Superoxide Dismutase In Liver Tissue Research Articles

Effects of Organic Apricot on Liver Regeneration After Partial Hepatectomy in Rats

BackgroundThe present study investigated the effects of (sun-dried organic apricot/SDOA) supplementation in chow on liver regeneration after partial hepatectomy/(PH) in rats. MethodIn this study, 28 female rats were randomized into four groups. On the 7th day of the study, group 1 underwent laparoscopic intervention while a PH was performed on the other three cohorts. On day 28, all rats were humanely killed. Blood and liver tissue samples were subjected to biochemical determinations, histological examinations, and measurement of tissue oxidative stress enzyme activity. ResultsSerum levels of alanine transaminase (ALT), alkaline phosphatase (ALP), and liver tissue glutathione (GSH) activities were affected by PH and/or SDOA consumption (P < .05). Moderately staining cell counts in group 4 were significantly different from the other three groups (P < .05). However, no significant differences were detected among all groups in regard to aspartate aminotransferase (AST) serum levels or liver tissue superoxide dismutase (SOD), malondialdehyde (MDA), catalase (CAT) or glutathione peroxidase (GSHpx) activities (P < .05). ConclusionThe 5% SDOA supplementation over a 21-day feeding period showed a beneficial effect on liver regeneration in rats, as reflects by Ki-67 finding although there was no change in ALT or ALP or in liver tissue GSH activity.

Effect of Ginger Extract on Liver Damage in Experimental Obstructive Jaundice Produced by Main Bile Duct Ligation

Background : Obstructive jaundice is one of the most important surgical causes of childhood jaundices. The aim of this study is to investigate effects of ginger (Gingiber officinalis) extracts on liver damage in experimental obstructive jaundice produced by main bile duct ligation.Materials and Methods : Forty two Wistar-albino rats were randomly allocated into 7 groups (n = 6). Nothing was performed in the control (C) group. Only laparatomy was performed in the sham (Sh) group. The ginger 1 and 2 (Gi and G2) groups received only 100 and 200 mg/kg/day doses of ginger extract for 1 week orally. In study group, common bile duct ligation was done. In treatment 1 and 2 (T and T2) groups common bile duct ligation was followed by administration of 100 and 200 mg/kg/day doses of ginger extract for 1 week orally from the third post operative day, respectively. Blood samples and liver were harvested in order to evaluate the serum aspartate aminotransferase (AST), alanine amino transferase (ALT), gama glutamyltransferase (GGT), total bilirubin (bil), superoxide dismutase (SOD), glutathione (GSH), malondialdehyde (MDA) and liver tissue SOD, GSH, MDA levels and liver apoptosis. Results were analyzed by Mann-Whitney U test statistically.Results : Ginger administration did not result in any differences of serum or tissue levels of the studied parameters and liver apoptosis between the groups statistically (except AST levels in group T2). Tissue GSH and serum SOD levels were only mildly increased in groups receiving ginger alone.Conclusions : There is no evidence for protective, inhibitive and decreasing effects of ginger extract on liver injury in experimental obstructive jaundice with these findings.

The effects of L-carnitine and N-acetylcysteine on carbontetrachloride induced acute liver damage in rats

To investigate the effects of L-carnitine (LCAR) and N-acetylcysteine (NAC) on carbon tetrachloride (CCl4)-induced acute liver damage in rats. Totally, 40 rats in 5 groups were included in the study. The first group was the control group. Group 2 received CCl4 (2 ml/kg). Group 3 was given CCl4 + NAC (150 mg/kg). The rats in the Group 4 were administered CCl4 + LCAR (100 mg/kg), and the rats in the Group 5 were given CCl4 + NAC + LCAR. Both CCl4 and the treatment protocols were administered via intraperitoneal route for 10 days. Tissue oxidative stress and antioxidant markers were investigated in liver tissue and serum liver enzymes were measured. The levels of blood liver enzymes (ALT and AST) increased significantly in the Group 2. However, they decreased markedly in all treatment groups. While malondialdehyde and myeloperoxidase levels in the liver tissue samples increased significantly in the 2nd group, those levels were determined to be decreased significantly in all treatment groups. When the liver tissue antioxidant levels were evaluated; reduced glutathione and catalase decreased markedly in the 2nd group, but increased following the administration of NAC and LCAR. The activities of liver tissue superoxide dismutase did not differ significantly among the groups. In the histopathologic evaluation of liver tissues, on the other hand, diffuse hepatosteatosis was observed in all groups except the control group and there was no significant difference among the groups from the point of steatosis. LCAR and NAC were concluded to have beneficial effects on the acute liver damage induced by CCl4 administration (Tab. 1, Fig. 5, Ref. 52). Text in PDF www.elis.sk.

Effects of Erdosteine in Experimental Sepsis Model in Rats

Objective Erdosteine is a mucolytic agent that is known to possess antioxidant effects. This study investigated the effects of erdosteine on endothelin-1 (ET-1) levels and oxidative stress parameters superoxide dismutase (SOD) and malondialdehyde (MDA) in a rat sepsis model. Methods Four groups of Wistar albino rats (n=8 per group) were randomly allocated to the following groups: sham (group 1), sepsis (group 2), erdosteine control (group 3) and a sepsis group pretreated with erdosteine (group 4). Sepsis was induced using E. Coli ATCC 25922 inoculation. Serum ET-1, liver tissue SOD and MDA levels were determined in all groups. Results ET-1 levels were significantly higher in group 2 compared to groups 1, 3 and 4 (p&lt;0.001, p=0.002 and p&lt;0.001, respectively). Similarly, MDA levels in groups 1, 3 and 4 were significantly lower relative to group 2 (p&lt;0.001, p=0.022 and p=0.010, respectively). Additionally, SOD activities in these same three groups were found to be significantly higher than those in group 2 (p&lt;0.001, p=0.004 and p=0.028, respectively). Conclusion In conclusion, erdosteine decreases ET-1 levels and ameliorates oxidative stress parameters induced by sepsis in an experimental rat model of sepsis.

Hepatoprotective effect of ghrelin on carbon tetrachloride-induced acute liver injury in rats

Background & AimsRecent studies have revealed that ghrelin may be an antioxidant and antiinflammatory agent. Oxidative stress are considered to play a prominent causative role in the development of various hepatic disorders. We investigated whether ghrelin plays a protective role against carbon tetrachloride (CCl4)-induced acute liver injury in rats. MethodsForty adult male Sprague–Dawley rats were randomly divided into four equal groups as; control, ghrelin, CCl4 and ghrelin plus CCl4. Evaluations were made for lipid peroxidation, enzyme activities and biochemical parameters. Pathological histology was also performed. ResultsCCl4 treatment increased plasma and liver tissue malondialdehyde (MDA) content and plasma nitric oxide (NO) level, and decreased erythrocyte and liver tissue superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) activities when compared to control group. At the same time, CCl4 treatment increased the serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alcaline phosphatase (ALP) activities. By contrast, ghrelin pretreatment reduced plasma and liver MDA content and plasma NO level, and increased erythrocyte and liver tissue SOD, CAT and GPx activities when compared with CCl4-treated group. Moreover, both ghrelin alone and ghrelin plus CCl4 treatment elevated serum glucose level. The CCl4-induced histopathological changes were also reduced by the ghrelin pretreatment. ConclusionOur results show that ghrelin can be proposed to protect the liver against CCl4-induced oxidative damage in rats, and the hepatoprotective effect may be correlated with its antioxidant and free radical scavenger effects.

Protective effect of probucol on liver injury induced by carbon tetrachloride in rats

To explore protective effect of probucol on liver injury induced by carbon tetrachloride (CCl4) in rats. We used CCl4 to induce a rat model of liver injury. Some of those rats were treated with an oral administration of probucol. Liver function, blood lipid, liver tissue malondialdehyde (MDA), superoxide dismutase (SOD), and degree of liver fibrosis were analyzed. Probucol significantly decreased the elevation of serum aspartate transaminase, total bile acid, alkaline phosphatase and cholesterol, and improved liver histopathological changes (including fatty infiltration, inflammation cell infiltration, and fibrosis), decreased liver tissue MDA level, and increased liver tissue SOD level in liver injury rats. For the first time, we demonstrated that probucol has protective effect against liver injury in animal experiment. The antioxidant action of probucol may play an important role in its hepatoprotective mechanism. Probucol also can reduce serum cholesterol. Thus, probucol may have the potential use in clinical liver diseases in which oxidative stress may be present, especially for the patients with hypercholesterolemia.

Sulforaphane protects liver injury induced by intestinal ischemia reperfusion through Nrf2-ARE pathway

To investigate the effect of sulforaphane (SFN) on regulation of NF-E2-related factor-2 (Nrf2)-antioxidant response element (ARE) pathway in liver injury induced by intestinal ischemia/reperfusion (I/R). Rats were divided randomly into four experimental groups: control, SFN control, intestinal I/R and SFN pretreatment groups (n = 8 in each group). The intestinal I/R model was established by clamping the superior mesenteric artery for 1 h and 2 h reperfusion. In the SFN pretreatment group, surgery was performed as in the intestinal I/R group, with intraperitoneal administration of 3 mg/kg SFN 1 h before the operation. Intestine and liver histology was investigated. Serum levels of aspartate aminotransferase (AST), and alanine aminotransferase (ALT) were measured. Liver tissue superoxide dismutase (SOD), myeloperoxidase (MPO), glutathione (GSH) and glutathione peroxidase (GSH-Px) activity were assayed. The liver transcription factor Nrf2 and heme oxygenase-1 (HO-1) were determined by immunohistochemical analysis and Western blotting analysis. Intestinal I/R induced intestinal and liver injury, characterized by histological changes as well as a significant increase in serum AST and ALT levels (AST: 260.13 +/- 40.17 U/L vs 186.00 +/- 24.21 U/L, P < 0.01; ALT: 139.63 +/- 11.35 U/L vs 48.38 +/- 10.73 U/L, P < 0.01), all of which were reduced by pretreatment with SFN, respectively (AST: 260.13 +/- 40.17 U/L vs 216.63 +/- 22.65 U/L, P < 0.05; ALT: 139.63 +/- 11.35 U/L vs 97.63 +/- 15.56 U/L, P < 0.01). The activity of SOD in the liver tissue decreased after intestinal I/R (P < 0.01), which was enhanced by SFN pretreatment (P < 0.05). In addition, compared with the control group, SFN markedly reduced liver tissue MPO activity (P < 0.05) and elevated liver tissue GSH and GSH-Px activity (P < 0.05, P < 0.05), which was in parallel with the increased level of liver Nrf2 and HO-1 expression. SFN pretreatment attenuates liver injury induced by intestinal I/R in rats, attributable to the antioxidant effect through Nrf2-ARE pathway.

Prophylaxis with carnosol attenuates liver injury induced by intestinal ischemia/reperfusion

To investigate the possible protective effects of carnosol on liver injury induced by intestinal ischemia reperfusion (I/R). Rats were divided randomly into three experimental groups: sham, intestinal I/R and carnosol treatment (n = 18 each). The intestinal I/R model was established by clamping the superior mesenteric artery for 1 h. In the carnosol treatment group, surgery was performed as in the intestinal I/R group, with intraperitoneal administration of 3 mg/kg carnosol 1 h before the operation. At 2, 4 and 6 h after reperfusion, rats were killed and blood, intestine and liver tissue samples were obtained. Intestine and liver histology was investigated. Serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT) and interleukin (IL)-6 were measured. Liver tissue superoxide dismutase (SOD) and myeloperoxidase (MPO) activity were assayed. The liver intercellular adhesion molecule-1 (ICAM-1) and nuclear factor kappaB (NF-kappaB) were determined by immunohistochemical analysis and western blot analysis. Intestinal I/R induced intestine and liver injury, characterized by histological changes, as well as a significant increase in serum AST and ALT levels. The activity of SOD in the liver tissue decreased after I/R, which was enhanced by carnosol pretreatment. In addition, compared with the control group, carnosol markedly reduced liver tissue MPO activity and serum IL-6 level, which was in parallel with the decreased level of liver ICAM-1 and NF-kappaB expression. Our results indicate that carnosol pretreatment attenuates liver injury induced by intestinal I/R, attributable to the antioxidant effect and inhibition of the NF-kappaB pathway.

The Effect of Seaweed Eucheuma cottonii on Superoxide Dismutase (SOD) Liver of Hypercholesterolemic Rats

Intracellular antioxidant superoxide dismutase (SOD) was reported decreased in the liver and kidney of hypercholesterolemic rats. This study was conducted to observe the effect of seaweed Eucheuma cottonii powder on the profile of blood cholesterol and the level of SOD in liver tissues of hypercholesterolemic rats by using immunohistochemical technique. Twenty male Wistar rats were used for this study. Those rats were divided into four groups; (i) negative control group (A), (ii) hypercholesterolemia group treated by 5% seaweed powder (B), (iii) hypercholesterolemia group treated by 10% seaweed powder (C), and (iv) Positive control group or hypercholesterolemia group (D). The experiment was carried out for 35 days. Hypercholesterolemia condition (> 130 mg/dl), except group A, was achieved by feeding the rats with commercial diet containing 1% cholesterol. Drinking water was given ad libitum for 40 days. The results showed that seaweed powder decreased the total cholesterol, low density lipoprotein (LDL), triglyceride, and increased the level of high density lipoprotein (HDL) and SOD status in the liver tissues of hypercholesterolemic rats. The treatment of 10% seaweed powder gave better results than that of 5%. These results suggested that dietary fiber such in the seaweed powder has antioxidant activity.

Hypothetical mode of action of earthworm extract with hepatoprotective and antioxidant properties

The hepatoprotective potential of earthworm extract (EE) (Lampito mauritii, Kinberg) was evaluated against paracetamol-induced liver injury in Wistar albino rat, in comparison with silymarin, the standard hepatoprotective drug. We observed a reduction in liver antioxidants, such as glutathione (GSH), superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT) and in serum total protein, and an increase in serum alkaline phosphatase (ALP), serum aspertate aminotranferase (AST), serum alanine aminotranferase (ALT), bilirubin and liver thiobarbituric acid reactive substances (TBARS) due to liver injury in the paracetamol-administered rats (2 g/kg). On the contrary, increased activities of liver GSH, SOD, GPx, CAT and serum total protein level, and decrease in the contents of serum ALP, AST, ALT, bilirubin and liver TBARS were observed in rats administered with different doses of EE (100, 200 and 300 mg/kg), which are similar to the activities of hepatoprotective drug silymarin (150 mg/kg). The mode of action of EE as evidenced by the above parameters may suggest that EE, on the one hand, prevents the formation of the reactive oxygen groups, or scavenges these groups, thereby preventing the damage on the hepatic cells, and, on the other hand, modulates the genes responsible for synthesis of antioxidant enzymes such as GPx, CAT and SOD in liver tissue and decreases the serum enzymatic activities such as ALP, AST and ALT.

Potential effects of L-NAME on alcohol-induced oxidative stress

Nitric oxide (NO) is a highly reactive oxidant synthesized from L-arginine by nitric oxide synthase (NOS). NO may cause injury through the generation of potent radicals. Nw- nitro-L-arginine methyl ester (L-NAME) is a non-selective inhibitor of NOS. We aimed to evaluate whether L-NAME treatment had protective effects against oxidative stress in rats intragastrically fed with ethanol during a 4 wk-period. Thirty-six male Wistar rats were divided into 3 equal groups: group 1 (control group-isocaloric dextrose was given), group 2 (6 g/kg.d ethanol-induced group) and group 3 (both ethanol 6 g/kg.d and L-NAME 500 mg/L in drinking water-given group). Animals were sacrificed at the end of 4 wk-experimental period, and intracardiac blood and liver tissues were obtained. Biochemical measurements were performed both in plasma and in homogenized liver tissues. Alanine amino transferase (ALT), aspartate amino transferase (AST), malondialdehyde (MDA), NO, superoxide dismutase (SOD), catalase (CAT) and glutathione (GSH) levels were measured by spectrophotometry. ALT and AST in group 2 (62 U/L and 128 U/L, respectively) were higher than those in group 1 (24 U/L and 38 U/L) and group 3 (37 U/L and 81 U/L) (P<0.001 for both). Plasma and tissue levels of MDA in group 2 (4.66 micromol/L and 0.55 nmol/mg protein) were higher than in group 1 (2.65 micromol/L and 0.34 nmol/mg protein) and group 3 (3.43 micromol/L and 0.36 nmol/mg protein) (P<0.001 for both). Plasma and liver tissue levels of NO in group 2 (54.67 micromol/L and 586.50 nmol/mg protein) were higher than in group 1 (34.67 micromol/L and 435.33 nmol/mg protein) and group 3 (27.50 micromol/L and 412.75 nmol/mg protein) (P<0.001 for both). Plasma and liver tissue SOD activities in group 2 (15.25 U/mL and 5.38 U/ mg protein, respectively) were lower than in group 1 (20.00 U/mL and 8.13 U/ mg protein) and group 3 (19.00 U/mL and 6.93 U/ mg protein) (P<0.001 for both). Plasma and liver tissue CAT activities in group 2 (145 U/mL and 37 U/ mg protein, respectively) were lower than in group 1 (176 U/mL and 73 U/mg protein) and group 3 (167 U/mL and 61 U/mg protein) (P<0.001 for both). Meanwhile, erythrocytes and liver tissue levels of GSH in group 2 (4.12 mg/g Hb and 5.38 nmol/mg protein, respectively) were lower than in group 1 (5.52 mg/g Hb and 4.49 nmol/mg protein) and group 3 (5.64 mg/g Hb and 4.18 nmol/mg protein) (P<0.001 for both). Our findings show that L-NAME may produce a restorative effect on ethanol-induced liver damage via decreasing oxidative stress and increasing antioxidant status.

Relationship between superoxide dismutase (SOD) and viral liver diseases.

Immunohistochemical evaluation of Cu, Zn- and Mn-superoxide dismutase (SOD) activity in various viral liver diseases was performed by the peroxidase-conjugated antibody indirect method. Anti-human Cu, Zn-SOD (rabbit) and anti-human Mn-SOD (guinea-pig) derived and purified from SOD of human erythrocytes and placentas were used to determine SOD distribution in liver tissues. SOD in the liver tissues was detected in 68 inpatients of our unit. They consisted of 23 cases with chronic hepatitis caused by hepatitis B virus (13) and hepatitis C virus (10), 24 with liver cirrhosis caused by hepatitis B virus (5) and hepatitis C virus (19) (15: compensatory, 9: decompensatory) and 21 with hepatocellular carcinoma caused by hepatitis B virus (2) and hepatitis C virus (18) complicated of liver cirrhosis. In viral liver diseases, SODs in the liver tissues were distributed to hepatocytes mainly in the pattern of cytoplasmic diffusion. The incidence of immunohistochemical Cu, Zn-SOD and Mn-SOD were 47.8% and 56.5% in chronic hepatitis, 93.3% and 86.7% in compensated liver cirrhosis, 11.1% and 22.2% in decompensated liver cirrhosis, respectively. The aggression of viral liver disease was accompanied with the decrease of SOD concentration in the liver tissues. Hepatocellular carcinoma cells were negative for Mn-SOD in all cases, and weakly positive for Cu, Zn-SOD in 2 out of 21 cases. Comparatively strongly positive SOD findings were obtained from normal regions neighboring carcinomas. A close relationship between the depletion of SOD in liver tissues and carcinogenesis in viral liver diseases was observed.

Activities, electrophoretic profiles and immunolocalization of superoxide dismutase in human liver specimens.

In order to elucidate active oxygen in liver diseases, activities, electrophoretic profiles and immunolocalization of superoxide dismutase (SOD) in human liver specimens were investigated. Activities and electrophoresis were studied using liver homogenates in 41 cases and immunolocalization of Cu, Zn SOD was observed in 87 cases. Total SOD activity in acute viral hepatitis (AVH) and fatty liver (FL) groups was significantly lower than that in non-specific reactive hepatitis (NSRH) group. Cu, Zn SOD activity in AVH, FL and chronic active hepatitis (CAH) groups was also significantly lower than that in NSRH group. However, no difference of Mn SOD activity, was found between NSRH group and others. Decreased activity of superoxide dismutase in liver tissues suggests the release of this enzyme from the injured hepatocytes. In electrophoretic patterns of superoxide dismutase, 3 bands of Cu, Zn SOD isozymes and 8 to 10 bands of Mn SOD isozymes were recognized. Immunocytochemical investigation revealed the localization of Cu, Zn SOD in the cytoplasm of hepatocytes. Two different distribution of Cu, Zn SOD was observed in the lobules: a diffuse localization pattern and a focal one. The latter was found in the cases of liver diseases with severe parenchymal lesion. These findings suggest that superoxide radical anion and its scavenger, superoxide dismutase, may play an important role in the pathogenesis of liver cell necrosis.