Lipid Peroxidation In Hepatic Tissues Research Articles

Hepatoprotective Effect of Vitamin-E (α-Tocopherol) on Trichloroethylene and Toluene Induce Liver Damage in Rats

This study was design to investigate the harmful effect of trichloroethylene and toluene on the hepatic cell of rats and possible protective effect of vitamin-E (α-tocopherol) on these detrimental effects. This study aimed to evaluate organic solvents which are persistent and uninterrupted ecological pollutants that are capable to cause numerous dysfunctions in target tissues of exposed animal as well as humans. This study suggests that trichloroethylene (TCE) and toluene when administered in rats changes their metabolic disposition. Therefore, investigation work performed as to (a) Compare the rate of lipid peroxidation in hepatic tissues, (b). To study the concomitant effect on reduced glutathione in liver of rats subjected to TCE and toluene with vitamin-E (VE) to protect the damage of liver cells.

Repeatedly heated mix vegetable oils-induced atherosclerosis and effects of Murraya koenigii

BackgroundStatins are considered as standard drugs to control cholesterol levels, but their use is also associated with renal hypertrophy, hemorrhagic stroke, hepatomegaly, and myopathy. Murraya koenigii is an herb that is used in traditional cuisine and as a medicine in South Asia. Here we assessed the antidyslipidemic and antiatherosclerotic effects of this spice in repeated heated mix vegetable oils (RHMVO)-induced atherosclerotic models.MethodsAqueous extract of M. koenigii leaves (Mk LE) was prepared and its phytoconstituents were determined. Rabbits were divided into 5 groups (n = 10). Except for the control group, all the other four groups were treated with RHMVO for 16 weeks (dose = 2 ml/kg/day) to induce dyslipidemia and atherosclerosis. These groups were further treated for 10 weeks either with 300 and 500 mg/kg/day Mk LE, lovastatin, RHMVO, or left untreated. Body and organ weights were measured along with oxidative stress and tissue damage parameters. Lipid profile and hepatic function markers were studied. Atheroma measurement and histopathological examination were also performed in control and treated groups.ResultsMk LE significantly (p < 0.05) attenuated RHMVO-induced dyslipidemia and atheroma formation. Furthermore, fat accumulation and lipid peroxidation in hepatic tissues were reduced by Mk LE in a dose-dependent manner. Our results indicated that the antidyslipidemic effects of Mk LE in 500 mg/kg/day dose were comparable to lovastatin. Additionally, oxidative stress markers were reduced much more significantly in Mk LE-500 than in the statin group (p < 0.05).ConclusionsThis study recommends Mk LE as a potent antioxidant and lipid-lowering natural medicine that can attenuate the RHMVO-induced atherosclerotic in optimal doses and duration. Therefore, Mk LE can be accessible, cheap, and free of adverse effects alternate to statins.

Chemical Compositions, Antiobesity, and Antioxidant Effects of Proanthocyanidins from Lotus Seed Epicarp and Lotus Seed Pot.

Lotus seed epicarp (LSE) and lotus seed pot (LSP) were characterized, and a total of 5 and 7 proanthocyanidins (PAs) were identified in purified LSE and LSP extract, respectively. Purified LSE and LSP PAs significantly suppressed the body weight and weight gain of white adipose tissue (WAT) and decreased the WAT cell size in high-fat diet-induced obese mice regardless of the daily food intake. LSE or LSP administration significantly lowered the serum leptin level and improved the serum and liver lipid profiles (including total cholesterol (TC), triglycerides (TG), high-density lipoprotein-cholesterol (HDL-C), and low-density lipoprotein-cholesterol (LDL-C) levels), increased activities of antioxidant enzymes (superoxide dismutase (SOD) and glutathione transferase (GST)) and reduced glutathione (GSH) concentration, and suppressed lipid peroxidation in hepatic tissue. LSP PAs were generally more effective than LSE PAs. Both extracts ameliorated obesity, insulin resistance, and oxidative damage in obese mice, suggesting they are good candidates for value-added functional food and nutraceutical ingredients.

Vitamin E inhibits cyclosporin A-induced CTGF and TIMP-1 expression by repressing ROS-mediated activation of TGF-β/Smad signaling pathway in rat liver

Cyclosporin A (CsA) is the most common immunosuppressive drug used in organ transplantation. However, the clinical use of CsA is often limited by several side effects including hepatotoxicity. In the present study, it was found that administration of CsA causes a rapid activation of TGF-β/Smad signaling cascade and subsequent expression of the profibrotic genes connective tissue growth factor (CTGF) and tissue inhibitors of matrix metallproteinases-1 (TIMP-1) in rat liver. In addition, Smad phosphorylation and subsequent CTGF and TIMP-1 expression were markedly reduced in the presence of neutralizing monoclonal TGFβ1–3 antibody. Furthermore, CsA administration significantly increased the serum levels of the liver enzymes alanine aminotransferase (ALT) and aspartate aminotransferase (AST) as well as lipid peroxidation in hepatic tissues. Moreover, significant reduction in the hepatic content of reduced glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT) was observed in CsA-alone-treated animals. Histopathological changes were also observed in CsA-alone-treated rats. Pretreatment of animals with Vitamin E (Vit E) before CsA administration significantly reduced TGF-β level as well as Smad phosphorylation and subsequent CTGF and TIMP-1 expression. Furthermore, administration of PEG-SOD clearly attenuated TGF-β/Smad signaling induced by CsA. Moreover, concomitant administration of Vit E along with CsA significantly ameliorated the histopathological changes and improved liver function as well as the antioxidant capacity. Finally, this study shows that the immunosuppressive efficiency of CsA was not altered in the presence of Vit E. These data may support the concept of using antioxidant therapy as a valuable approach for the prevention of CsA-induced tissue fibrosis.

Ethanol extract of Tetrapleura tetraptera fruit peels: Chemical characterization, and antioxidant potentials against free radicals and lipid peroxidation in hepatic tissues

The chemical and antioxidant properties of the ethanolic extract of Tetrapleura tetraptera fruit peels were investigated. Dried peels of T. tetraptera fruits were extracted with ethanol. The extract was subjected to preliminary phytochemical screening using standard procedures. GC–MS was used in identifying the secondary metabolites. The antioxidant properties of the extract were determined by its ferric reducing activity, 2,2′-diphenyl-1-picrylhydrazyl (DPPH) and nitric oxide (NO) radicals scavenging activities, and the inhibition of lipid peroxidation in hepatic tissues of albino male rats. Preliminary phytochemical screening revealed the presence of flavonoids, phenols, tannins, saponins, terpenoids and phlebotannin. GC–MS analysis revealed the presence of D-fructose, piperazine, octodrine, glycidol, glyceraldehydes, 6-octadecenoic acid and 9,12-octadecenoic acid, with D–fructose being the most predominant compound. The extract exhibited high antioxidant activities both in vitro and ex vivo, as indicated by its ability to scavenge DPPH and nitric oxide as well as inhibition of lipid peroxidation. This is further portrayed by its ferric reducing activity. These results suggest an antioxidant protective effect of the extract against oxidative hepatic damage and can be attributed to a synergetic action of the identified bioactive compounds.

Ameliorative role of melatonin against cypermethrin induced hepatotoxicity and impaired antioxidant defense system in Wistar rats

Recently, melatonin has attracted attention because of their strong free radical scavenging and antioxidant properties. The present study was designed to investigate the role of melatonin against cypermethrin induced hepatotoxicity in rats using qualitative, quantitative and biochemical approaches. Adult female Wistar rats were randomly divided into four groups; each group consists of six animals. Control group received vehicle, corn oil; Cypermethrin (CM) (250mg/kg bw); Melatonin (MEL) (10 mg/kg bw); CM+MEL treated group. Animals were treated orally, daily for a period of 4 weeks. Animals were sacrificed by decapitation and liver was used for various biochemical and histopathological examinations. The result of this study shows that in vivo administration of cypermethrin caused a significant induction of oxidative damage in liver tissue as evidenced by depletion of proteins, glutathione (GSH) and increased lipid peroxidation in hepatic tissue. Cypermethrin administration significantly enhanced the activities of enzymatic antioxidants (superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) glutathione reductase (GR) and glutathione-S- transferase (GST). Cypermethrin intoxication exhibited elevation in the activities of liver marker enzymes such as serum glutamate pyruvate transaminase (SGPT) serum glutamate oxaloacetate transaminase (SGOT) and Lactate dehydrogenase (LDH). Furthermore, the co-administration of melatonin mitigates the hepatotoxicity of cypermethrin by normalizing the biochemical and enzymatic parameters. The biochemical observations were supported by histopathological examination of liver. The findings of this investigation suggest that the melatonin may play a protective role against cypermethrin induced hepatotoxicity and oxidative damage in female albino rats.

ATTENUATING EFFECT OF UVARIA NARUM (DUNAL) WALL. LEAVES ON THIOACETAMIDE INDUCED HEPATIC INJURY

The objective of the present study was to evaluate the he patoprotective potential of U varia narum leaf extract at two different doses (200 and 400 mg / kg b.w.) against thioacetamide induced Hepatic injury . Thioacetamide at dose of 100 mg / kg induced l iver toxicity , which was ass essed by quantifying the serum h epatic biomarkers like SGPT, SGOT, ALP, total and direct bilirubin , serum biochemical parameters like albumin, total protein, cholesterol, triglycerides, glucose and urea and oxidative parameters like glutathione, catalas e, s uperoxide dismutase and lipid peroxidation in hepatic tissue. Further study was supported by histopathology studies. The results revealed that Silymarin (100 mg / kg b.w.) and Uvaria narum leaf extract at both doses prevented the elevation of serum hepatic biomarkers and also altered serum biochemical parameters dose de pendently. Whereas decrease in l ip id peroxidation and elevation in catalase, g lutathione and superoxide dismutase was observed in Silymarin and extract treated a nimals. Histopathological changes in hepatic tissue also supported the dose dep endent protective effect of Uvaria narum leaf extract . The results were comparable to reference standard Silymarin.

Beneficial effects of Allium sativum L. stem extract on lipid metabolism and antioxidant status in obese mice fed a high‐fat diet

This study was designed to examine the potential health benefits of Allium sativum L. (garlic) stem extract (ASSE) on obesity and related disorders in high-fat diet-induced obese mice. Obese mice were orally administered ASSE at doses of 100, 250 and 500 mg kg(-1) body weight day(-1) for 4 weeks. Consumption of ASSE significantly suppressed body weight gain and white adipose tissue (WAT) weight regardless of daily food intake. Obese mice fed ASSE also exhibited a significant decrease in WAT cell size. The decreased level of adiponectin and increased level of leptin in obese mice reverted to near normal mice levels in ASSE-treated mice. ASSE administration significantly improved lipid parameters of the serum and liver and inhibited fat accumulation in the liver by modulating the activities of hepatic lipid-regulating enzymes in obese mice. Administration of ASSE also led to significant increases in antioxidant enzymes and suppressed glutathione depletion and lipid peroxidation in hepatic tissue. These results suggest that ASSE may ameliorate obesity, insulin resistance and oxidative damage in high-fat diet-induced obese mice.

Protective Role of Moringa oleifera (Sajina) Seed on Arsenic-Induced Hepatocellular Degeneration in Female Albino Rats

In an attempt to develop new herbal therapy, an aqueous extract of the seed of Moringa oleifera was used to screen the effect on arsenic-induced hepatic toxicity in female rat of Wistar strain. Subchronic exposure to sodium arsenite (0.4 ppm/100 g body weight/day via drinking water for a period of 24 days) significantly increased activities of hepatic and lipid function markers such as alanine transaminase, aspartate transaminase, cholesterol, triglycerides, LDL along with a decrease in total protein and HDL. A notable distortion of hepatocellular histoarchitecture was prominent with a concomitant increase in DNA fragmentation following arsenic exposure. A marked elevation of lipid peroxidation in hepatic tissue was also evident from the hepatic accumulation of malondialdehyde and conjugated dienes along with suppressed activities in the antioxidant enzymes such as superoxide dismutase and catalase. However, co-administration of aqueous seed extract of M. oleifera (500 mg/100 g body weight/day for a period of 24 days) was found to significantly prevent the arsenic-induced alteration of hepatic function markers and lipid profile. Moreover, the degeneration of histoarchitecture of liver found in arsenic-treated rats was protected along with partial but definite prevention against DNA fragmentation induction. Similarly, generation of reactive oxygen species and free radicals were found to be significantly less along with restored activities of antioxidant enzymes in M. oleifera co-administered group with comparison to arsenic alone treatment group. The present investigation offers strong evidence for the hepato-protective and antioxidative efficiencies of M. oleifera seed extract against oxidative stress induced by arsenic.

Antihyperglycemic and antihyperlipidemic effect of Rumex patientia seed preparation in streptozotocin-diabetic rats

Background and objective: Rumex patientia (RP) could exert beneficial health effects to ameliorate metabolic diseases. The effect of subchronic feeding of RP seeds was evaluated on serum glucose and lipid profile in streptozotocin (STZ)-diabetic rats. Methods: Wistar rats were divided into control, RP-treated control, diabetic, glibenclamide-treated diabetic, and RP-treated diabetic groups. For induction of diabetes, streptozotcin was administered at a dose of 60 mg/kg. Meanwhile, RP-treated groups received RP seed powder mixed with standard pelleted food at a weight ratio of 6% for 4 weeks. Serum glucose and lipid levels were determined before the study and at 2nd and 4th weeks after the study in addition to the oxidative stress markers in hepatic tissue. Results: Serum glucose was significantly lower in RP-treated diabetic rats at 2nd and 4th weeks as compared to untreated diabetics ( p < 0.05 and p < 0.01, respectively). Serum total cholesterol and triglyceride levels did not show significant reductions in RP-treated diabetic rats as compared to untreated diabetics. Serum HDL-cholesterol, however, significantly increased ( p < 0.05) and LDL-cholesterol showed a significant reduction ( p < 0.05) in RP-treated diabetic rats as compared to untreated diabetics ( p < 0.05). RP also attenuated the increased malondialdehyde (MDA) content and reduced activity of superoxide dismutase (SOD) in hepatic tissue. Conclusion: Subchronic treatment of diabetic rats with RP could lessen the abnormal changes in blood glucose level and to improve lipid profile regarding HDL- and LDL-cholesterol in part due to its attenuation of lipid peroxidation in hepatic tissue.

Beneficial Interaction of Thymoquinone and Sodium Valproate in Experimental Models of Epilepsy: Reduction in Hepatotoxicity of Valproate

The antiepileptic potential of thymoquinone (TQ) was studied in mice by using pentylenetetrazole (PTZ) and maximal electroshock seizure (MES)-induced convulsion models. In this investigation, the combined treatment of TQ and sodium valproate (SVP) was also studied. The aim of this part was to minimize SVPinduced hepatotoxic implications, by reducing its antiepileptic dose. TQ in both PTZ- and MES- models increased SVP potency. The experiments dealing with the effects of TQ on the ED50 of SVP revealed that TQ reduced the ED50 of SVP in both the models. However, this potentiation of SVP antiepileptic response was relatively more significant in PTZ model at both 50 and 100 mg/kg doses of TQ. Although very well tolerated and effective, SVP is well known for its hapatotoxic implications. In the experiment dealing with subacute treatment, SVP (1300-1500mg/kg/day in drinking water) for 21 days, produced hepatotoxicity in mice, characterized by elevated serum ALT and AST, reduced levels of non protein sulfhydryls and increase in lipid peroxidation in hepatic cells. Hepato-protection was successfully achieved when TQ (5-5.5mg/kg/day) was combined with SVP in drinking water for the same duration. The protective activity of TQ was evident by averting any serum ALT rise seen in SVP treatment. Though there is no prevention to the rise in lipid peroxidation in hepatic tissue but the same time a significant recovery in glutathione was evident by TQ joint treatment. However, a combination of TQ and low dose of SVP may be useful strategy to minimize adverse reactions of SVP. From the results of the present study that disclosed a protective role of TQ against SVP toxic damage to the liver, it could be mentioned safely that TQ behaves as an antioxidant and protected liver against its harmful effects. It also protected against the liver enzyme induction seen in the case of SVP alone.

Oxidative stress in liver of brown bullhead and channel catfish following exposure to tert-butyl hydroperoxide

Reactive oxygen species (ROS) have been implicated in the etiology of liver neoplasia in mammals and fishes. Oxidation of DNA and lipid peroxidation may be important early markers of such damage in certain species and tissues. In this study, 8-hydroxy-2′-deoxyguanosine (8-OHdG) was measured in channel catfish ( Ictalurus punctatus) and brown bullhead ( Ameriurus nebulosus) liver after glutathione (GSH) depletion (with diethyl maleate/buthionine sulfoximine injection) and exposure to the exogenous oxidant, tert-butyl hydroperoxide ( t-BOOH). GSH depletion alone resulted in a significant increase in lipid peroxidation in hepatic tissue of brown bullhead, but not in channel catfish. GSH depletion alone did not result in a significant increase in 8-OHdG formation as assessed by high performance liquid chromatography and electrochemical detection in either species. Treatment with t-BOOH alone or in combination with GSH depletion did not affect levels of DNA oxidation in either species. These results suggest that liver cells from these species of fish are relatively insensitive to the formation of oxidative DNA damage following exposure to a severe oxidative stress, and that lipid peroxidation may be a more appropriate early marker of oxidative stress in liver of these species.