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Background/aims: Steroids have been shown to prevent intestinal oxidative stress. We investigated the effects of methylprednisolone on intestinal oxidative damage and bacterial translocation in thioacetamide-induced liver failure in rats., Materials and Methods: Group 1 (n=8) was the control group. In group 2 (n=8), the thioacetamide group, rats received 300 mg/kg intraperitoneal thioacetamide daily for 2 days. In group 3 (n=8), the thioacetamide+methylprednisolone group, treatment with methylprednisolone (30 mg/kg intraperitoneal) was commenced 48 h before the first dose of thioacetamide. In group 4 (n=8), the methylprednisolone group, the rats received only methylprednisolone (30 mg/kg intraperitoneal)., Results: Serious hepatic and intestinal oxidative damage and high bacterial translocation frequencies were observed in the thioacetamide group compared with those of the controls. Bacterial translocation frequency in the thioacetamide+methylprednisolone group was significantly lower than that in the thioacetamide group (p<0.05). Intestinal thiobarbituric acid-reactive substances and myeloperoxidase levels and tissue damage scores for the intestines in the thioacetamide+methylprednisolone group were lower than those in the thioacetamide group (p<0.01, p<0.01, and p<0.0001, respectively)., Conclusion: Our findings suggest that methylprednisolone reduces bacterial translocation by preventing intestinal oxidative damage in this model of acute liver failure in rats.

Aim/background: Pistacia terebinthus is used as a coffee substitute in the East and Southern Anatolia regions of Turkey. It contains unsaturated fatty acids, tocopherols, polyphenols and carotenoids. P. terebinthus has anti-inflammatory and potential antioxidant activity. In this study we evaluated the protective effects of P. terebinthus coffee (PTC) on thioacetamide (TAA)-induced liver injury in rats., Materials and Methods: Twenty-eight male Sprague-Dawley rats were equally randomized into four groups. Chronic liver injury was induced with TAA (100 mg/kg i.p. three times weekly). The first group of rats served as control and received only tap water (G1), and the remaining groups of rats received PTC, p.o (G2); TAA (G3); TAA plus PTC, p.o (G4), respectively., Results: After 8 weeks, PTC intake significantly reduced fibrosis/inflammation scores (p PTC intake reduced transforming growth factor beta (TGF-β) concentrations in the liver (p PTC intake., Discussion and Conclusion: PTC intake provided beneficial effects against TAA-induced liver injury in rats. PTC probably suppresses the proinflammatory cytokines through NF-κB signaling pathway.

Oxidative stress plays important role in the development of acute liver failure. In this study, we investigated effects of allopurinol (AP) upon thioacetamide (TAA)-induced liver injury and the potential mechanisms leading to amelioration in inflammation with AP treatment. Acute liver failure was induced by intraperitoneal administration of TAA (300 mg/kg/day for 2 days). Thirty-five rats were divided into five groups as control (group 1), TAA (group 2), TAA + 25AP (group 3), TAA + 50 AP (group 4), and TAA + 100AP (group 5). The number of animals in each group was seven. At the end of the study, histopathological, biochemical, and western blot analysis were done. TAA treatment significantly increased serum levels of aminotransferases, liver malondialdehyde (MDA), nuclear factor-kappa B (NF-қB ), activator protein-1 (AP-1), tumor necrosis factor-alpha (TNF-α), cyclooxygenase-2 (COX-2) and interleukin-6 (IL-6) levels, and the necro-inflammation scores. Nevertheless, nuclear factor E2-related factor-2 and heme oxygenase-1 (HO-1) expressions in the liver were decreased by TAA. AP treatment significantly lowered the serum levels of aminotransferases (P < 0.01) and liver MDA, NF-κB, AP-1, TNF-α, COX-2, and IL-6 expressions (P < 0.05). Moreover, AP restored the liver Nrf2 and HO-1 expressions and improved the necro-inflammation scores significantly. AP improves oxidative stress-induced liver damage by regulating cellular redox-sensitive transcriptor factors and expression of pro-inflammatory and antioxidant defense mechanisms. AP probably exerts these beneficiary features by its free radical scavenging ability in a dose-dependent manner.

Background and Study Aims: Oxidative stress plays an important role in development of intestinal injury after abdomino-pelvic radiation therapy. Teucrium polium (TP) is a medicinal plant which has antioxidant and anti-inflammatory properties. The aim of this study was to investigate the effect of TP on radiation-induced intestinal oxidative damage in rats., Materials and Methods: Group 1 (n = 8), the control group; Group 2 (n = 8), the RAD (radiation) group in which each rat received a single whole-body 800 cGy radiation performed with a LINAC ; Group 3 (n = 8), the RAD + TP group in which rats were exposed to radiation as in Group 2, followed by intragastric administration of 0.5 g/kg/daily TP extract for 7 consecutive days; and Group 4 (n = 8), the TP group, rats received only intragastric TP for 7 days., Results: Radiation led to intestinal damage, which was accompanied by an increase in intestinal thiobarbituric-acid-reactive substances (TBARS) and myeloperoxidase (MPO) levels, and a decrease in reduced glutathione (GSH) levels. Although TP significantly decreased intestinal MPO levels and inflammation scores, it neither reverted intestinal TBARS and GSH levels nor ameliorated other histological parameters of the disease., Conclusions: Our results suggest that TP reduces inflammation but does not ameliorate the increased oxidative stress conditions in radiation-induced intestinal damage in rats.

Abstract: Although proline is one of the major computable organic solutes that accumulate in many plant species in abiotic stresses, a hot debate continues about whether proline accumulation is a reaction to abiotic stress, or a plant''s response is associated with stress tolerance. The effects of proline on antioxidative system in grape leaves of Vitis vinifera L. cv., ‘Öküzgözü’ exposed to oxidative stress by H2O2 was investigated. Endogenous proline, hydrogen peroxide (H2O2), malondialdehyde (MDA) concentrations, percentage of electrolyte leakage (EL), and some of the antioxidant enzyme activities; such as superoxide dismutase (SOD), catalase (CAT), ascorbate peroxidase (APX), and guaiacol peroxidase (POD) were measured spectrophotometrically. Inhibitory effect of H2O2 on antioxidant enzyme activities, MDA, and EL was found. In the presence of proline, SOD and CAT activities decreased, while POD and APX activities increased. Proline pre-treatment resulted in a decrease in cellular H2O2 content, MDA, and EL, while cellular concentration of proline increased. Based on the finding, it was suggested that proline and H2O2 could play an important role in oxidative stress injury of grapevine leaves grown in vitro culture. Also, proline might have a direct positive effect on antioxidant enzyme system, membrane phase change, MDA, and EL. [Copyright &y& Elsevier]

Gingko biloba (GB) has antioxidant and platelet-activating factor (PAF) antagonistic effects. We investigated the protective effects of GB on thioacetamide (TAA)-induced fulminant hepatic failure in rats. Fulminant hepatic failure was induced in treatment groups by three intraperitoneal (ip) injections of TAA (350 mg/kg) at 24-hour intervals. Treatments with GB (100 mg/kg per day, orally) and N-acetylcysteine (20 mg/kg twice daily, sc) were initiated 48 hours prior to TAA administration. The liver was removed for histopathological examinations. Serum and liver thiobarbituric acid-reactive substance (TBARS) levels were measured for assessment of oxidative stress. Liver necrosis and inflammation scores and serum and liver TBARS levels were significantly higher in the TAA group compared to the control group (P <0.001, <0.001, 0.001, <0.001, respectively). Liver necrosis and inflammation scores and liver TBARS levels were significantly lower in the GB group compared to the TAA group (P <0.001, <0.001 and 0.01, respectively). GB ameliorated hepatic damage in TAA-induced fulminant hepatic failure. This may be due to the free radical-scavenging effects of GB. [ABSTRACT FROM AUTHOR]