Lipid Peroxidation In Rat Liver Research Articles

Effect of gold nanoparticles on glutathione and malondialdehyde levels in liver, lung and heart of rats

We studied the effect of gold nanoparticles (NPs) on oxidative stress markers including reduced glutathione (GSH) and malondialdehyde (MDA) in different organs of rats. Adult male Wistar-Kyoto rats were randomly divided into 3 groups of 5 animals each. One group served as control and received vehicle only. The remaining two groups were treated with 50μl of 10nm sized gold NPs, daily for 3 and 7days, respectively. The rats were sacrificed 24h after the last injection of NPs. Administration of gold NPs did not cause any significant change in GSH levels in liver, lung and heart on day 3 or day 7. There was no significant effect of gold NPs on MDA levels in lung and heart whereas significant increases in MDA levels were found in the liver of rats treated with gold nanoparticles on both 3 and 7days post-dosing (ANOVA F=7.113, P=0.010). In conclusion, the findings of this preliminary study suggest that gold NPs of 10nm diameter produce significant lipid peroxidation in rat liver however lungs and heart do not show any oxidative stress. Further studies are warranted to examine the effects of a broader dose range of gold NPs on the levels of free radical indices in different organs of rats.

Anti-Stress and Anti-Amnesic Effects of Coriandrum sativum Linn (Umbelliferae) Extract – an Experimental Study in Rats

Purpose: Coriandrum sativum Linn. ( Umbelliferae , C. sativum ) is cultivated throughout the world for its use as spice and as a folk medicine. This study deals with the anti-stress and anti-amnestic properties of C. sativum extract in rats. Methods: Urinary levels of vanillylmandelic acid (VMA) and ascorbic acid were used to evaluate antistress activity in rats, while conditioned avoidance response test in normal and scopolamine-induced amnesic rats was used to evaluate anti-amnesic effects. C. sativum extract was also evaluated for its antioxidant activities by inhibition of lipid peroxidation in brain and liver homogenates of the rats. Results: Daily administration of C. sativum extract (100, 200 and 300 mg/kg body weight) 1 h prior to induction of stress significantly decreased the stress-induced urinary levels of VMA from 382.79 ± 10.70 to 350.66 ± 15.15, 291.21 ± 16.53 and 248.86 ± 13.56 μg/kg/24 h and increased the ascorbic acid excretion levels from 66.73 ± 9.25 to 69.99 ± 7.37, 105.28 ± 13.74 and 135.32 ± 12.54 μg/kg/24 h at 100, 200 and 300 mg/kg, respectively, in a dose-dependent fashion without affecting the normal levels in control groups. The amnesic deficits (acquisition, retention and recovery) induced by scopolamine (1mg/kg, i.p.) in rats was reversed by C. sativum dose dependently. The extract also inhibited lipid peroxidation in both rat liver and brain to a greater extent than the standard antioxidant, ascorbic acid. Conclusion: C. sativum may be useful remedy in the management of stress and stress related disorders on account of its multiple actions such as anti-stress, anti-amnestic and antioxidant effects. Keywords: C. sativum , Stress, Lipid peroxidation, Vanillylmandelic acid, Memory.

Effects of Subacute and Subchronic Treatment of Synthetic Plant Growth Regulators on Liver Damage Serum Biomarkers Tissue Antioxidant Defense Systems and Lipid Peroxidation in Rats

The present study was aimed to investigate the effects of some synthetic plant growth regulators; s-Naphthoxy acetic acid (s-NOA) and 4-Chlorophenoxy acetic acid (4-CPA) at 10 and 20 ppm dosages on liver damage, antioxidant defense system and lipid peroxidation in rats. Rats were divided into 12 groups as control, s-NOA and 4-CPA at 10 and 20 ppm dosages application groups. Serum marker enzymes and biochemical parameters were selected as biomarkers for liver damage. Antioxidant defense systems as SOD, GR, CAT, GSH-Px, GST and G6PD enzyme activities and GSH and MDA contents were determined in tissues as the indicators of oxidative stress. At the end of experiments, the statistically significant changes were observed in the levels of TPRO, TALB, TCHOL, TBIL, AST, ALT and LDH as liver damage serum biomarkers in rats exposed to 10 and 20 ppm of s-NOA and 4-CPA as compared with controls. MDA levels increased in all the tissues of rats exposed to s-NOA and 4-CPA dosages whereas the fluctuation in SOD, GR, CAT, GSH-Px, GST and G6PD enzyme activities and GSH levels were observed compared with controls. It could be concluded that the treatments of s-NOA and 4-CPA dosages may induce liver damage and oxidative stress.

Omega-3 fatty acids enhance mitochondrial superoxide dismutase activity in rat organs during post-natal development

The protection of the developing organism from oxidative damage is ensured by antioxidant defense systems to cope with reactive oxygen species (ROS), which in turn can be influenced by dietary polyunsaturated fatty acids (PUFAs). PUFAs in membrane phospholipids are substrates for ROS-induced peroxidation reactions. We investigated the effects of dietary supplementation with omega-3 PUFAs on lipid peroxidation and antioxidant enzyme activities in rat cerebrum, liver and uterus. Pups born from dams fed a diet low in omega-3 PUFAs were fed at weaning a diet supplying low α-linolenic acid (ALA), adequate ALA or enriched with eicosapentaenoic acid (EPA) plus docosahexaenoic acid (DHA). Malondialdehyde (MDA), a biomarker of lipid peroxidation, and the activities of superoxide dismutase 1 (SOD1), SOD2, catalase (CAT) and glutathione peroxidase (GPX) were determined in the three target organs. Compared to low ALA feeding, supplementation with adequate ALA or with EPA+DHA did not affect the cerebrum MDA content but increased MDA content in liver. Uterine MDA was increased by the EPA+DHA diet. Supplementation with adequate ALA or EPA+DHA increased SOD2 activity in the liver and uterus, while only the DHA diet increased SOD2 activity in the cerebrum. SOD1, CAT and GPX activities were not altered by ALA or EPA+DHA supplementation. Our data suggest that increased SOD2 activity in organs of the growing female rats is a critical determinant in the tolerance to oxidative stress induced by feeding a diet supplemented with omega-3 PUFAs. This is may be a specific cellular antioxidant response to ROS production within the mitochondria.

Effects of long‐term exposure to low levels of organophosphorous pesticides and their mixture on altered antioxidative defense mechanisms and lipid peroxidation in rat liver

Organophosphorous pesticides, commonly used in agriculture for achieving better quality products, are toxic substances that have harmful effects on human health. Recent research on pesticides, especially pesticide mixtures, has shown that they are one of the key environmental health issues. The aim of the present study was to investigate whether dichlorvos, acephate, dimethoate and phorate, either used separately or in combination, can induce oxidative damage in rat livers. The levels of superoxide dismutase, glutathione peroxidase, catalase and lipid peroxidation products (malondialdehyde) were used as criteria. Low, middle and high doses of pesticides in drinking water were continuously administered orally to rats ad libitum for 24 weeks. Results show that the antioxidative defense mechanisms and lipid peroxidation in the rat livers display different responses, depending on the pesticide treatments and doses. The parameters for acephate, dichlorvos, phorate and dimethoate in the low-dose group, and the corresponding low-dose co-treated group were not altered. The oxidative damage in rat livers showed different responses with increasing pesticide dose according to the different pesticide treatments. The combination group of dichlorvos, acephate, dimethoate and phorate displayed different responses compared with the single pesticide-treated group. However, these responses did not constitute the sum of the response produced by each pesticide in the liver.

Gum resin of Boswellia serrata inhibited human monocytic (THP-1) cell activation and platelet aggregation

Ethnopharmacological relevanceStem bark gum resin extract of Boswellia serrata is traditionally used in India for its hemostatic, antiinflammatory and cardiovascular health effects and it is named as Śallakī in Ayurvedic medicine. Aim of the studyThis study was conducted to evaluate the antioxidative and antithrombotic properties of stem bark gum resin extracts of Boswellia serrata (BS). Materials and methodsThe inhibitory activity of the BSWE and BSAE on FeCl3 induced lipid peroxidation (in vitro) in rat liver and heart homogenates was measured spectrophotometrically. Their effect on H2O2 induced reactive oxygen species (ROS) generation in human monocytic (THP-1) cells was investigated by tracking intensity of a cell permeable fluorescent dye, H2DCFDA and subjecting the cell samples to confocal microscopy. Further, the effect of BSAE and BSWE on ADP-induced platelet aggregation was assessed using a multimode detection plate reader, plasma coagulation times using an automated blood coagulation analyzer and on human blood clotting factors Xa and XIa using chromogenic substrate. Phytomarker analysis of the water (BSWE) and hydroalcoholic (BSAE) extracts of BS-gum resin was done through HPLC using a standard compound AKβBA. ResultsBSAE and BSWE inhibited, to varied extents, the lipid peroxidation in liver (80%) and heart (50%) tissue homogenates of male Wistar rats. Further, BSAE (30μgdwt/mL) and BSWE (300μgdwt/mL) attenuated ≥60% of H2O2 mediated ROS generation in THP-1 cells. In case of standard compounds, ascorbate (20μgdwt/mL) and butylated hydroxytoluene (BHT) (10μgdwt/mL) completely scavenged ROS in the cells. BSAE and BSWE at 3mgdwt/mL completely inhibited ADP induced platelet aggregation and activities were comparable to 20μg/mL of heparin. The extracts also showed very high activity in prolonging coagulation time periods. Both types of extracts extended prothrombin time (PT) from ∼13 to >60s and activated partial thromboplastin time (APTT) from ∼32s to >90s. BSAE inhibited clotting factors Xa and XIa remarkably at 6μg of dwt where as BSWE did not show much effect on FXa and showed 30% inhibition on FXIa at 120μg. 10μg of heparin was required to inhibit about 30% activity of the above factors. HPLC analyses suggested that BSAE and BSWE had AKβBA of 9% (w/w) and 7.8% (w/w) respectively. ConclusionPresent study demonstrated antioxidant and antithrombotic anticoagulant activities of water and hydroalcoholic extracts of Boswellia serrata's gum resin. We suggest that BS-gum resin as a good source for lead/therapeutic compounds possessing antioxidant, antiplatelet and anticoagulant activities.

Long-term Exposure to Acetaminophen is a Crucial for Activity of Selected Antioxidative Enzymes and Level of Lipid Peroxidation Process in Rat Liver

Background: Our aim was to investigate the effect of intra-oesophageal acetaminophen instillation on the selected antioxidative enzymes activity: superoxide dismutase isoenzymes (MnSOD, Cu/ZnSOD), glutathione peroxidase (GPX), glutathione-S-transferase (GST), glutathione reductase (GR) and lipid peroxidation in rat liver after 4, 8 and 12 weeks of exposure. Material and methods: Male Wistar FL strain rats weighing 150-160 g were treated with paracetamol by intra- oesophageal instillation at a dose of 2.4 g/kg b.w every day up to 12 weeks. During the whole experiment rats were kept in a night-and-day’s cycle lasting twelve hours, with standard feed ad libitum . Rats were sacrificed after 4, 8 and 12 weeks of the study. The collected tissue liver was homogenized and the above mentioned enzymes were determined in the supernatants. Results: The current study revealed the presence of paracetamol-induced changes in the activities of antioxidative enzymes in comparison to the control values. Our results suggested that long term exposure to PC (8 and 12 weeks) decreased activity of GPX enzyme and increased activity of GST and GR enzymes as well as increased level of lipid peroxidation process in rat liver. These changes in the activity of antioxidative enzymes may be involved in paracetamol toxicity of the liver after a longer time of exposure to PC. The cited literature and our findings show that excessive use of paracetamol-containing preparations can have a harmful effect upon liver metabolism and suggest the need for further research.

ChemInform Abstract: Synthesis and Antioxidant Properties of Some New Flavone Derivatives on Lipid Peroxidation in the Rat Liver.

A series of 2'-, 3'-, 4'- and 6-substituted flavone derivatives was synthesized and their in vitro effects on rat liver microsomal NADPH-dependent lipid peroxidation (LP) levels were determined. Retinoic acid, at 10(-4) M concentration, decreased the LP level by about 34%. A significant decrease in male liver microsomal LP level was noted for the compounds 3d, 1a, 3b and 4b at a concentration of 10(-4) M (100%, 95%, 75% and 62%, respectively).

Tissue protective effect of xanthine oxidase inhibitor, polymer conjugate of (styrene–maleic acid copolymer) and (4-amino-6-hydroxypyrazolo[3,4-d]pyrimidine), on hepatic ischemia–reperfusion injury

The detrimental role of superoxide anion (O(2)(-)) has been well documented in the pathogenesis of ischemia-reperfusion (I/R) injury. Our and other studies suggested that one critical source of O(2)(-) generation may be xanthine oxidase (XO). We thus hypothesized that I/R injury could be protected by inhibiting XO activity, which would reduce the amount of O(2)(-) and hence reduce pathogenic consequences. Among various XO inhibitors, we previously found 4-amino-6-hydroxypyrazolo[3,4-d]pyrimidine (AHPP) exhibited potent XO inhibitory activity. Here, we report that the covalent conjugate of AHPP with amphipathic styrene-maleic acid copolymer (SMA-AHPP) showed protective effect against I/R-induced injury in a rat hepatic I/R model. Liver ischemia was induced by occluding both the portal vein and the hepatic artery for 30 min, and followed by reperfusion. SMA-AHPP was administered via the tail vein two hours before ischemia was initiated. A remarkable increase of liver enzymes in plasma (aspartate aminotransferase, AST; alanine aminotransferase, ALT and lactate dehydrogenase, LDH) was detected three hours after reperfusion, whereas prior injection of SMA-AHPP greatly suppressed this increase of AST, ALT and LDH. Moreover, induction of inflammatory cytokines, i.e. tumor necrosis factor-alpha (TNF-alpha), interleukin-12 (IL-12) and monocyte chemotactic protein-1 (MCP-1) by I/R were significantly inhibited by SMA-AHPP treatment. Accordingly, cytotoxic effect or apoptosis in the liver caused by I/R was clearly reduced by SMA-AHPP pretreatment. Furthermore, thiobarbituric acid-reactive substance assay showed a significant decrease of lipid peroxidation in rat liver after the administration of SMA-AHPP, which is parallel with the decreased XO activity after SMA-AHPP treatment, indicating the involvement of reactive oxygen species generated by XO. In addition, SMA-AHPP was found to bind to albumin, thus to exhibit prolonged in vivo (plasma) half-life. These results suggest that SMA-AHPP exerted a potent cytoprotective effect against I/R injury in rat liver, by inhibiting XO activity and the subsequent generation of O(2)(-).

Effects of cisplatin on lipid peroxidation and the glutathione redox status in the liver of male rats: The protective role of selenium

The role of oxidative stress in cisplatin (CP) toxicity and its prevention by pretreatment with selenium (Se) was investigated. Male Wistar albino rats were injected with a single dose of cisplatin (7.5 mg CP/kg b.m., i.p.) and selenium (6 mg Se/kg b.m, as Na2SeO3, i.p.) alone or in combination. The results suggest that CP intoxication induces oxidative stress and alters the glutathione redox status: reduced glutathione (GSH), oxidized glutathione (GSSG) and the GSH/GSSG ratio (GSH RI), resulting in increased lipid peroxidation (LPO) in rat liver. The pretreatment with selenium prior to CP treatment showed a protective effect against the toxic influence of CP on peroxidation of the membrane lipids and an altering of the glutathione redox status in the liver of rats. From our results we conclude that selenium functions as a potent antioxidant and suggest that it can control CP-induced hepatotoxicity in rats.

Identification of carotenoids from green alga Haematococcus pluvialis by HPLC and LC-MS (APCI) and their antioxidant properties.

Haematococcus pluvialis, a green alga accumulates astaxathin upto 2-3% on dry weight basis. In the present study, identification of carotenoids from Haematococcus cyst cell extract by HPLC and LC-MS (APCI) and their antioxidant properties were evaluated in vitro model systems. The extract exhibited 89% and 78% antioxidant activity in beta-carotene linoleate model, and hydroxyl radical scavenging model at 9 ppm of total carotenoid respectively. The extract also showed 80%, 85% and 79% antioxidant activity against lipid peroxidation in kidney, brain and liver of rats. Low-density lipoprotein oxidation induced by Cu2+ ions also protected (45%, 64% and 75%) by the extract in a dose dependent manner with different carotenoid levels. Thiobarbituric acid reactive substances concentration in the blood, liver, and kidney of rat was also significantly (p<0.005) decreased in H. pluvialis treated rats. Potent antioxidant activity is attributable to various carotenoids present in the extract.

Mechanism of action of novel naphthofuranquinones on rat liver microsomal peroxidation

In order to elucidate the effect on mammal systems of new derivatives from 2-hydroxy-3-allyl-naphthoquinone, α-iodinated naphthofuranquinone (NPPN-3223), β-iodinated naphthofuranquinone (NPPN-3222) and β-methyl naphthofuranquinone (NPPN-3226) synthesized as possible trypanocidal agents, their effect on rat liver microsomal lipid peroxidation was investigated. They (a) inhibited NADPH-dependent, iron-catalyzed microsomal rat liver lipid peroxidation; (b) did not inhibit the tert-butyl hydroperoxide-dependent lipid peroxidation; (c) did not inhibit ascorbate–lipid peroxidation with the exception of NPPN-3226 which did inhibit it; (d) stimulated NADPH oxidation and microsomal oxygen uptake; (e) increased superoxide anion formation by NADPH-supplemented microsomes and (f) stimulated ascorbate oxidation. The three drugs were reduced to their seminaphthofuranquinone radical by the liver NADPH–P450 reductase system, as detected by ESR measurements. These results support the hypothesis that naphthofuranquinones reduction by microsomal NADPH–P450 reductase and semiquinone oxidation by molecular oxygen diverts electrons, preventing microsomal lipid peroxidation. In addition, hydroquinones and/or semiquinones formed by naphthofuranquinones reduction would be capable of lipid peroxidation inhibition and on interacting with the lipid peroxide radicals can lead to an antioxidant effect as we suggested for NPPN-3226 in close agreement to the inhibition of ascorbate–lipid peroxidation. Due to the properties of these molecules and their incoming structure developments, naphthofuranquinones would be considered as potentially promising therapeutic agents, mainly against Chagas disease.

Influence of thyroid dysfunction on liver lipid peroxidation and antioxidant status in experimental rats

The purpose of this study was to evaluate the effects of dysthyroidism on lipid peroxidation, antioxidants status, liver, and serum dysfunction parameters in the hypo-/hyperthyroidism-induced rats. Hypothyroidism and hyperthyroidism conditions were induced for 5 weeks by administration of 0.05% benzythiouracile (BTU) and l-thyroxine sodium salt (0.0012%), in drinking water, respectively. The enzymatic activities of glutathione peroxidase (GPx), superoxide dismutase (SOD), catalase (CAT) and the lipid peroxidation product; thiobarbituric acid reacting substances (TBARS) were measured in liver as indicators of oxidative damage. However, liver dysfunction parameters represented by the activities of aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), lactate dehydrogenase (LDH), and gamma glutamyl transferase (GGT), were measured in serum. In hyperthyroidism rats, the TBARS contents of liver have significantly increased compared to those in hypothyroid rats and the controls (p<0.001), associated with a fall of the total antioxidant status (TAS) in the serum of the hyperthyroid rats. The SOD, CAT, and GPx activities in liver of hyperthyroid rats have significantly increased compared to hypothyroid rats and the controls (p<0.001). The AST, ALT, LDH, GGT, and ALP activities increased in the hyperthyroidism rats (p<0.05).We conclude that thyroid dysfunction induces oxidative stress and modifies some biochemical parameters of liver. Our results show the occurrence of a state of oxidizing stress in relation to hyperthyroidism.

In vitro and in vivo antioxidant activity of Pinus koraiensis seed extract containing phenolic compounds

Abstract A polyphenolics extract from Pinus koraiensis seed (PKS) has been investigated for its in vivo and in vitro antioxidant activity. The total phenolic content of PKS extract was 264 mg of gallic acid equivalents/g dry material. The extract was found to show remarkable scavenging activity on 2,2-diphenyl-picrylhydrazyl (DPPH) (EC 50 0.023 ± 0.004 mg/ml), OH (EC 50 0.391 ± 0.055 mg/ml), O 2 - (EC 50 4.37 ± 0.19 mg/ml), as well as a high and dose-dependent reducing power. The extract also showed strong suppressive effect on rat liver lipid peroxidation and erythrocyte haemolysis. Ageing and radiation models were used to evaluate the antioxidant effect in vivo . PKS extract highly inhibited oxidative damage induced by d -galactose and γ-ray. The results have indicated that intragastric administration of the extract can increase levels of superoxide dismutase (SOD) and glutathione (GSH), and decrease malondialdehyde (MDA) content.

Comparative effect of N-substituted dehydroamino acids and α-tocopherol on rat liver lipid peroxidation activities

Free radical damage has been associated with a growing number of diseases and conditions, such as autoimmune diseases, neurodegenerative disorders and multiple types of cancer. Some dehydroamino acids and corresponding peptides can function as radical scavengers. In this study the in vitro effects on rat liver lipid peroxidation levels of fourteen N-substituted dehydroamino acid derivatives and α-tocopherol were investigated. α-Tocopherol is a powerful antioxidant that is beneficial in the treatment of many free radical related diseases. The results indicated that all the compounds showed very good inhibitory effect on the lipid peroxidation compound with α-tocopherol at 1 mM concentrations and the inhibition rate was in the range of 70–79 % with the exception of compound 5. At 0.1 mM concentrations compounds 1, 2 and 9 were found more active than α-tocopherol. The results confirmed that molecules such as dehydroamino acids which have reactive double bonds can act as a guard in vitro against oxidants.

Ameliorative effect of ajwain extract on hexachlorocyclohexane-induced lipid peroxidation in rat liver

Effect of ajwain extract on hexachlorocyclohexane-induced oxidative stress and toxicity in rats were investigated. Six groups of rats were maintained for 12 weeks as (1) Control; (2) HCH (300 mg/kg body weight) injected (3) 1% ajwain extract incorporated diet (4)1% ajwain extract incorporated diet + HCH (5) 2% ajwain extract incorporated diet and (6) 2% ajwain extract incorporated diet + HCH. Results revealed that HCH administration lead to an increase in hepatic lipid peroxidation associated with reduction in, levels of glutathione (GSH), activity of superoxide dismutase (SOD), catalase and glucose-6-phosphate dehydrogenase. Prefeeding of ajwain extract resulted in decreased hepatic levels of lipid peroxides and increased GSH, GSH-peroxidase, G-6-PDH, SOD, catalase and glutathione S-transferase (GST) activities. At the same time there was a significant reduction in hepatic levels of HCH-induced raise in lipid peroxides as a result of the prefeeding the extract. Prefeeding of ajwain extract at 1% level to rats injected with HCH reverted the significant changes in catalase, G-6-PDH, GST and -glutamyl transpeptidase. HCH-induced formation of micronuclei in femur bone marrow was also reduced significantly. It was concluded that HCH administration resulted in hepatic free radical stress, causing toxicity, which could be reduced by the dietary ajwain extract.

Formaldehyde Content in the Rui Fish (Labeo rohita) in Bangladesh and Effect of Formaldehyde on Lipid Peroxidation in Rat Liver and Intestinal Tissues

Formaldehyde Content in the Rui Fish (Labeo rohita) in Bangladesh and Effect of Formaldehyde on Lipid Peroxidation in Rat Liver and Intestinal Tissues

Protective effect of caffeic acid phenethyl ester on tert-butyl hydroperoxide-induced oxidative hepatotoxicity and DNA damage

Increased oxidative stress and associated high levels of free radical generation have been described to occur during the pathogeneses of various diseases in animal models. In the present work, we investigated the protective effects of the phenethyl ester of caffeic acid (CAPE), an active component of honeybee propolis, on tert-butyl hydroperoxide ( t-BHP)-induced hepatotoxicity in a cultured HepG2 cell line and in rat liver. CAPE was found to significantly reduce t-BHP-induced oxidative injury in HepG2 cells, as determined by cell cytotoxicity, and lipid peroxidation and reactive oxygen species (ROS) levels in a dose-dependent manner. Furthermore, CAPE protected HepG2 cells against t-BHP-induced oxidative DNA damage, as determined by the Comet assay. Consistently, CAPE reduced hydroxyl radical-induced 2-deoxy- d-ribose degradation by ferric ion-nitrilotriacetic acid and H 2O 2, and also removed the superoxide anion generated by a xanthine/xanthine oxidase system. Our in vivo study showed that pretreatment with CAPE prior to the administration of t-BHP significantly and dose-dependently prevented increases in the serum levels of hepatic enzyme markers (alanine aminotransferase and aspartate aminotransferase) and reduced lipid peroxidation in rat liver. Moreover, histopathological evaluation of livers consistently revealed that CAPE reduced liver lesion induction by t-BHP. Taken together, these results suggest that the protective effects of CAPE against t-BHP-induced hepatotoxicity may, at least in part, be due to its ability to scavenge ROS and protect DNA from oxidative stress-induced damage.

Antiperoxidative Effect of Withania somnifera Root Powder on Liver Lipid Peroxidation and Antioxidant Status in Adjuvant-induced Arthritic Rats

Antiperoxidative Effect of Withania somnifera Root Powder on Liver Lipid Peroxidation and Antioxidant Status in Adjuvant-induced Arthritic Rats

IN VITRO ANTI‐OXIDANT AND DNA PROTECTIVE EFFECTS OF THE NOVEL 3‐HYDROXY‐3‐METHYLGLUTARYL COENZYME A REDUCTASE INHIBITOR ROSUVASTATIN

1. Free radical-induced lipid peroxidation and changes in protein and nucleic acid structures can result in various human ailments, including ageing, neurodegenerative disorders and cancer. High body fat or dietary fat further enhances the free radical-mediated pathogenesis of various diseases. 2. In the present study, the in vitro anti-oxidant and DNA protective effects of the novel cardiovascular drug rosuvastatin were evaluated. Anti-oxidant activity was evaluated on the basis of inhibition of lipid peroxidation, scavenging of superoxide radical and the reduction of ferric ions (Fe(3+)). Inhibition of lipid peroxidation was determined using Fenton's reaction-induced lipid peroxidation in rat liver and brain homogenates and liver mitochondria. Superoxide radical-scavenging activity was evaluated by scavenging of the superoxide anion generated by photo illumination of riboflavin and Fe(3+)-reducing activity was determined by the ferric-reducing anti-oxidant power (FRAP) assay. DNA protection was evaluated according to changes in H(2)O(2)-induced pBR322 plasmid DNA and Fenton's reaction-induced-fragmentation of rat liver DNA. 3. The results indicate that rosuvastatin (1.5 or 2 mg/mL) is able to protect against lipid peroxidation. Furthermore, H(2)O(2)-induced changes in pBR322 plasmid DNA and fragmentation of hepatic DNA were alleviated by rosuvastatin. However, rosuvastatin did not show any superoxide anion-scavenging activity. The protective mechanism of rosuvastatin can be correlated with the reducing equivalent donating property or direct hydroxyl radical-scavenging activity of the drug. 4. The pleiotropic activities of rosuvastatin exhibited suggest its clinical advantages against oxidative stress-induced human ailments in addition to its widely using hypolipidaemic effect.