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

2017 ◽  
Vol 37 (9) ◽  
pp. 991-1004 ◽  
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.

scholarly journals Metabolic changes in the lymphocytes during influenza

2012 ◽  
Vol 93 (4) ◽  
pp. 580-584
Author(s):  
I V Sergeeva ◽  
N I Kamzalakova ◽  
E P Tikhonova ◽  
G V Bulygin
Keyword(s):  
Nicotinamide Adenine Dinucleotide ◽  
Tricarboxylic Acid Cycle ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Tricarboxylic Acid ◽  
Nicotinamide Adenine ◽  
Control Group ◽  
Healthy Individuals ◽  
Acid Cycle ◽  
Intracellular Enzymes ◽  
Glucose 6 Phosphate Dehydrogenase

Aim. To assess the nature and intensity of metabolic processes in lymphocytes of patients with influenza according to the activity of intracellular enzymes in comparison to the severity of the disease. Methods. Determined were the enzymatic parameters of lymphocytes of 45 patients aged 18 to 42 years with a diagnosis of «influenza». Two groups of patients were formed: with moderate (24 patients) and severe (21 patients) course of the disease. Used as controls were the values the activity of intracellular enzymes of lymphocytes of 37 practically healthy individuals of comparable age. Results. In patients with a moderately severe course of the influenza compared with the controls noted was a significant increase in activity of glucose-6-phosphate dehydrogenase (3.17±0.53 and 2.74±0.31 mkE/10 000 cells, p 0.05) and glycerol-3-phosphate dehydrogenase (57.33±±5.65 and 0.84±0.16 mkE/10 000 cells respectively, p 0.001). The activity of lactate dehydrogenase was lower in patients than in controls (0.40±0.08 and 0.84±0.08 mkE/10 000 cells respectively, p 0.001). Indicators of nicotinamide adenine dinucleotide and nicotinamide adenine dinucleotide phosphate dependant isocitrate dehydrogenases in lymphocytes of patients were lower than in the controls: the first indicator in the patients was 0.17±0.02 mkE/10 000 cells, in controls - 1.95±0.25 mkE/10 000 cells (p 0.001), and for the second indicator these values were respectively 0.09±0.01 and 31.02±±2.20 mkE/10 000 cells (p 0.001). In patients with a moderately severe course of influenza the activity of nicotinamide adenine dinucleotide and nicotinamide adenine dinucleotide phosphate dependant glutamate dehydrogenases was significantly higher compared with healthy individuals: 63.67±5.32 and 0.34±0.06 mkE/10 000 cells, 1.45±0.18 and 0.11±0.02 mkE/10 000 cells respectively (p 0.001). The activity of nicotinamide adenine dinucleotide dependant malate dehydrogenase in patients was equal to 86.46±12.30 mkE/10 000 cells (in the control group 84.16±13.70 mkE/10 000 cells), and the activity of nicotinamide adenine dinucleotide phosphate dependant malate dehydrogenase was equal to 1.34±±0.25 mkE/10 000 cells (in the control group 0.33±0.07 mkE/10 000 cells, p 0.001). The activity of glutathione reductase was also higher in patients with the moderately severe course of the influenza: 5.86±0.25 mkE/10 000 cells, while the value in healthy individuals was 1.28±0.30 mkE/10 000 cells (p 0.001). In the group of patients with a severe course of influenza the activity of almost all (except for glucose-6-phosphate dehydrogenase) enzymes was higher than during the moderately severe course of disease. Conclusion. At the peak of the diseases noted were opposite changes in the activity of reactions of the pentose phosphate cycle and glycolysis. With a high functional load on the cells there is a significant reduction in the intensity of the reactions of the initial phase of the tricarboxylic acid cycle, which reduces the energy efficiency of the cycle, while the intense influx of metabolites to supply the tricarboxylic acid cycle with substrates of the amino acid metabolism provides enhanced transport of amino acids into the lymphocytes.

Polymorphism C242T of the gene of the p22phox subunit for nicotinamide adenine dinucleotide phosphate oxidase, and erythrocytic antioxidant enzymes, in patients with tetralogy of Fallot

2007 ◽  
Vol 17 (3) ◽  
pp. 295-300 ◽  
Author(s):  
António Guerra ◽  
Carla Rego ◽  
Constança Coelho ◽  
Nuno Guimarães ◽  
Catarina Thiran ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Tetralogy Of Fallot ◽  
Nicotinamide Adenine Dinucleotide ◽  
Reductase Activity ◽  
Tyrosine Phosphatase ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Nicotinamide Adenine ◽  
Long Term Follow Up ◽  
Markers Of Oxidative Stress ◽  
Blood Pressures

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.

scholarly journals Advanced Oxidation Protein Products Promote Inflammation in Diabetic Kidney through Activation of Renal Nicotinamide Adenine Dinucleotide Phosphate Oxidase

Endocrinology ◽  
2008 ◽  
Vol 149 (4) ◽  
pp. 1829-1839 ◽  
Author(s):  
Xiao Yun Shi ◽  
Fan Fan Hou ◽  
Hong Xin Niu ◽  
Guo Bao Wang ◽  
Di Xie ◽  
...  
Keyword(s):  
Nadph Oxidase ◽  
Nicotinamide Adenine Dinucleotide ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Advanced Oxidation ◽  
Diabetic Rats ◽  
Nicotinamide Adenine ◽  
Control Group ◽  
Advanced Oxidation Protein Products ◽  
Renal Inflammation ◽  
Diabetic Kidney

The involvement of inflammatory processes has been recognized in development and/or progression of diabetic nephropathy. However, the mechanisms involved in the pathogenesis of renal inflammation have not been completely understood. In this study, we tested the hypothesis that accumulation of advanced oxidation protein products (AOPPs), which occurs in diabetes, may promote inflammatory responses in diabetic kidney. Streptozotocin-induced diabetic rats were randomized to iv injection of vehicle, native rat serum albumin (RSA), and AOPPs-modified RSA (AOPPs-RSA) in the presence or absence of oral administration of apocynin. A control group was followed concurrently. Compared with RSA- or vehicle-treated diabetic rats, AOPPs-RSA-treated animals displayed significant increase in renal macrophage infiltration and overexpression of monocyte chemoattractant protein-1 and TGF-β1. This was associated with deteriorated structural and functional abnormalities of diabetic kidney, such as glomerular hypertrophy, fibronectin accumulation, and albuminuria. AOPP challenge significantly increased nicotinamide adenine dinucleotide phosphate (NADPH) oxidase-dependent superoxide generation in renal homogenates and up-regulated membrane expression of renal NADPH oxidase subunits p47phox and gp91phox. All these AOPPs-induced perturbations in diabetic kidney could be prevented by the NADPH oxidase inhibitor apocynin. These data suggest that chronic accumulation of AOPPs may promote renal inflammation in diabetes probably through activation of renal NADPH oxidase.

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