scholarly journals Dietary Supplementation with Chitosan Oligosaccharides Alleviates Oxidative Stress in Rats Challenged with Hydrogen Peroxide

Animals ◽  
2019 ◽  
Vol 10 (1) ◽  
pp. 55 ◽  
Author(s):  
Ruixia Lan ◽  
Qingqing Chang ◽  
Lilong An ◽  
Zhihui Zhao

Oxidative stress is induced by excessive oxidative radicals, which directly react with biomolecules, and damage lipids, proteins and DNA, leading to cell or organ injury. Supplementation of antioxidants to animals can be an effective way to modulate the antioxidant system. Chitosan oligosaccharides (COS) are the degraded products of chitosan or chitin, which has strong antioxidant, anti-inflammatory, and immune-enhancing competency. Therefore, the current study was conducted to evaluate the hypothesis that dietary supplementation with COS alleviates the damage caused by oxidative stress in Sprague Dawley rats challenged with hydrogen peroxide (H2O2). The rats were randomly divided into three groups: CON, control group, in which rats were fed a basal diet with normal drinking water; AS, H2O2 group, in which rats were fed the basal diet and 0.1% H2O2 in the drinking water; ASC, AS + COS group, in which rats were fed the basal diet with 200 mg/kg COS, and with 0.1% H2O2 in the drinking water. In vitro, COS exhibited better radical scavenging capacity of 1, 1-diphenyl-2-picrylhydrazyl (DPPH), superoxide anion (O2−), H2O2, and ferric ion reducing antioxidant power (FRAP) than butylated hydroxy anisole (BHA). In vivo, dietary supplementation with COS alleviated the H2O2-induced oxidative damage, evidenced by comparatively increasing activity of SOD, CAT, GSH-Px, GSH, and T-AOC, and comparatively decreasing level of MDA in serum, liver, spleen, and kidney. COS also comparatively alleviated the H2O2-induced inflammation. In conclusion, COS supplementation reduced lipid peroxidation and restored antioxidant capacity in Sprague Dawley rats, which were challenged with H2O2.

2019 ◽  
Vol 8 ◽  
pp. 1250
Author(s):  
Esmat Radmanesh ◽  
Mahin Dianat ◽  
Narges Atefipour

Background: Many risk factors, including nutritional ones, contribute to cardiovascular diseases (CVDs). Increased fructose consumption, for example, can lead to an increase in CVD risk factors, i.e. an increase in blood lipids and the development of insulin resistance. Materials and Methods: In the present study, Sprague Dawley rats were divided into two groups:  control group (free access to tap drinking water for seven weeks), and a group that received fructose 10% in drinking water for seven weeks, (n ═8 per each group). In all groups, before starting the test period and seven weeks after it, electrocardiogram was recorded by Power lab system. Unpaired t-test and two-way ANOVA were used for data analysis. Also, oxidative stress parameters were measured. Results: In the group received high doses of fructose, a significant reduction (P <0.05) was observed in the PR interval (P<0.001) and a significant increase (P<0.05) in the QTc interval. However, there was no significant change in the RR interval and the voltage of the QRS complex. A significant decrease in catalase, superoxide dismutase and glutathione peroxidase (P<0.05) and a significant increase (P<0.05) in malondialdehyde and lactate dehydrogenase were observed in the group that received fructose in comparison with the control group at the end of the experiment. Conclusion: According to our results, the chance of arrhythmias in the rats receiving high doses of fructose was possibly due to the increased oxidative stress in the healthy rats. [GMJ.2019;8:e1250]


Author(s):  
Eman A. Al-Rekabi ◽  
Dheyaa K. Alomer ◽  
Rana Talib Al-Muswie ◽  
Khalid G. Al-Fartosi

The present study aimed to investigate the effect of turmeric and ginger on lipid profile of male rats exposed to oxidative stress induced by hydrogen peroxide H2O2 at a concentration of 1% given with consumed drinking water to male rats. Methods: 200 mg/kg from turmeric and ginger were used, and the animals were treatment for 30 days. Results: the results showed a significant increase in cholesterol, triglycerides, low density lipoprotein (LDL), very low density lipoprotein (VLDL), whereas it explained a significant decrease in high density lipoprotein (HDL) of male rats exposed to oxidative stress when compared with control group. the results showed a significant decrease in cholesterol, triglycerides, (LDL), (VLDL), whereas it explained a significant increase in (HDL) of rats treated with turmeric and ginger at dose 200 mg/kg when compared with male rats exposed to oxidative stress.


Hypertension ◽  
2000 ◽  
Vol 36 (suppl_1) ◽  
pp. 723-723
Author(s):  
Qing-Feng Tao ◽  
Diego Martinez vasquez ◽  
Ricardo Rocha ◽  
Gordon H Williams ◽  
Gail K Adler

P165 Aldosterone through its interaction with the mineralocorticoid receptor (MR) plays a critical role in the development of hypertension and cardiovascular injury (CVI). Normally, MR is protected by 11β-hydroxysteroid dehydrogenase (11β-HSD) which inactivates glucocorticoids preventing their binding to MR. We hypothesis that if activation of MR by either aldosterone or glucocorticoids induces hypertension and CVI, then the inhibition of 11β-HSD with glycyrrhizin (GA), a natural inhibitor of 11β-HSD, should induce damage similar to that observed with aldosterone. Sprague-Dawley rats were uninephrectomized, and treated for 4 weeks with 1% NaCl (in drinking water) for the control group, 1% NaCl + aldosterone infusion (0.75 μg/h), or 1% NaCl + GA (3.5 g/l in drinking water). After 4 weeks, aldosterone and GA caused significant increases in blood pressure compared to control rats ([mean ± SEM] 211± 9, 205 ± 12, 120 ± 9 mmHg, respectively, p<0.001). Both aldosterone- and GA-treated rats had a significant increase in proteinuria (152.2 ± 8.7 and 107.7 ± 19.5 mg/d, respectively) versus controls (51.2 ± 9.5 mg/d). There was a significant increase (p<0.001) in heart to body weight ratio in the rats treated with aldosterone or GA compared with control (3.92 ± 0.10, 3.98 ± 0.88, and 3.24 ± 0.92 mg/g, respectively). Hearts of GA and aldosterone treated rats showed similar histological changes consisting of biventricular myocardial necrosis and fibrinoid necrosis of small coronary arteries and arterioles. These data suggests that in rodents activation of MR by either aldosterone or corticosterone leads to severe hypertension, vascular injury, proteinuria and myocardial infarction. Thus, 11β-HSD plays an important role in protecting the organism from injury.


Animals ◽  
2020 ◽  
Vol 10 (11) ◽  
pp. 2045
Author(s):  
Hamada Elwan ◽  
Mostafa Abdelhakeam ◽  
Sally El-Shafei ◽  
Atef Abd El-Rahman ◽  
Zienhom Ismail ◽  
...  

Animals fed with a high amount of a wide range of antioxidants in their diet are significantly protected against oxidative stress. Powerful antioxidant substances such as vitamin E, vitamin C, and carotenoids are present naturally in red-hot pepper (RHP). This study hypothesized that using RHP may provide protection against oxidative stress and enhance animal physiological responses. Thus, this study aimed to investigate the effect of feeding New Zealand white rabbits with RHP-supplemented diets on their physiological and biochemical responses. New Zealand White rabbits (age = 6 weeks, n = 48) were split equally into three groups (n = 16 in each group). One group was fed a basal diet only (control group), with the other two groups fed a basal diet along with 1 and 2% RHP. Mass spectrometric analysis for the RHP methanolic extract showed some phenolic compounds, such as p-coumaric, sinapinic acids, vanillic, and luteolin, as well as catechin and its isomers. Hepatic antioxidant enzymes (SOD, GSH, GSH-Px, and CAT) were significantly elevated (p < 0.05) by feeding rabbits diets supplemented with 1 or 2% RHP. The addition of RHP significantly enhanced immune-responses; phagocytic activity, chemotaxis, TIg, IgG, IgM, and IgA increased when growing rabbits were fed RHP compared with the control group. In conclusion, dietary supplementation of 1 or 2% RHP may play a role as an enhancer of growth and immune response in growing rabbits.


2016 ◽  
Vol 40 (3-4) ◽  
pp. 621-632 ◽  
Author(s):  
Qing Zhao ◽  
Jianyong Yin ◽  
Zeyuan Lu ◽  
Yiwei Kong ◽  
Guangyuan Zhang ◽  
...  

Background: Sulodexide is a powerful antithrombin agent with reno-protective property. However, whether it has beneficial effects on Contrast-Induced Nephropathy (CIN) remained elusive. In the current study, we evaluated the therapeutic effects of Sulodexide on CIN and investigated the potential mechanisms. Methods: CIN model was induced by intravenous injection of indomethacin, followed by Ioversol and L-NAME. Sprague-Dawley rats were divided into 4 groups: control group, CIN group, CIN+vehicle group (CIN rats pretreated with vehicle) and CIN+ Sulodexide (CIN rats pretreated with Sulodexide). Sulodexide or an equivalent volume of vehicle was intravenously delivered 30 min before the induction of CIN. All the animals were sacrificed at 24h after CIN and tissues were harvested to evaluate renal injury, kidney oxidative stress and apoptosis levels. Plasma antithrombin III (ATIII) activities were also measured. Results: Compared to the untreated CIN group, improved renal function, reduced tubular injury, decreased levels of oxidative stress and apoptosis were observed in CIN rats receiving Sulodexide injection. In addition, we also found that ATIII activity was significantly higher in Sulodexide-administered group than that in vehicle-injected CIN rats. For in vitro studies, HK2 cells were exposed to Ioversol and the cyto-protective effects of Sulodexide were also determined. Sulodexide pretreatment protected HK2 cells against the cytotoxicity of Ioversol via inhibiting caspase-3 activity. Preincubation with Sulodexide could also attenuate H2O2-induced increases in ROS, apoptosis and caspase-3 levels. Conclusions: Taken together, Sulodexide could protect against CIN through activating ATIII, and inhibiting oxidative stress, inflammation and apoptosis.


2012 ◽  
Vol 36 (0A) ◽  
pp. 62-69
Author(s):  
Hazim J. Al – Daraji

This study was conducted to evaluate the effect of adding different levels of rocket salad seeds powder to the diet on seminal plasma traits of roosters subjected to oxidative stress induced by hydrogen peroxide. A total of 60 Hy – line laying breeder roosters 57 weeks old were used in this study. Roosters were randomly distributed into 5 treatments with 3 replicates each. Each replicate constituted of 4 roosters (12 roosters for each treatment). Experimental treatments were as following: T1: Males fed control diet and normal water, T2: Males fed diet supplemented with 3 gm rocket salad powder / kg of diet + 0.25 ml hydrogen peroxide (0.5%) / litter of water, T3: Males fed diet supplemented with 3 gm rocket salad powder / kg of diet + 0.5 ml hydrogen peroxide (0.5%) / litter of water, T4: Males fed diet supplemented with 3 gm rocket salad powder / kg of diet + 1 ml hydrogen peroxide (0.5%) / litter of water, and T5: Males fed control diet and drink tap water supplemented with 1 ml hydrogen peroxide (0.5%) / litter of water. Males were treated with hydrogen peroxide (6%) and rocket salad for 12 weeks starting from 59 week of male ages. Results revealed that treated the roosters with hydrogen peroxide without adding rocket salad powder to the diet of these roosters (T5) resulted in highly significant (p< 0.01) decrease as regards concentrations of phospholipids, cholesterol, glutathione, the activity of superoxide desmutase and catalase, and total antioxidant activity in seminal plasma and highly significant (p< 0.01) increase concerning concentrations of tyrosine and malondialdehyde as compared with control group (T1) and rocket salad powder treatments (T2, T3, T4) after 12 weeks of experiment. However, supplementing diet of roosters with rocket salad powder (T2, T3, T4) resulted in highly significant (p< 0.01) increase with relation to concentrations of phospholipids, cholesterol, glutathione, the activity of superoxide desmutase and catalase, and total antioxidant activity in seminal plasma and highly significant (p< 0.01) decrease respecting concentrations of tyrosine and malondialdehyde as compared with (T5) In conclusion adding rocket salad powder to the diet of roosters had important role in limiting the negative effect of oxidative stress induced by hydrogen peroxide on seminal plasma quality of roosters. Therefore, dietary supplementation with rocket salad powder could be used as one of important tools for improving semen quality of roosters.


Hypertension ◽  
2000 ◽  
Vol 36 (suppl_1) ◽  
pp. 688-688
Author(s):  
Nosratola D Vaziri ◽  
Xiu Q Wang ◽  
Fariba Oveisi ◽  
Behdad Rad

59 Several recent studies have shown that certain forms of genetic and acquired hypertension (HTN) are associated with oxidative stress and respond favorably to antioxidant therapy. We hypothesize that oxidative stress, per se, may cause HTN via (among other mechanisms) enhanced oxidation and inactivation of nitric oxide (NO). To test this hypothesis, Sprague-Dawley rats were subjected to oxidative stress by glutathione (GSH) depletion using GSH synthase inhibitor, buthionine sulfoximine (BSO, 30 mmol/L in drinking water), for two weeks. The control group was given drug-free drinking water. In parallel experiments, subgroups of animals were provided vitamin E-fortified chow and vitamin C-supplemented drinking water. Arterial blood pressure, urinary excretion of NO metabolites (NO 2 +NO 3 , NOx), and liver tissue GSH were measured. In addition, plasma, kidney, heart, liver and aorta were tested by Western blot analysis for nitrotyrosine, which is the footprint of NO inactivation by reactive oxygen species (ROS). The BSO-treated group showed a three-fold fall in hepatic tissue GSH content (0.99±0.3 vs 3.4±0.3 μmol/g wet tissue, P<0.001), a marked elevation in blood pressure (203±3 vs 120±2 mmHg, P<0.001) and a significant reduction in urinary excretion of NO metabolites, nitrate + nitrite (316±23 vs 595±29 μmol/g creatinine, P<0.01), suggesting depressed NO availability. This was associated with a significant accumulation in all tested tissues of nitrotyrosine (P<0.05 for all comparisons). Administration of vitamins E+C ameliorated HTN (156±4 mmHg, P<0.01), improved urinary NOx excretion (392±28 μmol/g creatinine, P<0.05) and mitigated nitrotyrosine accumulation (despite persistent GSH depletion) in the BSO-treated animals. However, vitamins E+C treatment had no effect on any of the above parameters in the control group (data not shown). In conclusion, GSH depletion resulted in perturbation of the NO system and severe HTN in normal animals. The effects of BSO were mitigated by concomitant antioxidant therapy despite GSH depletion, supporting the notion that oxidative stress was involved in the pathogenesis of HTN in this model.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Hyoeun Yoo ◽  
Hyun-Sook Kim

AbstractAging, a critical risk factor of several diseases, including neurodegenerative disorders, affects an ever-growing number of people. Cacao supplementation has been suggested to improve age-related neuronal deficits. Therefore, this study investigated the protective effects of raw cacao powder on oxidative stress-induced aging. Male Sprague–Dawley rats were divided into 4 groups: Control (C), d-galactose-induced aging (G), d-galactose injection with 10% (LC), and 16% (HC) cacao powder mixed diet. d-galactose (300 mg/3 mL/kg) was intraperitoneally injected into all but the control group for 12 weeks. Cacao supplemented diets were provided for 8 weeks. The levels of serum Malondialdehyde (MDA), Advanced Glycation End-products (AGEs), brain and liver MDA, the indicators of the d-galactose induced oxidative stress were significantly decreased in LC and HC but increased in G. The Acetylcholinesterase (AChE) activity of brain showed that the cholinergic impairment was significantly lower in LC, and HC than G. Furthermore, the expression levels of catalase (CAT), phospho-Akt/Akt, and procaspase-3 were significantly increased in LC and HC. In conclusion, cacao consumption attenuated the effects of oxidative stress, cholinergic impairment and apoptosis, indicating its potential in future clinical studies.


Author(s):  
Murtala Bello ABUBAKAR ◽  
Boon Suen ANG

Background: Exposure to petrol is common among individuals working in oil refineries, oil fields, filling stations, automobile mechanical workshops. Exposure to petrol is associated with a number of health hazards including hepatotoxicity and oxidative stress. Honey is rich in many antioxidants such as catalase, flavonoids, thiamine, riboflavin, pyridoxine, pantothenic acid, ascorbic acid and nicotinic acid and was recently reported to reduce petrol-induced hepatotoxicity and nephrotoxicity. Materials and Methods: A total of 32 male Sprague-Dawley rats were randomly divided into four groups: control group (exposed to ambient air daily), petrol exposed group


Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Masahito Kajiya ◽  
Yousuke Inai ◽  
Taro Morimoto ◽  
Tatsuo Iwasaki ◽  
Kousuke Endo ◽  
...  

Background: Hydrogen peroxide (H 2 O 2 ) is a well recognized candidate for EDHF. The aim of this study was to examine H 2 O 2 -EDHF function in coronary arterial microvessels under conditions of increased oxidative stress in RV of pulmonary hypertension (PH). Methods: Monocrotaline (60 mg/kg SC) was administrated in 5 week-age male Sprague-Dawley rats to induce PH (PH; n=52). Saline was injected in control rats (n=47). After 3 weeks, RV coronary arterioles (CA; 30 –100 μm) and small arteries (CSA; 100 –200 μm) were visualized in vivo using our intravital videomicroscopy. After cyclooxigenase blockade, Acetylcholine (ACh; 2 μg/kg/min IV) induced vasodilation was evaluated under three conditions; ACh alone, N ω nitro-L-arginine methyl ester (L-NAME), L-NAME+catalase. Differences of percentage vasodilation between ACh alone and L-NAME, and between L-NAME and L-NAME+catalase were used as relative indices for the contributions of NO and H 2 O 2 -EDHF, respectively. Malondialdehyde (MDA) in plasma was measured with colormetric assay. Superoxide production in RV was determined by lucigenin-derived chemiluminescence. Results: RV systolic pressure was significantly increased in PH (75±13 vs. 31±3 mmHg; p<0.05). In PH, Ach-induced vasodilation was significantly reduced in both CA and CSA compared with control (CA; 5.2±1.5% vs. 10.8±3.5%, CSA; 3.8±1.0% vs. 6.0±1.9%, both p<0.05). Inhibition of vasodilation by L-NAME in PH was markedly decreased for both CA (from 4.0% to 1.0%) and CSA (from 3.6% to 1.0%) (both p<0.05). Suppression of vasodilation by the addition of catalase in PH was decreased for CA (from 5.2% to 3.1%, p<0.05), but maintained or even increasing tendency for CSA (from 1.7% to 2.0%, NS). Notably, the relative contribution of H 2 O 2 -EDHF in PH was greatly increased for both CA (from 48% to 60%) and CSA (from 28% to 53%) (both p<0.05). Plasma MDA and RV superoxide in PH were markedly higher than those in control (MDA; 1.63±0.53 vs. 0.93±0.11 μm, superoxide; 290±52 vs 158±25 cpm/mg, both p<0.05). Collectively, increased oxidative stress may augment H 2 O 2 produciton and contribute to the robust EDHF function. Conclusion: Under conditions of increased oxidative stress in PH, H 2 O 2 -EDHF plays a crucial role against NO dysfunction in RV coronary microcirculation.


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