Liver Oxidative Stress Status Research Articles

Effect of the Bitis arietans snake venom obtained from Kaltungo, Nigeria on Liver Oxidative Stress Status and Histological changes in Wistar Albino Rats

The venom of the Nigerian Bitis arietans (puff adder) was assessed for its ability to trigger venom-induced necrosis as well as oxidative stress in the liver of Wistar albino rats. The snake was captured in Kaltungo Gombe state and the venom was milked and lyophilized accordingly. A single LD50 dose (1.5mg/kg) was administered and the rats were monitored for two weeks and the liver homogenate samples were analyzed for the changes in oxidative stress markers. Histopathology of the liver tissue was conducted to assess the necrotic effect of the venom. The Malondialdehyde (MDA) values were not significantly changed while the superoxide dismutase (SOD) and reduced glutathione (GSH) levels were affected significantly. One week after venom administration, the branching and anastomoses of the hepatocytes in the liver tissue were observed to be not clearly demarcated due to the severity of the necrosis with disintegrated nuclei especially in the wall of the central vein. There was almost total disintegration of the wall of the central vein two weeks after venom administration. The results of this study indicate that the Nigerian puff adder venom can also trigger oxidative stress and promote necrosis in the liver tissue of Wistar albino rats.

Chlorella vulgaris supplementation effects on performances, oxidative stress and antioxidant genes expression in liver and ovaries of New Zealand White rabbits

Oxidative stress is an exclusive biochemical complication affecting reproduction; hence, dietary antioxidant supplementation for its attenuation is a required nutrition – reproduction improvement strategy. On this background, Chlorella vulgaris (a natural antioxidant) was supplemented to grower female rabbits to maturity. The rabbits were thirty-five in number randomly distributed into five experimental groups in a completely randomized design. Control group was fed only basal feed while treatment groups were fed diets containing 40 %, 60 %, 80 % and 100 % Chlorella vulgaris biomass as T1, T2, T3 and T4 respectively at 500 mg per animal body weight (kg) along with the basal feed daily. Performance records were obtained, blood was collected, and at the end uterus, ovaries and liver were removed from sacrificed animals for analysis. Serum, uterus and liver oxidative stress status were determined while RNA isolated from liver and ovaries samples were used for antioxidant genes expression analysis. Oxidative stress status and antioxidant enzymes activities were determined using chemical assays while antioxidant gene expression levels were determined using real-time quantitative PCR system. There was significant difference in feed intake (p < 0.014), final body weights (p < 0.008), empty carcass weights (p < 0.001) and commercial carcass weights (p < 0.001) of the rabbits as results of the microalgae supplementation. There was also significant difference in malondialdehyde (MDA) concentrations (p < 0.050), total antioxidant capacity (TAC) (p < 0.050) and protein carbonyl (PCO) concentrations (p < 0.050) due to the supplementation of the microalgae; in addition, supplementation of the microalgae significantly improved activities of superoxide dismutase (SOD) (p < 0.050), catalase (CAT) (p < 0.050) and reduced glutathione (GSH) concentration (p < 0.050). Furthermore, there was significant difference in relative expression of primary antioxidant genes sod1 (p < 0.050) and gpx1 (p < 0.050); however, there was no significant difference in relative expression of bre (p > 0.050) and ucp1 (p > 0.050). The study concluded from the outcomes stated above that supplementation of microalgae Chlorella vulgaris improved performances of rabbits through attenuation of oxidative stress, enhancement of antioxidant enzymes activities as well as up-regulation of primary antioxidant genes. Hence, it was recommended as dietary supplement for protection against oxidative stress and improved productivity in rabbits and other food producing mammalian species. In addition, further studies into assessment of its effects on expression of transcripts and immune modulation genes in rabbits and other animals is warranted as future studies in order to established its potential as beneficial nutraceutical for animals and human.

Hydroxytyrosol prevents reduction in liver activity of \u0394-5 and \u0394-6 desaturases, oxidative stress, and depletion in long chain polyunsaturated fatty acid content in different tissues of high-fat diet fed mice

BackgroundEicosapentaenoic acid (EPA, C20:5n-3), docosahexaenoic acid (DHA, C22:6n-3) and arachidonic acid (AA, C20:4n-6) are long-chain polyunsaturated fatty acids (LCPUFAs) with relevant roles in the organism. EPA and DHA are synthesized from the precursor alpha-linolenic acid (ALA, C18:3n-3), whereas AA is produced from linoleic acid (LA, C18:2n-6) through the action of Δ5 and Δ6-desaturases. High-fat diet (HFD) decreases the activity of both desaturases and LCPUFA accretion in liver and other tissues. Hydroxytyrosol (HT), a natural antioxidant, has an important cytoprotective effects in different cells and tissues.MethodsMale mice C57BL/6 J were fed a control diet (CD) (10% fat, 20% protein, 70% carbohydrates) or a HFD (60% fat, 20% protein, 20% carbohydrates) for 12 weeks. Animals were daily supplemented with saline (CD) or 5 mg HT (HFD), and blood and the studied tissues were analyzed after the HT intervention. Parameters studied included liver histology (optical microscopy), activity of hepatic desaturases 5 and 6 (gas-liquid chromatography of methyl esters derivatives) and antioxidant enzymes (catalase, superoxide dismutase, glutathione peroxidase, and glutathione reductase by spectrophotometry), oxidative stress indicators (glutathione, thiobarbituric acid reactants, and the antioxidant capacity of plasma), gene expression assays for sterol regulatory element-binding protein 1c (SREBP-1c) (qPCR and ELISA), and LCPUFA profiles in liver, erythrocyte, brain, heart, and testicle (gas-liquid chromatography).ResultsHFD led to insulin resistance and liver steatosis associated with SREBP-1c upregulation, with enhancement in plasma and liver oxidative stress status and diminution in the synthesis and storage of n-6 and n-3 LCPUFAs in the studied tissues, compared to animals given control diet. HT supplementation significantly reduced fat accumulation in liver and plasma as well as tissue metabolic alterations induced by HFD. Furthermore, a normalization of desaturase activities, oxidative stress-related parameters, and tissue n-3 LCPUFA content was observed in HT-treated rats over control animals.ConclusionsHT supplementation prevents metabolic alterations in desaturase activities, oxidative stress status, and n-3 LCPUFA content in the liver and extrahepatic tissues of mice fed HFD.

Effect of 3-keto-1,5-bisphosphonates on obese-liver's rats.

Obesity is associated with an oxidative stress status, which is defined by an excess of reactive oxygen species (ROS) vs. the antioxidant defense system. We report in this present work, the link between fat deposition and oxidative stress markers using a High Fat Diet-(HFD) induced rat obesity and liver-oxidative stress. We further determined the impact of chronic administration of 3-keto-1, 5-BPs 1 (a & b) (40μg/kg/8 weeks/i.p.) on liver's level. In fact, exposure of rats to HFD during 16 weeks induced body and liver weight gain and metabolic disruption with an increase on liver Alanine amino transférase (ALAT) and Aspartate aminotransférase (ASAT) concentration. HFD increased liver calcium level as well as free iron, whereas, it provoked a decrease on liver lipase activity. HFD also induced liver-oxidative stress status vocalized by an increase in reactive oxygen species (ROS) as superoxide radical (O2), hydroxyl radical (OH) and Hydrogen peroxide (H2O2). Consequently, different deleterious damages as an increase on Malon Dialdehyde MDA, Carbonyl protein PC levels with a decrease in non-protein sulfhydryls NPSH concentrations, have been detected. Interestingly, our results demonstrate a decrease in antioxidant enzymes activities such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidases (GPx) and peroxidases (POD). Importantly, 3-keto-1,5-bisphosphonates treatment corrected the majority of the deleterious effects caused by HFD, but it failed to correct some liver's disruptions as mineral profile, oxidative damages (PC and NPSH levels) as well as SOD and lipase activities. Our investigation point that 3-keto-1,5-bisphosphonates could be considered as safe antioxidant agents on the hepatic level that should also find other potential biological applications.

Featured Article: Oxidative stress status and liver tissue defenses in diabetic rats during intensive subcutaneous insulin therapy.

Long-term insulin delivery can reduce blood glucose variability in diabetic patients. In this study, its impact on oxidative stress status, inflammation, and liver injury was investigated. Diabetes was induced in Wistar rats with a single dose of streptozotocin (100 mg/kg). Untreated rats and rats administered Insuplant® (2 UI/200 g/day) through a subcutaneous osmotic pump for one or four weeks were compared with non-diabetic controls. Body weight, fructosamine level, total cholesterol, Insulin Growth Factor-1 (IGF-1) level, lipid peroxidation, and total antioxidant capacity were measured. Hepatic injury was determined through the measurement of glycogen content, reactive oxygen species (ROS) production, and macrophage infiltration. Liver oxidative stress status was evaluated through the measurement of superoxide dismutase (SOD), catalase (CAT), and nicotinamide adenine dinucleotide phosphate-oxidase (NADPH oxidase) expression, and p38 mitogen-activated protein kinase (p38MAPK) activation. Induction of diabetes led to increased plasma oxidative stress and inflammation. Moreover, ROS production and macrophage infiltration increased in addition to SOD, CAT, and NADPH oxidase expression. Intensive insulin therapy improved metabolic control in diabetic animals as seen by a restoration of hepatic glycogen, plasma IGF-1 levels, and a decrease in plasma oxidative stress. However, insulin treatment did not result in a decrease in acute inflammation in diabetic rats as seen by continued ROS production and macrophage infiltration in the liver, and a decrease of p38MAPK activation. These results suggest that the onset of diabetes induces liver oxidative stress and inflammation, and that subcutaneous insulin administration cannot completely reverse these changes. Targeting oxidative stress and/or inflammation in diabetic patients could be an interesting strategy to improve therapeutic options.

Liver oxidative stress of the grey mullet Mugil cephalus presents seasonal variations in Ennore estuary

The objective of this study was to determine the liver oxidative stress status of grey mullets living in heavy-metal-rich polluted Ennore estuary compared with unpolluted Kovalam estuary. Fish were collected from both estuaries during the monsoon and summer seasons from October 2004 to September 2006. Fish liver homogenate (N = 20 per group) was prepared for evaluating oxidative stress parameters. Fish living in the polluted estuary had significantly higher lipid oxidation products, conjugated dienes (0.346 +/- 0.017 vs 0.141 +/- 0.012 DA233/mg protein), lipid hydroperoxides (0.752 +/- 0.032 vs 0.443 +/- 0.03 nmol/mg protein), and lipid peroxides (3.447 +/- 0.14vs 1.456 +/- 0.096 nmol MDA/mg protein) than those of the unpolluted estuary during the summer. In contrast, significantly lower levels of superoxide dismutase (20.39 +/- 1.14 vs 53.63 +/- 1.48 units/mg protein) and catalase (116 +/- 6.87vs 153 +/- 8.92 units/mg protein) were detected in the liver of fish from the polluted estuary (Ennore) compared to fish from the unpolluted estuary (Kovalam) during the summer. Variations in most of the oxidative stress parameters were observed between the summer and monsoon seasons, indicating the importance of seasonal variation for estuaries and their inhabitants.

Oxidative stress in gill, erythrocytes, liver and kidney of Nile tilapia ( Oreochromis niloticus) from a polluted site

A comparison between some pro- and antioxidant parameters in erythrocyte, gill, liver and kidney of Nile tilapia, O. niloticus from a fish farm (Control group) and from a polluted site in the Billings Reservoir (Reservoir group) was done. No hematological alterations were observed in blood of Billings fish. The erythrocyte oxidative stress was characterized by increased oxygen uptake and decreased induction time (induced by t-butyl hydroperoxide, t-BHP) evidencing a higher susceptibility to oxidative damage. Moreover, beside the augmented erythrocyte superoxide dismutase (SOD), glucose-6-phosphate dehydrogenase (G6PDH) and glutathione peroxidase activities, a decrease in both catalase (CAT) activity and total glutathione content (GSH), in erythrocytes of Reservoir fish was observed. The higher cytochrome b 5 levels observed in the gill microsomal fraction is likely to be the cause of the enhanced oxyradical production. This fact, associated with the diminished CAT and G6PDH activities, accounts for a gill oxidative stress of Reservoir fish. Except for the NADPH-cytochrome P-450 (c) reductase activity, the other liver pro-oxidant parameters were greatly increased in the Reservoir fish. These results together with the increase in SOD activity and decrease in CAT, glutathione reductase (GR) and G6PDH activities indicated a liver oxidative stress status. The observed increases in kidney NADH cytochrome c reductase and in both cytochromes P-450 and b 5 contents were not reflected in enhanced oxyradical production, suggesting a well coupled P-450 catalytic cycle in this tissue. However, the antioxidant enzymes had a similar pattern in liver. The decrease in GSH observed in kidney is probably associated with conjugation reactions for subsequent excretion. All these results furnish useful data for future investigations of polluted aquatic sites in order to provide a data base relating the presence of pollutants to biological effects at a molecular level.