scholarly journals Inhibitory Response ofRaphanus sativuson Lipid Peroxidation in Albino Rats

2008 ◽  
Vol 5 (1) ◽  
pp. 55-59 ◽  
Author(s):  
P. Chaturvedi
Keyword(s):  
Lipid Peroxidation ◽  
Methanol Extract ◽  
Reduced Glutathione ◽  
Cumene Hydroperoxide ◽  
Thiobarbituric Acid ◽  
Control Group ◽  
Thiobarbituric Acid Reactive Substance ◽  
Experimental Control ◽  
Reactive Substance

In the present study, inhibitory effect of the methanol extract ofRaphanus sativusroot on lipid peroxidation has been carried out in normal rats. Graded doses of methanol extract of root of the plant (40, 80 and 120 mg kg−1body weight) were administered orally for 15 days to experimental treated rats. Distilled water was administered to experimental control rats. At the end of experiment, rats were killed by decapitation after ether anesthesia. Blood and liver were collected to measure thiobarbituric acid reactive substance, reduced glutathione and activity of catalase. Results indicated that the extract ofR. sativusroot reduced the levels of thiobarbituric acid reactive substance significantly in all experimental treated groups (P < 0.05) as compared to the experimental control group. It also increased the levels of reduced glutathione and increased the activity of catalase.In vitroexperiments with the liver of experimental control and experimental treated rats were also carried out against cumene hydroperoxide induced lipid peroxidation. The extract inhibitedin vitrocumene hydroperoxide induced lipid peroxidation.R. sativusinhibits lipid peroxidationin vivoandin vitro. It provides protection by strengthening the antioxidants like glutathione and catalase. Inclusion of this plant in every day diet would be beneficial.

Resistance of erythrocytes from Brown trout (Salmo trutta m. trutta L.) affected by ulcerative dermal necrosis syndrome

2011 ◽  
Vol 14 (3) ◽  
pp. 443-448 ◽  
Author(s):  
N. Kurhalyuk ◽  
H. Tkachenko ◽  
K. Pałczyńska
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Brown Trout ◽  
Salmo Trutta ◽  
Thiobarbituric Acid ◽  
Control Group ◽  
Thiobarbituric Acid Reactive Substance ◽  
Tbars Level ◽  
Reactive Substance ◽  
Brown Trout Salmo Trutta

Resistance of erythrocytes from Brown trout (Salmo trutta m. trutta L.) affected by ulcerative dermal necrosis syndrome In the present work we evaluated the effect of ulcerative dermal necrosis (UDN) syndrome on resistance of erythrocytes to haemolytic agents and lipid peroxidation level in the blood from brown trout (Salmo trutta m. trutta L.). Results showed that lipid peroxidation increased in erythrocytes, as evidenced by high thiobarbituric acid reactive substance (TBARS) levels. Compared to control group, the resistance of erythrocytes to haemolytic agents was significantly lower in UDN-positive fish. Besides, UDN increased the percent of hemolysated erythrocytes subjected to the hydrochloric acid, urea and hydrogen peroxide. Results showed that UDN led to an oxidative stress in erythrocytes able to induce enhanced lipid peroxidation level, as suggested by TBARS level and decrease of erythrocytes resistance to haemolytic agents.

Bitter Melon Protects Against Lipid Peroxidation Caused by Immobilization Stress in Albino Rats

2009 ◽  
Vol 79 (1) ◽  
pp. 48-56 ◽  
Author(s):  
Chaturvedi
Keyword(s):  
Lipid Peroxidation ◽  
Immobilization Stress ◽  
Reduced Glutathione ◽  
Cumene Hydroperoxide ◽  
Liver Homogenate ◽  
Thiobarbituric Acid ◽  
Albino Rats ◽  
Bitter Melon ◽  
Protective Effects

In the present study, protective effects of bitter melon (Momordica charantia) extract on lipid peroxidation induced by immobilization stress in rats have been assessed. Graded doses of extract (50, 100, and 150 mg/kg body weight) were administered orally to rats subjected to immobilization stress for two hours for seven consecutive days. Stress was applied by keeping the rats in a cage where no movement was possible. After seven days, rats were killed by decapitation after ether anesthesia. Blood and liver were collected to measure thiobarbituric acid reactive substances, reduced glutathione, and catalase. In vitro effects of M. charantia extract on lipid peroxidation in liver homogenate of normal, control, and rats pretreated with extract were carried out against cumene hydroperoxide-induced lipid peroxidation. Results reveal that in vivo M. charantia inhibited stress-induced lipid peroxidation by increasing the levels of reduced glutathione and activities of catalase. These results were further supported by in vitro results. In vitro inhibition of lipid peroxidation was indicated by low levels of thiobarbituric acid in the liver homogenate from pretreated rats and normal rats when incubated with both cumene hydroperoxide and extract. Inhibition was also noted in the homogenate where the rats were pretreated but the mixture contained no extract. Thus this plant provides protection by strengthening the antioxidants like reduced glutathione and catalase. Inclusion of this plant in the daily diet would be beneficial.

scholarly journals Protective effects of molsidomine against doxorubicin-induced renal damage in rats

2016 ◽  
Vol 39 (1) ◽  
pp. 7 ◽  
Author(s):  
Fatih Oguz ◽  
Ali Beytur ◽  
Ediz Sarihan ◽  
Hilal K Oguz ◽  
Recep Bentli ◽  
...  
Keyword(s):  
Renal Damage ◽  
Reduced Glutathione ◽  
Kidney Injury ◽  
Thiobarbituric Acid ◽  
Kidney Damage ◽  
Control Group ◽  
Thiobarbituric Acid Reactive Substance ◽  
Protective Effects ◽  
Reactive Substance ◽  
Group 4

Purpose: The purpose of this study was to investigate the therapeutic and protective effects of molsidomine (MLS) against doxorubicin (DOX)-induced renal damage in rats. Methods: Forty rats were randomly divided into five groups (control, MLS, DOX, DOX+MLS and MLS+DOX groups). Thiobarbituric acid reactive substance (TBARS), reduced glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), nitric oxide (NO) and glutathione peroxidase (GPx) levels were determined from kidney tissues and blood urea nitrogen (BUN), creatinine (Cr) and albumin (Alb) levels also determined. Results: DOX treatment caused a significant increase in TBARS levels and a significant decrease in the GSH and CAT levels compared with the control group. In comparison, MLS administration before DOX injection caused a significant decrease in TBARS levels and also increases in GSH and CAT levels, whereas treatment of MLS after DOX injection did not show any beneficial effect on these parameters. All groups showed a significant increase in NO levels compared to the control group. There were no significant differences among the all groups for BUN and Cr levels. Serum level of Alb decreased in the DOX-treated groups when compared with control and MLS groups. The histopathological findings were in accordance with the biochemical results. MLS treatment reversed the DOX-induced kidney damage in group 4. MLS treatment before DOX injection exerted a protective effect against DOX-induced kidney damage. Conclusions: MLS shows promise as a possible therapeutic intervention for the prevention of kidney injury associated with DOX treatment. Additional studies are warranted.

scholarly journals Evaluation of theIn VitroandIn VivoAntioxidant Potentials ofSudarshanaPowder

2018 ◽  
Vol 2018 ◽  
pp. 1-5 ◽  
Author(s):  
Weerakoon Achchige Selvi Saroja Weerakoon ◽  
Pathirage Kamal Perera ◽  
Dulani Gunasekera ◽  
Thusharie Sugandhika Suresh
Keyword(s):  
Antioxidant Activity ◽  
Antioxidant Capacity ◽  
Thiobarbituric Acid ◽  
Trolox Equivalent Antioxidant Capacity ◽  
Control Group ◽  
Thiobarbituric Acid Reactive Substance ◽  
Trolox Equivalent ◽  
Antioxidant Effects

Sudarshanapowder (SP) is one of the most effective Ayurveda powder preparations for paediatric febrile conditions. The objective of the present study was to evaluate thein vitroandin vivoantioxidant potentials of SP. Thein vitroantioxidant effects were evaluated using ABTS radical cation decolourization assay where the TROLOX equivalent antioxidant capacity (TEAC) was determined. Thein vivoantioxidant activity of SP was determined in Wistar rats using the Lipid Peroxidation (LPO) assay in serum. Thein vitroassay was referred to as the TROLOX equivalent antioxidant capacity (TEAC) assay. For thein vivoassay, animals were dosed for 21 consecutive days and blood was drawn to evaluate the MDA level. Thein vitroantioxidant activity of 0.5 μg of SP was equivalent to 14.45 μg of standard TROLOX. The percentage inhibition against the radical formation was50.93±0.53%. The SP showed a statistically significant (p<0.01) decrease in the serum level of thiobarbituric acid-reactive substance in the test rats when compared with the control group. These findings suggest that the SP possesses potent antioxidant activity which may be responsible for some of its reported bioactivities.

scholarly journals Exposure of precision-cut rat liver slices to ethanol accelerates fibrogenesis

2010 ◽  
Vol 299 (3) ◽  
pp. G661-G668 ◽  
Author(s):  
Courtney S. Schaffert ◽  
Michael J. Duryee ◽  
Robert G. Bennett ◽  
Amy L. DeVeney ◽  
Dean J. Tuma ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Cytokine Production ◽  
Smooth Muscle Actin ◽  
Thiobarbituric Acid ◽  
Ethanol Metabolism ◽  
Thiobarbituric Acid Reactive Substance ◽  
Ethanol Treatment ◽  
Liver Slices

Ethanol metabolism in the liver induces oxidative stress and altered cytokine production preceding myofibroblast activation and fibrogenic responses. The purpose of this study was to determine how ethanol affects the fibrogenic response in precision-cut liver slices (PCLS). PCLS were obtained from chow-fed male Wistar rats (200–300 g) and were cultured up to 96 h in medium, 25 mM ethanol, or 25 mM ethanol and 0.5 mM 4-methylpyrazole (4-MP), an inhibitor of ethanol metabolism. Slices from every time point (24, 48, 72, and 96 h) were examined for glutathione (GSH) levels, lipid peroxidation [thiobarbituric acid-reactive substance (TBARS) assay], cytokine production (ELISA and RT-PCR), and myofibroblast activation [immunoblotting and immunohistochemistry for smooth muscle actin (SMA) and collagen]. Treatment of PCLS with 25 mM ethanol induced significant oxidative stress within 24 h, including depletion of cellular GSH and increased lipid peroxidation compared with controls ( P < 0.05). Ethanol treatment also elicited a significant and sustained increase in interleukin-6 (IL-6) production ( P < 0.05). Importantly, ethanol treatment accelerates a fibrogenic response after 48 h, represented by significant increases in SMA and collagen 1α(I) production ( P < 0.05). These ethanol-induced effects were prevented by the addition of 4-MP. Ethanol metabolism induces oxidative stress (GSH depletion and increased lipid peroxidation) and sustained IL-6 expression in rat PCLS. These phenomena precede and coincide with myofibroblast activation, which occurs within 48 h of treatment. These results indicate the PCLS can be used as in vitro model for studying multicellular interactions during the early stages of ethanol-induced liver injury and fibrogenesis.

scholarly journals Lycium europaeum Extract: A New Potential Antioxidant Source against Cisplatin-Induced Liver and Kidney Injuries in Mice

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Ilhem Rjeibi ◽  
Anouar Feriani ◽  
Anouar Ben Saad ◽  
Jazia Sdayria ◽  
Issam Saidi ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Antioxidant Activity ◽  
Animal Studies ◽  
Methanol Extract ◽  
Reduced Glutathione ◽  
Protective Effects ◽  
Dpph Radical ◽  
Phytochemical Composition ◽  
Liver And Kidney

This study was designed to assess the protective effects of Lycium europaeum methanol extract (LEM) on liver and kidney injuries induced by cisplatin. The phytochemical composition, the antioxidant activity, and hepatorenal injury biomarkers were investigated. Results revealed that LEM exhibited a significant antioxidant activity in vitro on DPPH radical and H2O2 scavenging assays. In the animal studies, treatment with LEM significantly reduced the effects of cisplatin intoxication on serum liver biomarkers and serum renal biomarkers. Meanwhile, LEM diminishes significantly the effect of cisplatin on the level of lipid peroxidation in liver and kidney tissues. The activities of the antioxidant enzymes (reduced glutathione, glutathione peroxidase, superoxide dismutase, and catalase) were increased in groups pretreated with LEM and quercetin. Additionally, the normal histological structures of the liver and kidney were restored after treatment with LEM. This work clearly demonstrated that L. europaeum may be useful as a drug with hepato-nephroprotective potentials.

scholarly journals Evaluation of the Effect of Ceftriaxone on Lipid Peroxidation and Antioxidant Levels in Mice

2019 ◽  
Vol 12 (1) ◽  
pp. 245-250
Author(s):  
Kunjumon Dayana ◽  
Megaravalli R. Manasa
Keyword(s):  
Lipid Peroxidation ◽  
Body Weight ◽  
Antioxidant Enzymes ◽  
Free Radicals ◽  
Defense Mechanisms ◽  
Thiobarbituric Acid ◽  
Generation Cephalosporin ◽  
Control Group ◽  
Thiobarbituric Acid Reactive Substance ◽  
Albino Mice

Lipid peroxidation generates free radicals. These free radicals are scavenged by antioxidant defense mechanisms. An imbalance between the free radicals generation and antioxidant mechanisms can result in tissue damage. Several drugs are known to induce lipid peroxidation which can be responsible for their toxic potential. Hence the current study was planned to assess the effect of ceftriaxone, a third generation cephalosporin, on lipid peroxidation and levels of antioxidants in albino mice. Ceftriaxone was injected intraperitoneally at two doses - 100 mg/kg body weight; 200 mg/kg body weight – to albino mice. TBARS (Thiobarbituric acid reactive substance) levels in plasma, erythrocytes as well as tissue and the antioxidant enzymes activities were estimated. The data from ceftriaxone groups was analyzed with control group using ANOVA and Dunnett’s test as post hoc. Ceftriaxone (100 mg/kg body weight) did not alter TBARS levels compared to control. Ceftriaxone - 200 mg/kg body weight, has significantly increased TBARS levels. The activities of antioxidant enzymes were significantly decreased by ceftriaxone at these doses. The present study demonstrates that ceftriaxone has the potential for lipid peroxidation induction and reduction in the antioxidant enzymes acitivities in albino mice.

Involvement of hydrogen and lipid peroxides in acute tobacco smoking-induced platelet hyperactivity

1995 ◽  
Vol 268 (2) ◽  
pp. H679-H685 ◽  
Author(s):  
D. Blache
Keyword(s):  
Reduced Glutathione ◽  
Plasma Concentrations ◽  
Lipid Peroxides ◽  
Thiobarbituric Acid ◽  
Thiobarbituric Acid Reactive Substance ◽  
Lipid Hydroperoxides ◽  
Platelet Activity ◽  
Induced Aggregation ◽  
Platelet Hyperaggregability

Previous studies have established that cigarette smoking results in acute platelet hyperaggregability. We investigated whether changes in plasma oxidative properties could occur after smoking and whether such changes could be responsible for this enhanced platelet activity. In the present work, we report that platelets from nonsmokers become hyperactive after incubation with plasma prepared from blood of smokers obtained 10 min after smoking. This effect was not observed with presmoking plasma and could be inhibited in vitro by adding either catalase or reduced glutathione plus peroxidase to plasma or 2,6-di-tert-butyl-p-cresol (BHT) to platelets before incubation. Comparison of pre- and postsmoking plasma showed that smoking resulted in a decrease in vitamin E (18%, P < 0.01) and increases in conjugated diene (35%, P < 0.001), thiobarbituric acid-reactive substance (23%, P < 0.02), and free fatty acid (FFA, 40%, P < 0.005) plasma concentrations. The FFA fraction was peroxidized to a higher extent when extracted from postsmoking than from presmoking plasma. This peroxidized FFA fraction enhanced the thrombin-induced aggregation of platelets from nonsmokers. This increased response was inhibited either when the peroxidized FFA fractions were isolated from plasma treated with reduced glutathione and peroxidase or by pretreatment of the platelets with BHT. We conclude that the enhanced formation of lipid hydroperoxides found in postsmoking plasma seems to be responsible for the acute and marked platelet hyperactivity observed after smoking.

Cardioprotective effects of carvedilol on acute autoimmune myocarditis: anti-inflammatory effects associated with antioxidant property

2004 ◽  
Vol 286 (1) ◽  
pp. H83-H90 ◽  
Author(s):  
Zuyi Yuan ◽  
Keisuke Shioji ◽  
Yasuki Kihara ◽  
Hiroyuki Takenaka ◽  
Yoko Onozawa ◽  
...  
Keyword(s):  
Inflammatory Cytokines ◽  
Antioxidant Properties ◽  
Thiobarbituric Acid ◽  
Experimental Models ◽  
Left Ventricular ◽  
Thiobarbituric Acid Reactive Substance ◽  
Autoimmune Myocarditis ◽  
Reactive Substance

Carvedilol, a new β-blocker with antioxidant properties, has been shown to be cardioprotective in experimental models of myocardial damage. We investigated whether carvedilol protects against experimental autoimmune myocarditis (EAM) because of its suppression of inflammatory cytokines and its antioxidant properties. We orally administered a vehicle, various doses of carvedilol, racemic carvedilol [ R(+)-carvedilol, an enantiomer of carvedilol without β-blocking activity], metoprolol, or propranolol to rats with EAM induced by porcine myosin for 3 wk. Echocardiographic study showed that the three β-blockers, except R(+)-carvedilol, suppressed left ventricular fractional shortening and decreased heart rates to the same extent. Carvedilol and R(+)-carvedilol, but not metoprolol or propranolol, markedly reduced the severity of myocarditis at the two different doses and suppressed thickening of the left ventricular posterior wall in rats with EAM. Only carvedilol suppressed myocardial mRNA expression of inflammatory cytokines and IL-1β protein expression in myocarditis. In addition, carvedilol and R(+)-carvedilol decreased myocardial protein carbonyl contents and myocardial thiobarbituric acid-reactive substance products in rats with EAM. The in vitro study showed that carvedilol and R(+)-carvedilol suppressed IL-1β production in LPS-stimulated U937 cells and that carvedilol and R(+)-carvedilol, but not metoprolol or propranolol, suppressed thiobarbituric acid-reactive substance products in myocardial membrane challenged by oxidative stress. It was also confirmed that probucol, an antioxidant, ameliorated EAM in vivo. Carvedilol protects against acute EAM in rats, and the superior cardioprotective effect of carvedilol compared with metoprolol and propranolol may be due to suppression of inflammatory cytokines associated with the antioxidant properties in addition to the hemodynamic modifications.

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