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Lipid Peroxidation Products and Nitric Oxide in the Evaluation of Benign and Malignant Pleural Effusion  [PDF]
Tandon R.,J.K. Mishra,Manish Shankar,Hari D. Khanna
Journal of Stress Physiology & Biochemistry , 2012,
Abstract: Background: Pleural effusion is a common complication of various diseases. Free radicals are known to produce damage in many biological tissues. Free radicals exert their cytotoxic effect by causing lipid peroxidation which is believed to be responsible for the exudation of fluid into the pleural space.Aim: Evaluation of the association of benign and malignant pleural effusion with the free radical induced pleurisy by measurement of lipid peroxidation products and nitric oxide activity.Methods: Case control study was conducted on 50 cases of benign pleural effusion, 50 cases of malignant pleural effusion and 15 cases of healthy controls. Malondialdehyde (MDA) levels were measured by spectrophotometric method with TBA. Nitric Oxide activity was measured by spectrophotometric method using Griess reaction.Results: Our results showed significant increase of MDAs level in both groups of patients: benign and malignant in comparison with control group. Significant increase in the concentrations of nitrate/nitrite depicting total nitric oxide was observed in benign as well as malignant group in comparison to control healthy group.Conclusion: These results suggest that determination of biomarkers of oxidative stress products may be useful in the diagnosis and treatment of patients.
Supratim Ray
International Journal of Pharmaceutical Sciences and Research , 2012,
Abstract: The study was designed with an aim to evaluate the antiperoxidative potential of ascorbic acid on busulfan-induced lipid peroxidation. The study was performed in vitro using goat liver as lipid source. This evaluation was done by measuring the 4-hydroxy-2-nonenal (4-HNE) and nitric oxide (NO) content of liver tissue homogenates as markers of lipid peroxidation. The study reveals the lipid peroxidation induction capacity of busulfan and the antiperoxidative potential of ascorbic acid on busulfan-induced lipid peroxidation.
Nevin Atalay Güzel,Serkan Hazar,Deniz Erbas
Journal of Sports Science and Medicine , 2007,
Abstract: The purpose of this study was to determine the changes of oxidative response and exercise-induced muscle damage after two different resistance exercise protocols. Whether training with low or high intensity resistance programs cause alterations in the activities of lipid peroxidation, nitric oxide (NOx), and creatine kinase (CK) activity in human plasma was investigated. Twenty untrained males participated into this study. Ten of the subjects performed high intensity resistance (HR) exercise circuit and the rest of them performed low intensity resistance (LR) exercise circuit of 4 different exercises as a single bout. Venous blood samples were drawn pre-exercise, immediately after the exercise, and at the 6th, 24th, 48th and the72nd hours of post-exercise. Samples were analyzed for markers of muscle damage (CK), lipid peroxidation (MDA) and NOx. NOx production increased in HR group (p < 0.05). The MDA response to the two different resistance exercise protocol in this study caused a significant increase between pre and post-exercise values in both groups (p < 0.05). Also, there was a significant difference in the MDA level between the two groups in post-exercise values (p < 0.05) and higher values were observed in HR group. CK activities showed a significant increase in all post exercise values (p < 0.05) of both groups but there were no difference between HR and LR groups. These findings support that high intensity resistance exercise induces free radical production more than low intensity resistance exercise program
The in Vivo Antioxidant Effects of (−)-Epigallocatechin-3-Gallate Consumption in Healthy Postmenopausal Women Measured by Urinary Excretion of Secondary Lipid Peroxidation Products  [PDF]
Chelsey Fiecke, Mindy Kurzer, Chi Chen, A. Saari Csallany
Food and Nutrition Sciences (FNS) , 2019, DOI: 10.4236/fns.2019.101002
Abstract: The present study was carried out to determine whether the consumption of epigallocatechin (EGCG), the major bioactive green tea catechin, exerts a positive effect on lowering in vivo lipid peroxidation, a measure of oxidative stress, in healthy postmenopausal women. Urinary excretion of secondary lipid peroxidation products, a measure of in vivo lipid peroxidation, was determined in 40 participants randomly assigned to consume a green tea catechin extract (843.0 ± 44.0 mg EGCG/d) or placebo capsules for 12 months. Urine samples were analyzed for individual polar and nonpolar lipophilic aldehydes and related carbonyl compounds by high-performance liquid chromatography (HPLC) at the beginning and at the end of the 12-month intervention period. Results show that two nonpolar aldehydes, nonanal and decatrienal, were both 48% lower (p < 0.005) following consumption of EGCG. These results indicate that a modest degree of in vivo antioxidant activity exists with long-term EGCG consumption, which could slightly limit oxidative damage associated with lipid peroxidation and the onset and progression of chronic diseases.
Effect of Ginsenosides on Malondialdehyde, Nitric Oxide and Endothelin-1 Production in Vascular Endothelial Cells Suffering from Lipid Peroxidation Injury  [PDF]
Tan Jun,Zhu Liancai,Wang Bochu
International Journal of Pharmacology , 2007,
Abstract: Ginsenosides are the main effective substance in Panax ginseng and have bioactivity to improve cardiovascular function. In this study, effect of ginsenosides on malondialdehyde (MDA), Nitric Oxide (NO) and endothelin-1 (ET-1) production in human vascular endothelial cells strain VEC304 treated with diamide was studied. The treatment of VEC304 with 0.01 μL · L-1 diamide significantly increased MDA production (p<0.01), significantly decreased NO production (p<0.05) and slightly increased ET-1 production in cells, indicating that diamide induced lipid Peroxidation injury for VEC304. While after VEC304 injured by lipid peroxidation were treated with ginsenosides, MDA production and ET-1 production in cells were decreased significantly (p<0.01) by 29.81 and 38.18%, respectively and NO production in cells was increased significantly (p<0.01) by 6.04 times. The results implied that Panax ginseng and ginsenosides work effectively on cardiovascular diseases probably by anti-oxidation and increasing NO production and decreasing ET-1 production in VEC.
Efficacy of piperine, an alkaloidal constituent of pepper on nitric oxide, antioxidants and lipid peroxidation markers in L-NAME induced hypertensive rats
Kumar S, Saravana Kumar M, Raja B
International Journal of Research in Pharmaceutical Sciences , 2010,
Abstract: A pharmacological inhibition of nitric oxide synthase (NOS) in rats produces vasoconstriction which causes hypertension. We have investigated that whether piperine ameliorates Nω-Nitro-L-arginine methyl ester hydrochloride (L-NAME) - induced hypertension. Treatment of rats with L-NAME (40 mg/kg in drinking water for 4 weeks) caused a sustained decrease in the nitrite/nitrate concentrations (NOx) in plasma compared with control rats. Piperine restored the plasma NO metabolites concentration in L-NAME-treated hypertensive rats. Moreover, piperine significantly restored enzymatic (superoxide dismutase, catalase, glutathione peroxidase), non-enzymatic antioxidants (vitamin C, vitamin E and reduced glutathione) and decreased the levels of lipid peroxidation markers, compared to the L-NAME-treated group. Histopathological findings of piperine treated hypertensive rat heart confirmed the biochemical findings of this study. Taken together, these results suggest that L-NAME-induced hypertension is associated with decreased release of NO, an imbalance in antioxidant status and increased lipid peroxidation. Our results indicate that piperine attenuates hypertension on NO-deficient rats and that oxidative stress participates in the established phase of this type of hypertension.
A Diet with 3% of Energy from a Mixture of Omega-3 Fatty Acids Significantly Increases in Vivo Lipid Peroxidation in Postmenopausal Women  [PDF]
A. Saari Csallany, Cheryl E. Ainslie-Waldman, Lindsay R. Young, Chi Chen, Mindy S. Kurzer, Susan K. Raatz
Food and Nutrition Sciences (FNS) , 2016, DOI: 10.4236/fns.2016.712105
Abstract: Dietary omega-3 (n - 3) polyunsaturated fatty acids (PUFA) are recommended by public health organizations to reduce the risk of cardiovascular disease, and several epidemiological studies have suggested there is an inverse association between n - 3 intake and human cancers. However, n - 3 are susceptible to an increase in lipid peroxidation in the human body. As part of a crossover dietary intervention study of a diet (20% of energy from fat) with or without an additional 3% of energy from a mixture of n - 3 (with 5.36 g α-linolenic acid and 1.45 g eicosapentaenoic acid and docosahexaenoic acid per 2000 kcal per day), we measured total in vivo lipid peroxidation in healthy postmenopausal women (n = 15). Our results indicated that the diet with 3% of energy from n - 3 significantly increased the urinary concentrations of total polar lipophilic aldehydes and related compounds produced via lipid peroxidation (p < 0.05) as well as the α, β-unsaturated hydroxy aldehydes 4-hydroxy-2-trans - hexenal (p < 0.05) and 4-hydroxy-2-trans -decenal (p < 0.05) compared to the diet with less than 1% of energy from n - 3. This is also the first study to document the presence of 4-hydroxy-2-trans -decenal in the urine of individuals consuming n - 3. These results demonstrate that an increase in 3% of energy from dietary n – 3 increases in vivo lipid peroxidation.
In vitro inhibition of linoleic acid peroxidation by primary S-nitrosothiols
Simplicio, Fernanda I.;Seabra, Amedea B.;Souza, Gabriela F. P. de;Oliveira, Marcelo G. de;
Journal of the Brazilian Chemical Society , 2010, DOI: 10.1590/S0103-50532010001000013
Abstract: nitric oxide (?no) is an effective chain-breaking antioxidant in the inhibition of lipid peroxidation and circulates in vivo mainly as primary s-nitrosothiols (rsnos). in this work, the in vitro peroxidation of linoleic acid-sds comicelles (la-sds) catalyzed by soybean lipoxygenase (slo) and feii ions was monitored in the presence and absence of three primary rsnos: s-nitrosocysteine, s-nitroso-n-acetylcysteyne and s-nitrosoglutathione. kinetic measurements based on the formation of conjugated double bonds and fluorescent oxidized la-lysine adducts, showed that rsnos are more potent antioxidants than their corresponding free thiols (rshs) in equimolar conditions. these results are consistent with the blocking of la-sds peroxidation by rsnos through the inactivation of peroxyl/alkoxyl (loo?/lo?) radicals, leading to nitrogen-containing products of oxidized la, which release free ?no. these results indicate that endogenous rsnos may play a major role in the blocking of lipid peroxidation in vivo, through the primary inactivation of alkoxyl/peroxyl radicals and also of preformed lipid hydroperoxides.
The effects of taurine, melatonin and acetylcysteine on nitric oxide, lipid peroxidation and some antioxidants in cadmium induced liver injury  [cached]
Nurettin Aydo?du,Mehmet Kanter,Hakan Erba?,Kadir Kaymak
Erciyes Medical Journal , 2007,
Abstract: Purpose: Our aim was to investigate both the potential protective and therapeutic effects of taurine, melatonin and acetylcysteine in cadmium induced liver injury.Material and Methods: Ninety male Spraque Dawley rats were divided into nine groups. For the three months treatment period, drinking water was administered to Group 1 whereas 200 ppm CdCl2 to Group 2, 200 ppm CdCl2 and 1% taurine to Group 3, 200 ppm CdCl2 and 0.02% melatonin to Group 4 and 200 ppm CdCl2 and 0.5%acetylcysteine to Group 5. Groups 6, 7, 8 and 9 received 200 ppm CdCl2 in their drinking water for 3 months. After this period, for 7 days, 4% taurine to group 7, 0.08% melatonin to Group 8 and 2% acetylcysteine to group 9 were applied.Results: In liver tissues of cadmium received rats, the levels of glutathione (GSH) and the enzyme activities of superoxide dismutase (SOD) and glutathione peroxidase (GPx) were decreased. Thiobarbituric acid reactive substances (TBARS), nitric oxide (NO) and inducible nitric oxide synthase (iNOS) activities were increased. While, taurine, melatonin and acetylcysteine increased GSH levels, SOD and GPx activities, it decreased TBARS, NO and iNOS activities.Conclusion: Taurine, melatonin and acetylcysteine may have both protective and therapeutic effects in cadmium induced liver injuries.
Cisplatin-induced lipid peroxidation and its inhibition with Ascorbic acid  [cached]
Ray S,Roy K,Sengupta Chandana
Indian Journal of Pharmaceutical Sciences , 2006,
Abstract: The aim of the study was to investigate the antiperoxidative potential of ascorbic acid on cisplatin-induced lipid peroxidation, using some common laboratory markers. Goat liver was used as the lipid source. This in vitro evaluation was done by measuring the malondialdehyde, 4-hydroxy-2-nonenal, reduced glutathione, and nitric oxide content of tissue homogenates. The results suggest that cisplatin could induce lipid peroxidation to a significant extent, and it was also found that ascorbic acid has the ability to suppress the drug-induced toxicity.
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