009

Hum. Mutat.

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Methylmalonic aciduria (MMA) cobalamin deficiency type C (cblC) with homocystinuria (MMACHC) is the most frequent genetic disorder of vitamin B(12) metabolism. The aim of this work was to identify the mutational spectrum in a cohort of cblC-affected patients and the analysis of the cellular oxidative stress and apoptosis processes, in the presence or absence of vitamin B(12). The mutational spectrum includes nine previously described mutations: c.3G>A (p.M1L), c.217C>T (p.R73X), c.271dupA (p.R91KfsX14), c.331C>T (p.R111X), c.394C>T (p.R132X), c.457C>T (p.R153X), c.481C>T (p.R161X), c.565C>A (p.R189S), and c.615C>G (p.Y205X), and two novel changes, c.90G>A (p.W30X) and c.81+2T>G (IVS1+2T>G). The most frequent change was the known c.271dupA mutation, which accounts for 85% of the mutant alleles characterized in this cohort of patients. Owing to its high frequency, a real-time PCR and subsequent high-resolution melting (HRM) analysis for this mutation has been established for diagnostic purposes. All cell lines studied presented a significant increase of intracellular reactive oxygen species (ROS) content, and also a high rate of apoptosis, suggesting that elevated ROS levels might induce apoptosis in cblC patients. In addition, ROS levels decreased in hydroxocobalamin-incubated cells, indicating that cobalamin might either directly or indirectly act as a scavenger of ROS. ROS production might be considered as a phenotypic modifier in cblC patients, and cobalamin supplementation or additional antioxidant drugs might suppress apoptosis and prevent cellular damage in these patients.

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Section: Discussionmentioning

confidence: 61%

Genetic and cellular studies of oxidative stress in methylmalonic aciduria (MMA) cobalamin deficiency type C (cblC) with homocystinuria (MMACHC)

Richard¹,

Jorge‐Finnigan²,

García‐Villoria³

et al. 2009

Hum. Mutat.

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“…It has a high affinity for Cu 2+ and the mechanism of transferring copper from chelation with peptides to EDTA has been studied as early as 1968 [14]. In the studies of physiological and pathological activity of copper-dependent compounds, EDTA was often used as a classic Cu 2+ chelator in experiments to modulate copper concentrations in the cell, or to terminate biochemical process of copper-containing compounds [21][22][23]. EDTA binds to copper and prevents copperdependent biological events when it is added into media containing copper before the latter binds to targeted proteins or peptides.…”

Section: Polyaminocarboxylate Chelatorsmentioning

confidence: 99%

The significance of copper chelators in clinical and experimental application

Ding

Xie

Kang

2011

The Journal of Nutritional Biochemistry

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“…Yet, the negative effect can be prevented by antioxidants. The combined vitamin B supplementation causes a marked decrease in ROS, protein oxidation, and an enhancement of antioxidative enzymes [9,[14][15][16]. Subjects continuously exposed to low-grade oxidative stress, such as manual laborers [17] and patients suffering from schizophrenia [18] or chronic illnesses including cancer, might particularly benefit from the antioxidant and anti-inflammatory impact of the vitamin B in the prevention of lipid peroxidation [19,20].…”

Section: Introductionmentioning

confidence: 99%

A Randomized Pilot Trial to Evaluate the Bioavailability of Natural versus Synthetic Vitamin B Complexes in Healthy Humans and Their Effects on Homocysteine, Oxidative Stress, and Antioxidant Levels

Lindschinger¹,

Tatzber

Schimetta

et al. 2019

Oxidative Medicine and Cellular Longevity

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The vitamin B complex comprises 8 different water-soluble constituents that humans must sequester from the diet. This pilot study compared natural versus synthetic vitamin B complexes for their bioavailability, accumulation, and their impact on antioxidants, homocysteine levels, and oxidative stress. We conducted a double-blind randomized clinical trial with thirty healthy participants. They were randomly assigned to group N (natural) and group S (synthetic). Vitamin B was ingested daily for 6 weeks in the range of about 2.5 times above the recommended daily allowance. Blood samples were taken at baseline, 1.5 h, 4 h, 7 h (diurnal), 6 w (discontinuation of supplements), and 8 w (washout). Blood levels of thiamine (B 1 ), riboflavin (B 2 ), pyridoxine (B 6 ), folic acid (B 9 ), cobalamin (B 12 ), homocysteine, total antioxidants, peroxidase activity, polyphenols, and total peroxides were determined. Compared to initial values, serum levels of each B vitamin increased at the end of the supplementation period: i.e., B 1 (+23% N; +27% S), B 2 (+14% N; +13% S), B 6 (+101% N; +101% S), B 9 (+86% N; +153% S), and B 12 (+16% N) (p < 0:05). Homocysteine (-13% N) decreased, while peroxidase activity (+41% S) and antioxidant capacity increased (+26% N). Short-term effects were already observed after 1.5 h for B 9 (+238% N; +246% S) and after 4 h for vitamin B 2 (+7% N; +8% S), B 6 (+59% N; +51% S), and peroxidase activity (+58% N; +58% S). During the washout period, serum levels of B vitamins decreased except for thiamine and peroxidase activity, which increased further. This clinical pilot study revealed comparable bioavailability for both natural and synthetic B vitamins but did not show statistically noticeable differences between groups despite some favourable tendencies within the natural vitamin group, i.e., sustained effects for cobalamin and endogenous peroxidase activity and a decrease in homocysteine and oxidative stress levels.

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Vitamin B6 suppresses apoptosis of NM-1 bovine endothelial cells induced by homocysteine and copper

Cited by 27 publications

References 25 publications

Genetic and cellular studies of oxidative stress in methylmalonic aciduria (MMA) cobalamin deficiency type C (cblC) with homocystinuria (MMACHC)

Genetic and cellular studies of oxidative stress in methylmalonic aciduria (MMA) cobalamin deficiency type C (cblC) with homocystinuria (MMACHC)

The significance of copper chelators in clinical and experimental application

A Randomized Pilot Trial to Evaluate the Bioavailability of Natural versus Synthetic Vitamin B Complexes in Healthy Humans and Their Effects on Homocysteine, Oxidative Stress, and Antioxidant Levels

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