Passive Smoking Exacerbates Nicotinamide-Adenine Dinucleotide Phosphate Oxidase Isoform 2–Induced Oxidative Stress and Arterial Dysfunction in Children with Persistent Allergic Rhinitis

Background:Nicotinamide adenine dinucleotide phosphate oxidase of the vascular cell membrane is an important source of reactive oxygen species. The aim of our study was to evaluate the possible influence of the p22phox C242T gene polymorphism on blood pressure and some markers of oxidative stress in children with tetralogy of Fallot.Methods:After surgical repair in early life, we recruited 38 children, aged 11.7 plus or minus 3.2 years, including 185 healthy individuals as controls for the purposes of establishing frequencies of alleles and genotypes. From this latter group, we matched a sub-sample of 53 healthy caucasian children, aged 11.0 plus or minus 1.0 years, in order to compare enzymic activities.Results:The children with tetralogy of Fallot showed significantly lower values of low-molecular-weight protein tyrosine phosphatase, particularly in carriers of CC genotype for the p22phox gene, with values of 145.2 plus or minus 77.4 μmol/g Hb/h, compared to controls, at 344.4 plus or minus 100.4 μmol/g Hb/h (p less than 0.001). Methemoglobin reductase activity in the patients with tetralogy was also lower in those with the CC genotype, at 9.8 plus or minus 3.2 μmol/g Hb−1min−1compared to 24.2 plus or minus 11.8 μmol/g Hb−1min−1as measured in the controls (p less than 0.01). Lower systolic (p less than 0.05) and diastolic (p less than 0.01) blood pressures were also observed in the patients with tetralogy of Fallot.Conclusions:Patients with tetralogy of Fallot having the CC genotype may be at a higher state of oxidative stress than T allele carriers, a finding which could have prognostic implications. Long term follow-up of these patients, however, may be necessary in order to draw definite conclusions.

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Effect on oxidative stress, hepatic chemical metabolizing parameters, and genotoxic damage of mad honey intake in rats

Human & Experimental Toxicology ◽

10.1177/0960327117745691 ◽

2017 ◽

Vol 37 (9) ◽

pp. 991-1004 ◽

Cited By ~ 2

Author(s):

G Eraslan ◽

M Kanbur ◽

M Karabacak ◽

K Arslan ◽

Y Siliğ ◽

...

Keyword(s):

Oxidative Stress ◽

Nicotinamide Adenine Dinucleotide ◽

Nicotinamide Adenine Dinucleotide Phosphate ◽

Exposure Period ◽

Acute Stage ◽

Nicotinamide Adenine ◽

Control Group ◽

Antioxidant Enzyme Activities ◽

Subacute Stage ◽

Mad Honey

A total of 66 male Wistar rats were used and six groups (control: 10 animals and experimental: 12 animals) were formed. While a separate control group was established for each study period, mad honey application to the animals in the experimental group was carried out with a single dose (12.5 g kg−1 body weight (b.w.); acute stage), at a dose of 7.5 g kg−1 b.w. for 21 days (subacute stage), and at a dose of 5 g kg−1 b.w. for 60 days (chronic stage). Tissue and blood oxidative stress markers (malondialdehyde (MDA), nitric oxide (NO), 4-hydroxynonenal (HNE), superoxide dismutase, catalase, glutathione (GSH) peroxidase, and glucose-6-phosphate dehydrogenase), hepatic chemical metabolizing parameters in the liver (cytochrome P450 2E1, nicotinamide adenine dinucleotide (NADH)-cytochrome b5 reductase, nicotinamide adenine dinucleotide phosphate (NADPH)-cytochrome c reductase (CYTC), GSH S-transferase (GST), and GSH), and micronucleus and comet test in some samples were examined. Findings from the study showed that single and repeated doses given over the period increased MDA, NO, and HNE levels while decreasing/increasing tissue and blood antioxidant enzyme activities. From hepatic chemical metabolizing parameters, GST activity increased in the subacute and chronic stages and CYTC activity increased in the acute period, whereas GSH level decreased in the subacute stage. Changes in tail and head intensities were found in most of the comet results. Mad honey caused oxidative stresses for each exposure period and made some significant changes on the comet test in certain periods for some samples obtained. In other words, according to the available research results obtained, careless consumption of mad honey for different medical purposes is not appropriate.

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Impact of sperm morphology on DNA damage caused by oxidative stress induced by ?-nicotinamide adenine dinucleotide phosphate

Fertility and Sterility ◽

10.1016/j.fertnstert.2004.06.056 ◽

2005 ◽

Vol 83 (1) ◽

pp. 95-103 ◽

Cited By ~ 110

Author(s):

T SAID ◽

A AGARWAL ◽

R SHARMA ◽

A THOMASJR ◽

S SIKKA

Keyword(s):

Oxidative Stress ◽

Dna Damage ◽

Nicotinamide Adenine Dinucleotide ◽

Sperm Morphology ◽

Nicotinamide Adenine Dinucleotide Phosphate ◽

Nicotinamide Adenine

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Nebivolol Attenuates Redox-Sensitive Glomerular and Tubular Mediated Proteinuria in Obese Rats

Endocrinology ◽

10.1210/en.2010-1038 ◽

2010 ◽

Vol 152 (2) ◽

pp. 659-668 ◽

Cited By ~ 24

Author(s):

Javad Habibi ◽

Melvin R. Hayden ◽

James R. Sowers ◽

Lakshmi Pulakat ◽

Roger D. Tilmon ◽

...

Keyword(s):

Oxidative Stress ◽

Nitric Oxide ◽

Insulin Resistance ◽

Insulin Sensitivity ◽

Proximal Tubule ◽

Nicotinamide Adenine Dinucleotide ◽

Nicotinamide Adenine Dinucleotide Phosphate ◽

Male Rats ◽

Nicotinamide Adenine ◽

Specific Proteins

Abstract Obesity and insulin resistance-related proteinuria is associated with oxidative stress and impaired tissue bioavailable nitric oxide. Recent data suggest that nicotinamide adenine dinucleotide phosphate oxidase-mediated oxidative injury to the proximal tubule, like that seen in the glomerulus, contributes to proteinuria in insulin-resistant states. The vasodilator β-blocker nebivolol reduces nicotinamide adenine dinucleotide phosphate oxidase activity, increases bioavailable nitric oxide, and improves insulin sensitivity. To test the hypothesis that a treatment strategy that reduces oxidative stress and attenuates obesity-associated increases in glomerular and proximal tubule derived protein, we treated young Zucker obese (ZO) and age-matched Zucker lean male rats with nebivolol (10 mg · kg−1 · d−1) for 21 d. Compared with Zucker lean, ZO controls exhibited increased proteinuria and γ-glutamyl transpeptidase, reductions in systemic insulin sensitivity in association with increased renal renin, (pro)renin receptor, angiotensin II type 1 receptor, and mineralocorticoid receptor immunostaining, oxidative stress, and glomerular tubular structural abnormalities that were substantially improved with in vivo nebivolol treatment. Nebivolol treatment also led to improvements in glomerular podocyte foot-process effacement and improvement in podocyte-specific proteins (nephrin and synaptopodin) as well as proximal tubule-specific proteins (megalin and lysosomal-associated membrane protein-2) and proximal tubule ultrastructural remodeling in the ZO kidney. Our findings support the notion that obesity and insulin resistance lead to increased glomerulotubular oxidative stress and resultant glomerular and tubular sources of excess urine protein. Furthermore, the results of this study suggest the beneficial effect of nebivolol on proteinuria was derived from improvements in weight and insulin sensitivity and reductions in renal oxidative stress in a state of obesity and insulin resistance.

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