scholarly journals Effect of oral vitamin C ingestion on the vascular endothelial function and oxidative stress marker exposed to after transient heat-not-burn tobacco smoking

2020 ◽  
Vol 69 (2) ◽  
pp. 229-235
Author(s):  
Ayako Azuma ◽  
Hajime Miura ◽  
Mizuki Ishikawa ◽  
Yasuaki Tamura
Keyword(s):  
Oxidative Stress ◽  
Vitamin C ◽  
Endothelial Function ◽  
Tobacco Smoking ◽  
Oxidative Stress Marker ◽  
Vascular Endothelial ◽  
Vascular Endothelial Function ◽  
Oral Vitamin ◽  
Stress Marker ◽  
And Oxidative Stress

scholarly journals Vascular endothelial function and oxidative stress are related to dietary niacin intake among healthy middle-aged and older adults

2014 ◽  
Vol 116 (2) ◽  
pp. 156-163 ◽  
Author(s):  
Rachelle E. Kaplon ◽  
Lindsey B. Gano ◽  
Douglas R. Seals
Keyword(s):  
Oxidative Stress ◽  
Older Adults ◽  
Nadph Oxidase ◽  
Endothelial Function ◽  
Brachial Artery ◽  
Antioxidant Vitamin ◽  
Vascular Endothelial ◽  
Vascular Endothelial Function ◽  
Middle Aged ◽  
And Oxidative Stress

We tested the hypothesis that vascular endothelial function and oxidative stress are related to dietary niacin intake among healthy middle-aged and older adults. In 127 men and women aged 48–77 yr, brachial artery flow-mediated dilation (FMD) was positively related to dietary niacin intake [%change (Δ): r = 0.20, P < 0.05; mmΔ: r = 0.25, P < 0.01]. In subjects with above-average dietary niacin intake (≥22 mg/day, NHANES III), FMD was 25% greater than in subjects with below-average intake ( P < 0.05). Stepwise linear regression revealed that dietary niacin intake (above vs. below average) was an independent predictor of FMD (%Δ: β = 1.8; mmΔ: β = 0.05, both P < 0.05). Plasma oxidized low-density lipoprotein, a marker of systemic oxidative stress, was inversely related to niacin intake ( r = −0.23, P < 0.05) and was lower in subjects with above- vs. below-average niacin intake (48 ± 2 vs. 57 ± 2 mg/dl, P < 0.01). Intravenous infusion of the antioxidant vitamin C improved brachial FMD in subjects with below-average niacin intake ( P < 0.001, n = 33), but not above-average ( P > 0.05, n = 20). In endothelial cells sampled from the brachial artery of a subgroup, dietary niacin intake was inversely related to nitrotyrosine, a marker of peroxynitrite-mediated oxidative damage ( r = −0.30, P < 0.05, n = 55), and expression of the prooxidant enzyme, NADPH oxidase ( r = −0.44, P < 0.01, n = 37), and these markers were lower in subjects with above- vs. below-average niacin intake [nitrotyrosine: 0.39 ± 0.05 vs. 0.56 ± 0.07; NADPH oxidase: 0.38 ± 0.05 vs. 0.53 ± 0.05 (ratio to human umbilical vein endothelial cell control), both P < 0.05]. Our findings support the hypothesis that higher dietary niacin intake is associated with greater vascular endothelial function related to lower systemic and vascular oxidative stress among healthy middle-aged and older adults.

scholarly journals SUMO2 regulates vascular endothelial function and oxidative stress in mice

2019 ◽  
Vol 317 (6) ◽  
pp. H1292-H1300 ◽  
Author(s):  
Young-Rae Kim ◽  
Julia S. Jacobs ◽  
Qiuxia Li ◽  
Ravinder Reddy Gaddam ◽  
Ajit Vikram ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Function ◽  
Vascular Function ◽  
Ex Vivo ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Vascular Endothelial ◽  
Vascular Endothelial Function ◽  
Density Lipoprotein Receptor ◽  
Vascular Oxidative Stress

SUMOylation is a posttranslational modification of lysine residues. Modification of proteins by small ubiquitin-like modifiers (SUMO)1, -2, and -3 can achieve varied, and often unique, physiological and pathological effects. We looked for SUMO2-specific effects on vascular endothelial function. SUMO2 expression was upregulated in the aortic endothelium of hypercholesterolemic low-density lipoprotein receptor-deficient mice and was responsible for impairment of endothelium-dependent vasorelaxation in these mice. Moreover, overexpression of SUMO2 in aortas ex vivo, in cultured endothelial cells, and transgenically in the endothelium of mice increased vascular oxidative stress and impaired endothelium-dependent vasorelaxation. Conversely, inhibition of SUMO2 impaired physiological endothelium-dependent vasorelaxation in normocholesterolemic mice. These findings indicate that while endogenous SUMO2 is important in maintenance of normal endothelium-dependent vascular function, its upregulation impairs vascular homeostasis and contributes to hypercholesterolemia-induced endothelial dysfunction. NEW & NOTEWORTHY Sumoylation is known to impair vascular function; however, the role of specific SUMOs in the regulation of vascular function is not known. Using multiple complementary approaches, we show that hyper-SUMO2ylation impairs vascular endothelial function and increases vascular oxidative stress, whereas endogenous SUMO2 is essential for maintenance of normal physiological function of the vascular endothelium.

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