scholarly journals Comparison of coenzyme Q10 or fish oil for prevention of intermittent hypoxia-induced oxidative injury in neonatal rat lungs

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Christina D’Agrosa ◽  
Charles L. Cai ◽  
Faisal Siddiqui ◽  
Karen Deslouches ◽  
Stephen Wadowski ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Lung Injury ◽  
Fish Oil ◽  
Coenzyme Q10 ◽  
Intermittent Hypoxia ◽  
Oxidative Injury ◽  
Adverse Outcomes ◽  
Neonatal Rat ◽  
Antioxidant Systems

Abstract Background Neonatal intermittent hypoxia (IH) results in oxidative distress in preterm infants with immature antioxidant systems, contributing to lung injury. Coenzyme Q10 (CoQ10) and fish oil protect against oxidative injury. We tested the hypothesis that CoQ10 is more effective than fish oil for prevention of IH-induced lung injury in neonatal rats. Methods Newborn rats were exposed to two clinically relevant IH paradigms at birth (P0): (1) 50% O2 with brief hypoxia (12% O2); or (2) room air (RA) with brief hypoxia (12% O2), until P14 during which they were supplemented with daily oral CoQ10, fish oil, or olive oil from P0 to P14. Pups were studied at P14 or placed in RA until P21 with no further treatment. Lungs were assessed for histopathology and morphometry; biomarkers of oxidative stress and lipid peroxidation; and antioxidants. Results Of the two neonatal IH paradigms 21%/12% O2 IH resulted in the most severe outcomes, evidenced by histopathology and morphometry. CoQ10 was effective for preserving lung architecture and reduction of IH-induced oxidative stress biomarkers. In contrast, fish oil resulted in significant adverse outcomes including oversimplified alveoli, hemorrhage, reduced secondary crest formation and thickened septae. This was associated with elevated oxidants and antioxidants activities. Conclusions Data suggest that higher FiO2 may be needed between IH episodes to curtail the damaging effects of IH, and to provide the lungs with necessary respite. The negative outcomes with fish oil supplementation suggest oxidative stress-induced lipid peroxidation.

Coenzyme Q10 in combination with triple therapy regimens ameliorates oxidative stress and lipid peroxidation in chronic gastritis associated withH. pyloriinfection

2015 ◽  
Vol 55 (8) ◽  
pp. 842-847 ◽  
Author(s):  
Asghar Rahmani ◽  
Ghobad Abangah ◽  
Atefeh Moradkhani ◽  
Mohammad Reza Hafezi Ahmadi ◽  
Khairollah Asadollahi
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Triple Therapy ◽  
Chronic Gastritis ◽  
Coenzyme Q10

Expression Analysis of 4-Hydroxynonenal Modified Proteins in Schizophrenia Brain; Relevance to Involvement in Redox Dysregulation

2021 ◽  
Vol 18 ◽  
Author(s):  
Sobia Manzoor ◽  
Ayesha Khan ◽  
Beena Hasan ◽  
Shamim Mushtaq ◽  
Nikhat Ahmed
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Thiobarbituric Acid ◽  
Brain Regions ◽  
Protein Adducts ◽  
Antioxidant Systems ◽  
Control Group ◽  
Tbars Level ◽  
Elevated Expression ◽  
Modified Proteins

Background: Oxidative damage contributes to the pathophysiology of schizophrenia (SZ). Redox imbalance may lead to increased lipid peroxidation, which produces toxic aldehydes like 4-hydroxynonenal (4-HNE) ultimately leading to oxidative stress. Conversely, implications of oxidative stress points towards an alteration in HNE-protein adducts and activities of enzymatic and antioxidant systems in schizophrenia. Objectives: Present study focuses on identification of HNE-protein adducts and its related molecular consequences in schizophrenia pathology due to oxidative stress, particularly lipid peroxidation. Material and Methods: Oxyblotting was performed on seven autopsied brain samples each from cortex and hippocampus region of schizophrenia patients and their respective normal healthy controls. Additionally, thiobarbituric acid substances (TBARS), reduced glutathione (GSH) levels and catalase (CAT) activities associated with oxidative stress, were also estimated. Results: Obtained results indicates substantially higher levels of oxidative stress in schizophrenia patients than healthy control group represented by elevated expression of HNE-protein adducts. Interestingly, hippocampus region of schizophrenia brain shows increased HNE protein adducts compared to cortex. An increase in catalase activity (4.8876 ± 1.7123) whereas decrease in antioxidant GSH levels (0.213 ± 0.015µmol/ml) have been observed in SZ brain. Elevated TBARS level (0.3801 ± 0.0532ug/ml) were obtained in brain regions SZ patients compared with their controls that reflects an increased lipid peroxidation (LPO). Conclusion: Conclusion: We propose the role of HNE modified proteins possibly associated with the pathology of schizophrenia. Our data revealed increase lipid peroxidation as a consequence of increased TBARS production. Furthermore, altered cellular antioxidants pathways related to GSH and CAT also highlight the involvement of oxidative stress in schizophrenia pathology.

scholarly journals Oxidative stress in ageing

2017 ◽  
Vol 5 (11) ◽  
pp. 4826 ◽  
Author(s):  
Fasna K. A. ◽  
Geetha N. ◽  
Jean Maliekkal
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Free Radicals ◽  
Free Radical ◽  
Age Groups ◽  
The Body ◽  
Antioxidant Systems ◽  
Lipid Peroxidation Product ◽  
Free Radical Theory ◽  
Radical Theory

Background: Ageing is characterized by a gradual decline in body functions and decreased ability to maintain homeostasis. The free radical theory of ageing proposed by Harman D states that ageing is a result of cumulative damage incurred by free radical reactions. Free radicals are highly reactive molecular species with unpaired electrons; generated in the body by several physiological processes. Prime target to free radical attack are the polyunsaturated fatty acids of cell membranes causing lipid peroxidation. The free radicals are neutralized by the exogenous and endogenous antioxidant systems. Oxidative stress occurs when large number of free radicals are produced or the antioxidant activity is impaired. The present study is focused to find out the role of oxidative stress in ageing.Methods: A cross sectional observational study was undertaken to assess the oxidative stress in ageing; by determining the levels of lipid peroxidation product- malondialdehyde (MDA), the antioxidants- superoxide dismutase (SOD) and ceruloplasmin in various age groups. 150 healthy subjects were selected randomly and categorised into three different age groups of 20-30 years, 40-59 years and 60-90 years; with 50 subjects in each group. Results were expressed as mean ± standard deviation.Results: a significant elevation in serum MDA level and a decline in SOD were observed in 40-59 years and 60-90 years age groups. However, an elevated ceruloplasmin level was found in the above age groups.Conclusions: Aforementioned observations are suggestive of an association between oxidative stress and the progression of ageing process.

Lipid peroxidation-derived aldehydes and oxidative stress in the failing heart: role of aldose reductase

2002 ◽  
Vol 283 (6) ◽  
pp. H2612-H2619 ◽  
Author(s):  
Sanjay Srivastava ◽  
Bysani Chandrasekar ◽  
Aruni Bhatnagar ◽  
Sumanth D. Prabhu
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Aldose Reductase ◽  
Transcriptional Activation ◽  
Pressure Rise ◽  
Oxidative Injury ◽  
Left Ventricular ◽  
Protein Levels ◽  
Failing Heart ◽  
Before And After

Lipid peroxidation-derived aldehydes (LP-DA) can propagate oxidative injury and are detoxified by the aldose reductase (AR) enzyme pathway in myocardium. Whether there are alterations in the AR axis in heart failure (HF) is unknown. Sixteen instrumented dogs were studied before and after either 24 h or 4 wk of rapid left ventricular (LV) pacing (early and late HF, respectively). Six unpaced dogs served as controls. In early HF, there was subtle depression of LV performance (maximum rate of LV pressure rise, P < 0.05 vs. baseline) but no chamber enlargement, whereas in late HF there was significant ( P < 0.05) contractile depression and LV dilatation. Oxidative stress was increased at both time points, indexed by tissue malondialdehyde, total glutathione, and free C6–C9 LP-DA ( P < 0.025 vs. control). AR protein levels and activity decreased progressively during HF ( P < 0.025 early/late HF vs. control); however, AR mRNA expression decreased only in late HF ( P < 0.005 vs. early HF and control). DNA binding of tonicity-responsive enhancer binding protein (TonEBP, a transcriptional regulator of AR) paralleled AR mRNA, declining >50% in late HF ( P < 0.025 vs. control). We conclude that AR levels and attendant myocardial capacity to detoxify LP-DA decline during the development of HF. In early HF, decreased AR occurs due to a translational or posttranslational mechanism, whereas in late HF reduced TonEBP transcriptional activation and AR downregulation contribute significantly. Reduced AR-mediated LP-DA metabolism contributes importantly to LP-DA accumulation in the failing heart and thus may augment chronic oxidative injury.

scholarly journals The Mechanisms of Glutamine- and Fish Oil-Supplemented Resuscitation Fluids on Alleviating Oxidative Stress of the Lung and Liver in Rats with Trauma-Hemorrhagic Shock

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 429-429
Author(s):  
Bing-Xiang Liu ◽  
Hui-Chen Lo ◽  
Chien-Hsing Lee
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Fish Oil ◽  
Hemorrhagic Shock ◽  
Catalase Activity ◽  
Caspase 3 ◽  
Neutrophil Infiltration ◽  
Midline Laparotomy ◽  
Shed Blood ◽  
Main Factor

Abstract Objectives Oxidative stress has been demonstrated to be the cause of cellular and organ damage in patients with trauma hemorrhagic shock and reperfusion (THR). Our previous study showed that resuscitation fluids supplemented with glutamine and fish oil, the antioxidants with anti-inflammatory activities, may alleviate systemic inflammatory response and oxidative stress in the THR rats. The aim of this study was to further investigate the mechanisms of these supplements on alleviating THR-induced damage in the lung and liver, i.e., the 2 vulnerable organs in THR. Methods Male Wistar rats were suffered with 5 cm midline laparotomy and 2 catheterizations in the left carotid artery and right jugular vein individually for blood drawn to a mean arterial pressure 30 to 35 mmHg for 60 minutes and for resuscitation of shed blood and lactate Ringer's solution with or without L-alanyl-L-glutamine (13.5 mmole/kg/day) and/or fish oil (0.5 g/kg/day) within 10 minutes. The different resuscitation fluids were continuous infused (∼1.4 ml/h) for 42 hr. Normal healthy rats and intubation sham-operated rats were included as controls. Results In the lung, the THR-increased lipid peroxidation and toll-like receptor 4 (TLR4) were significantly decreased by glutamine with or without fish oil (one-way ANOVA, P &lt; 0.05). Fish oil was the main factor to decrease myeloperoxidase and activated caspase 3 in the lung of the THR rats (two-way ANOVA, P &lt; 0.05). In the liver, the THR-increased lipid peroxidation and TLR4 and the THR-decreased catalase activity were improved by glutamine and/or fish oil. In addition, fish oil was the main factor to decrease inducible and endothelial nitric oxide synthase (NOS) and to increase IkB and phosphorylated NF-kB and glutamine was the main factor to decrease activated caspase 3 in the liver of the THR rats. Conclusions These results suggest that fish oil may alleviate neutrophil infiltration and NOS activation and fish oil and glutamine may elevate catalase activity and alleviate apoptosis to attenuate the THR-induced damage in the lung and liver. Funding Sources MOST 102-2320-B-030-005-MY3.

scholarly journals Effect of corticosteroid (triamcinolone acetonide) and chlorhexidin on chemotherapy- induced oxidative stress in buccal mucosa of rats

2020 ◽  
pp. 014556131989440
Author(s):  
Sami Gümüş ◽  
Murat Yarıktaş ◽  
Mustafa Nazıroğlu ◽  
Abdülhadi Cihangir Uğuz ◽  
Giray Aynali ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Triamcinolone Acetonide ◽  
Buccal Mucosa ◽  
Inflammatory Cell ◽  
Chemotherapeutic Agent ◽  
Oxidative Injury ◽  
Cheek Pouch ◽  
Control Group ◽  
Ulcerative Lesions

Oral mucositis (OM) refers to erythematous and ulcerative lesions of the oral mucosa. This pathology can occur by various causes. Cancer therapy is one of the well-known causes of OM such as chemotherapy and/or with radiation therapy. It has been widely mentioned that oxidative stress parameters such as lipid peroxidation (LP) levels increase during cancer process. Glutathione (GSH) is one of the major intracellular enzymes to detoxify oxidant molecules. The aim of this study was to investigate and compare the effects of Triamcinolone Acetonide (TA), a synthetic steroid chlorhexidine (CHX), a chemical antiseptic, on 5- fluorouracil (5-FU), a chemotherapeutic agent and soft abrasion induced OM in buccal mucosa of rats. OM was induced in rats through a combination of 5-FU treatment and mild abrasion of the cheek pouch with a wire brush. Buccal mucosa lipid peroxidation (LP) levels were higher (p< 0.05) in 5-FU group than in control although LP levels were lower (p<0.05) in TA group than in control group. The reduced glutathione levels were lower (p<0.05) in 5-FU group than in the control group although its level was higher (p<0.05) in TA and CHX groups than in the 5-FU group. Glutathione peroxidase activity was also higher (p<0.05) in TA group than the 5- FU group. In histopathological analyses, treatment with TA reduced 5-FU induced inflammatory cell infiltration and ulceration (p<0.001) but not with CHX. In conclusion, we observed that TA and CHX treatment modulated chemotherapy induced oxidative injury in the rat OM. However, only TA histopathologically ameliorated the 5-FU induced OM of rats. These findings suggest that TA is a useful agent for management of experimental oxidative injury and OM caused by the chemotherapy.

Oxidative stress and antioxidative defense with an emphasis on plants antioxidants

1999 ◽  
Vol 7 (1) ◽  
pp. 31-51 ◽  
Author(s):  
Klara D Vichnevetskaia ◽  
D N Roy
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Free Radicals ◽  
Higher Plants ◽  
Cell Damage ◽  
Active Oxygen Species ◽  
Antioxidant Systems ◽  
Low Molecular Weight ◽  
Synthetic Antioxidants ◽  
Synthetic Antioxidant

Increased levels of active oxygen species or free radicals can create an oxidative stress. Concentration of free radicals in living cells increases as a result of exposure to environmental stresses that lead to aging, carcinogenesis, and immunodeficiencies in animals, and membrane leakage, senescence, chlorophyll destruction, and decreased photosynthesis in plants. The antioxidative system of higher plants consists of enzymes, low molecular weight compounds (among them peptides, vitamins, flavonoids, phenolic acids, alkaloids, etc.), and integrated detoxification chains. Enzymatic defense in plants include enzymes capable of removing, neutralizing, or scavenging oxy-intermediates. Catalases and superoxide dismutases are the most efficient antioxidant enzymes. Free radicals cause cell damage by a lipid peroxidation mechanism, which results in a blockade of natural antioxidant systems. Application of synthetic antioxidants can assist in coping with oxidative stress. There are very few publications on effects of synthetic antioxidants on plant growth and physiology. One of the examples of such synthetic antioxidant is 2-methyl-4-dimethylaminomethyl-5-hydroxybenzimidazole (Ambiol), which substantially promoted growth of agricultural and forestry plant species. Ambiol also demonstrated antitranspirant properties, increasing drought tolerance of conifers and agricultural species. The response of plants to Ambiol is under high genetic control. The identification of genes responsible for the reaction of plants to Ambiol may lead to attempts in genetic engineering of organisms with increased tolerance to oxidative stress. It seems impossible to find a universal scavenger trapping all free radicals active in the organism. However, analysis of the structure–activity relationships in antioxidants can contribute to the search for effective antioxidants.Key words: oxidative stress, lipid peroxidation, free radicals, natural and synthetic antioxidants, Ambiol.

scholarly journals Antioxidant and Anti-Inflammatory Activities of Caralluma Acutangula (Decne.) N.E.Br Extracts, a Medicinal Plant from Burkina Faso

2019 ◽  
Vol 9 (6) ◽  
pp. 155-161
Author(s):  
Pare Dramane ◽  
N’do Jotham Yhi-pênê ◽  
Hilou Adama
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Lipid Peroxidation ◽  
Secondary Metabolites ◽  
Acute Toxicity ◽  
Xanthine Oxidase ◽  
Antioxidant Systems ◽  
Nmri Mouse ◽  
Good Activity ◽  
Anti Inflammatory

Plants have always played an important role in health care in Africa. The stress, a situation of imbalance between oxidizing and antioxidant systems in favor of the prooxidants is responsible for the installation of several pathologies such as cancers, cardiovascular diseases, diabetes ... The objective of this study was to highlight the presence Secondary metabolites in C. acutangula extract and determine its antioxidant and anti-inflammatory potential. For the determination of the acute toxicity of the extract, a dose of 2000 mg / kg was administered to the NMRI Mouse. The methods of screening were used to detect secondary metabolites like tannins, steroids and terpen, flavonoids, coumarins. The antioxidant capacity was evaluated in vitro by determining the ability of the extract to inhibit lipid peroxidation, hydrogen peroxide, degradation of deoxyribose. The anti-inflammatory potential was evaluated on lipoxygenase and xanthine oxidase. Acute toxicity evaluated in NMRI mice showed that the ethanolic extract of C. acutangula show no toxicity. Tannins, steroids and terpen, flavonoids, coumarins have been detected in the extracts. C. acutangula showed good activity with an inhibition of 50.71 ± 2.51% at 100 μg / ml on lipid peroxidation, of 66.105 ± 1.26% on deoxyribose degradation and 8.625 ± 1.09% on hydrogen peroxide. It showed good activity on xanthine oxidase with an 81.5 ± 5.5% inhibition. For the effect on lipoxygenase it gave an inhibition of the enzyme at 43.11 ± 3.4%. This potential could be used in the fight against inflammatory diseases and that due to oxidative stress. Keywords: antioxidant, anti-inflammatory, oxidative stress, lipid peroxidation

scholarly journals Narrative Review of n-3 Polyunsaturated Fatty Acid Supplementation upon Immune Functions, Resolution Molecules and Lipid Peroxidation

Nutrients ◽  
2021 ◽  
Vol 13 (2) ◽  
pp. 662
Author(s):  
Gary P. Zaloga
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Fatty Acids ◽  
Fish Oil ◽  
Inflammatory Responses ◽  
Biological Effects ◽  
Scientific Evidence ◽  
Immune Functions ◽  
Pufa Supplementation ◽  
Fish Oil Supplementation

Fish oil supplementation is commonplace in human nutrition and is being used in both enteral and parenteral formulations during the treatment of patients with a large variety of diseases and immune status. The biological effects of fish oil are believed to result from their content of n-3 polyunsaturated fatty acids (PUFA), particularly docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA). These fatty acids are known to have numerous effects upon immune functions and are described as immunomodulatory. However, immunomodulatory is a nondescript term that encompasses immunostimulation and immunosuppression. The primary goal of this review is to better describe the immune effects of n-3 PUFA as they relate to immunostimulatory vs. immunosuppressive effects. One mechanism proposed for the immune effects of n-3 PUFA relates to the production of specialized pro-resolving mediators (SPMs). A second goal of this review is to evaluate the effects of n-3 PUFA supplementation upon production of SPMs. Although n-3 PUFA are stated to possess anti-oxidative properties, these molecules are highly oxidizable due to multiple double bonds and may increase oxidative stress. Thus, the third goal of this review is to evaluate the effects of n-3 PUFA upon lipid oxidation. We conclude, based upon current scientific evidence, that n-3 PUFA suppress inflammatory responses and most cellular immune responses such as chemotaxis, transmigration, antigen presentation, and lymphocyte functions and should be considered immunosuppressive. n-3 PUFA induced production of resolution molecules is inconsistent with many resolution molecules failing to respond to n-3 PUFA supplementation. n-3 PUFA supplementation is associated with increased lipid peroxidation in most studies. Vitamin E co-administration is unreliable for prevention of the lipid peroxidation. These effects should be considered when administering n-3 PUFA to patients that may be immunosuppressed or under high oxidative stress due to illness or other treatments.

scholarly journals Effect of iron deficiency anemia on lipid peroxidation and antioxidant systems

2012 ◽  
Vol 7 (4) ◽  
pp. 34-43 ◽  
Author(s):  
NL Madhikarmi ◽  
KRS Murthy
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Iron Deficiency ◽  
Iron Deficiency Anemia ◽  
Binding Capacity ◽  
Lipid Hydroperoxide ◽  
Nutritional Deficiencies ◽  
Deficiency Anemia ◽  
Antioxidant Systems ◽  
Enzymatic Antioxidants

Iron deficiency is one of the most widespread nutritional deficiencies in the world. Globally more than two billion people are suffering from iron deficiency anemia. The present study was designed to investigate the influence of a large number of factors known to be associated with oxidative stress. The case-control study determines the lipid peroxidation and antioxidants status in forty Iron deficiency anemia and forty healthy volunteers with their informed consent. All the parameters were assayed by spectrophotometric methods. Blood hemoglobin and plasma iron were decreased whereas total iron binding capacity was increased significantly in Iron deficiency anemia. The lipid peroxidation parameters like malondialdehyde, lipid hydroperoxide were significantly increased in Iron deficiency anemia. Both enzymatic; glutathione peroxidase, superoxide dismutase and catalase and non-enzymatic antioxidants; vitamin C, E and reduced glutathione were significantly decreased in Iron deficiency anemia case as compared to their healthy counterparts. Our findings suggest, increased lipid peroxidation products and reduced antioxidants system boost the oxidative stress state, hence deteriorating the condition of Iron deficiency anemia patients. Journal of College of Medical Sciences-Nepal,2011,Vol-7,No-4, 34-43 DOI: http://dx.doi.org/10.3126/jcmsn.v7i4.6739

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