The Effects of Hyperbaric Oxygen at Different Pressures on Oxidative Stress and Antioxidant Status in Rats.

Background: The optimal use of oxygen at greater than atmospheric pressures in any operational or therapeutic application (hyperbaric oxygen, HBO2) requires awareness of the fact that the beneficial effects of oxygen coexist with toxic effects depending on the pressure and duration of exposure. In this study, we aimed to investigate the effect of HBO2 therapy on oxidative stress and antioxidant status in commonly used protocol for acute HBO2 indications, such as carbon monoxide intoxication, central retinal artery occlusion, crush injury, gas gangrene, and to compare it with normobaric oxygen (NBO2) in healthy rats. Materials and Methods: Fifty-six male, young adult Wistar albino rats were randomly divided into seven groups and named as Group I through Group VII. Plasma malondialdehyde (MDA), superoxide dismutase (SOD), and erythrocyte glutathione (GSH) levels in control group were compared to the levels in other groups. Results: The increases in MDA levels and the decrease in SOD activities were statistically significant in HBO2 groups at the end of the first 24 h when compared to the control group, and the significant decrease in erythrocyte GSH level was only at 2.4 atmospheres absolute. Conclusions: The present study showed that pressure and frequency of exposure are important factors to consider when investigating HBO2-induced oxidative stress and antioxidant response.

Effects of Quercetin on Lipid and Protein Damage in the Liver of Streptozotocin-Induced Experimental Diabetic Rats.

Quercetin (QR) is part of a subclass of flavonoids called flavonols. We aimed to investigate the effect of QR on malondialdehyde (MDA), advanced oxidation protein products (AOPPs), and glutathione peroxidase (GSH-Px) activity in the liver of diabetic rats. We compared four groups of male adult Wistar albino rats: a control group, an untreated diabetic group, diabetic groups treated with QR, and QR group. Diabetes was induced by a single injection of streptozotocin (STZ) (50 mg/kg). Animals were kept in standard condition. On the 31st day of the study, the liver tissue was removed for biochemical parameters and histopathological evaluations. In an untreated diabetic group, liver MDA and AOPP levels were significantly higher than all groups. QR treatment significantly decreased the increased MDA, AOPP levels, and increased the decreased GSH-Px enzyme activity in liver tissues. The QR-treated rats in the diabetic group showed an improved histological appearance. Lesser vesicular vacuolization and fibrotic areas were observed in the QR-treated diabetic group than in the diabetic group. The STZ-induced liver injury is associated with oxidative stress, and coadministration of QR may reduce this damage effectively in a rat model. Our results are also supported by morphological improvement in liver tissue. Therefore, we think QR may be effective in treating hyperglycemia and oxidative damage in diabetes.

Selenium supplementation ameliorates electromagnetic field-induced oxidative stress in the HEK293 cells.

There is a widespread use of 2.4 GHz electromagnetic radiation emitting devices especially in communication and education. Recent studies show the adverse effects of electromagnetic fields (EMF) such as oxidative stress, cellular damage and apoptosis on tissues. Selenium (Se) has an antioxidant properties by inhibiting oxidative damage being within the structure of antioxidant enzymes like glutathione peroxidase (GSH-Px) and it has also regulatory function for cell cycle and apoptosis. The aim of this study was to investigate the effect of Se on 2.4 GHz frequency EMF exposed human embryonic kidney cells (HEK293) by means of alterations in apoptotic and oxidative stress parameters. Our study was planned as control, EMF, 100 nM Se + EMF, 200 nM Se + EMF groups. EMF groups were exposed to 2.4 GHz EMF for 1 h, element groups were incubated with two different doses of Se added cell culture medium for 48 h before EMF exposure. MDA levels were significantly higher whereas SOD and GSH-Px activities were significantly lower in EMF compared to control. 100 and 200 nM Se + EMF application decreased MDA levels, increased SOD and GSH-Px activities than EMF. Apoptosis and caspase-3 were statistically significantly higher but bcl-2 was lower in EMF than control. Apoptosis and caspase-3 were lower in 100 and 200 nM Se + EMF, although bcl-2 were higher than EMF. In conclusion, Se has protective effects against 2.4 GHz EMF-induced oxidative stress by reducing lipid peroxidation, regulating SOD and GSH-Px activity. Also, Se has inhibitory effect on 2.4 GHz EMF induced apoptosis by increasing the expression of anti-apoptotic protein bcl-2 and suppressing apoptosis regulatory protein caspase-3.

The Effects of Hyperbaric Oxygen Treatment on Total Antioxidant Capacity and Prolidase Activity after Bile Duct Ligation in Rats.

BACKGROUND: Hyperbaric oxygen (HBO) therapy may improve cholestasis, increase hepatic regeneration, and decrease oxidative stress in liver. In this study, we aimed to investigate the effects of HBO therapy on hepatic oxidative stress parameters, such as total thiol groups (T-SH), protein carbonyl (PCO), and total antioxidant capacity (TAC) as well as the predictive value of the noninvasive biochemical marker, sialic acid (SA), and prolidase activity in bile duct ligation (BDL)-induced oxidative damage and fibrosis in rats. METHODS: We divided 32 adult male Sprague Dawley rats into four groups: sham, sham + HBO, BDL, and BDL + HBO; each group contained eight animals. We placed the sham + HBO and BDL + HBO groups in an experimental hyperbaric chamber, in which we administered pure oxygen at 2.5 atmospheres for 90 min on 14 consecutive days. RESULTS: The application of BDL significantly increased PCO levels and prolidase activity, and decreased T-SH and TAC levels. HBO significantly decreased PCO levels and prolidase activity and increased T-SH and TAC levels in the liver tissues. There was no significant difference in sialic acid levels between any groups. CONCLUSIONS: These results indicate that HBO therapy has hepatoprotective effects on BDL-induced injury by decreasing PCO and prolidase activity and increasing antioxidant activities. We therefore suggest that HBO therapy may be useful after BDL-induced injury.

Hemostasis vs. epidural fibrosis?: A comparative study on an experimental rat model of laminectomy.

AIM: The aim of this study was to evaluate the histopathological and biochemical impact and effectiveness of two hemostatic agents, Ankaferd blood stopper (ABS) and Microporous Polysaccharide Hemospheres (MPH), on epidural fibrosis in an experimental rat laminectomy model. MATERIAL AND METHODS: Twenty adult Wistar albino rats were divided into MPH-treated (n=6), ABS-treated (n=6) and control (n=8) groups. Laminectomy of the lumbar spine was performed in all animals and treatment groups were exposed to MPH and ABS while closure was applied in control group as per usual. Epidural fibrosis was evaluated in all groups macroscopically, histopathologically, biochemically and with electron microscopy four weeks later. RESULTS: Statistically, it was found that MPH-treated group had significantly less epidural fibrosis compared to ABS-treated and control groups. CONCLUSION: We compared two hemostatic agents for their propensity to cause adhesions in the present study. Our results show that MPH significantly reduces epidural scar formation and dural adhesion in a rat model of laminectomy while ABS increases postoperative fibrosis.

The effect of coenzyme Q10 on venous ischemia reperfusion injury.

BACKGROUND: Coenzyme Q10 (CoQ10) is a lipid-soluble benzoquinone with antioxidant features that make it important in the treatment of ischemia reperfusion injury. In this study, we aimed to investigate the beneficial effect of CoQ10 in the treatment of venous ischemia/reperfusion injury. METHODS: Eighteen Sprague-Dawley male rats were randomly divided into two equal groups: the control group and an experimental group (n = 9 rats). The experimental group received CoQ10 orally, and the control group received a control diet for 8 wk. An inferior epigastric island flap was raised, and the inferior epigastric vein was clamped for 9 h; the flap was then reperfused. All rats were sacrificed on postoperative day 5. The flap survival rate and levels of CoQ10, malondialdehyde, glutathione, and superoxide dismutase were assessed, and flap tissues were examined under a light microscope (×200 magnification) after being stained with Hematoxylin & Eosin. RESULTS: The flap survival rate and levels of CoQ10, glutathione, and superoxide dismutase were significantly higher, but level of malondialdehyde was lower in the experimental group. The mean flap survival rates and plasma levels of CoQ10 were 51% ± 24% and 251 ± 11 ng/mL in the control group, whereas they were 88% ± 7% and 692.8 ± 79.7 ng/mL in the experimental group with statistically significant differences (P < 0.001). Polymorphonuclear leukocyte infiltration was higher, and surface epithelial integrity was more impaired in the control group. CONCLUSIONS: We concluded that CoQ10 supplementation has a beneficial effect on venous ischemia and/or reperfusion injury and improves flap survival rate.

Antioxidant and renoprotective effects of sphingosylphosphorylcholine on contrast-induced nephropathy in rats.

Contrast induced nephropathy (CIN) is a major cause of morbidity, and increased costs as well as an increased risk of death. This study was evaluated effects of exogenous sphingosylphosphorylcholine (SPC) administration on CIN in rats. Eight animals were included in each of the following eight groups: control, control phosphate-buffered solution (PBS), control SPC 2, control SPC 10, CIN, CIN PBS, CIN SPC 2 and CIN SPC 10. The induced nephropathy was created by injected with 4 g iodine/kg body weight. SPC was administered 3 d at a daily two different doses of 2 µm/mL and 10 µm/mL intraperitoneally. The severity of renal injury score was determined by the histological and immunohistochemical changes in the kidney. Malondialdehyde (MDA), nitric oxide (NO) and superoxide dismutase (SOD) were determined to evaluate the oxidative status in the renal tissue. Treatment with 2 and 10 µM SPC inhibited the increase in renal MDA, NO levels significantly and also attenuated the depletion of SOD in the renal injuryCIN. These data were supported by histopathological findings. The inducible nitric oxide synthase positive cells and apoptotic cells in the renal tissue were observed to be reduced with the 2 and 10 µM SPC treatment. These findings suggested that 2 and 10 µM doses can attenuate renal damage in contrast nephropathy by prevention of oxidative stress and apoptosis. The low and high dose SPC may be a promising new therapeutic agent for CIN.

Fluoxetine ameliorates imbalance of redox homeostasis and inflammation in an acute kidney injury model.

Ischemia-reperfusion (IR) has been reported to be associated with augmented reactive oxygen radicals and cytokines. Currently, we aimed to examine the influence of fluoxetine, which is already used as a preoperative anxiolytic, in the context of IR induced by occlusion of infrarenal abdominal aorta (60 min of ischemia) and its effects on renal oxidative status, inflammation, renal function, and cellular integrity in reperfusion (120 min post-ischemia). Male rats were randomly assigned as control, IR, and pretreated groups. The pretreated group animals received fluoxetine (20 mg/kg, i.p.) once daily for 3 days. Renal tissue oxidative stress, myeloperoxidase activity, proinflammatory cytokines (tumor necrosis factor-α, interleukin-1ß, interleukin-6), histology, and function were assessed. As an anti-inflammatory cytokine, interleukin-10 was also assessed. IR led to a significant increase in lipid hydroperoxide, malondialdehyde, and pro-oxidant antioxidant balance and decrease in superoxide dismutase activity and ferric reducing/antioxidant power level (p < 0.05), but fluoxetine was able to restore these parameters. High concentrations of tumor necrosis factor-α, interleukin-1ß, interleukin-6, and myeloperoxidase activity caused by IR were significantly decreased in kidney tissue with fluoxetine. In addition, interleukin-10 levels were high in fluoxetine pretreated group. IR resulted in disrupted cellular integrity, infiltration of tissue with leukocytes, and decreased serum creatinine-urea levels (p < 0.05). Fluoxetine significantly restored impaired redox balance and inflammation parameters of rats subjected to IR to baseline values. This beneficial effect of fluoxetine on redox balance might be addressed to an improvement in renal function.

Effects of Ankaferd on anastomotic healing of colon.

BACKGROUND: Ankaferd (Ankaferd blood stopper®, ABS) is a recently developed topical hemostatic agent. ABS is a standardized mixture of the plants Thymus vulgaris, Glycyrrhiza glabra, Vitis vinifera, Alpinia officinarum, and Urtica dioica. Through its effects on the endothelium, blood cells, angiogenesis, cellular proliferation, vascular dynamics, and cell mediators; Ankaferd plays a part in inflammation and hemostasis processes. The aim of this experimental study is to assess the effects of ABS on the left colonic anastomoses under normal, septic, and ischemic conditions. METHODS: Forty-eight Wistar Albino male rats were divided into six weight-matched equal groups: A, anastomosis in normal condition (n = 8); AA, anastomosis with ABS in normal condition (n = 8); AS, anastomosis in septic condition (n = 8); AAS, anastomosis with ABS in septic condition (n = 8); AI, anastomosis in ischemic condition (n = 8); and AAI, anastomosis with ABS in ischemic condition (n = 8). Blood and tissue samples were taken for the histopathological and biochemical studies after the anastomotic bursting pressures were measured. RESULTS: Higher hydroxyproline levels (p = .048) and angiogenesis (p = .038) were observed in the sepsis-induced rats compared to the control group. The inflammatory activity, fibrosis, and granulation were comparable in all experimental groups. Ankaferd improved the angiogenesis under septic conditions (AAS) when compared to the control group (AI; p = .038). CONCLUSIONS: ABS may support anastomotic healing in septic conditions. Topical ABS application controlling the mucosal bleeding at the cut ends of the colon may also improve the anastomotic wound healing by means of increasing mechanical strength and positively affecting angiogenesis. Further studies shall focus on the clinical importance of those findings.

The effects of atorvastatin on oxidative stress in L-NAME-treated rats.

OBJECTIVES: Current evidence suggests that the beneficial vascular effects of statins are not limited to the statins' lipid-lowering properties; these drugs can also improve vascular endothelial cell function. Nω-nitro-l-arginine methyl ester (L-NAME) is a potent synthetic nitric oxide inhibitor, and long-term oral L-NAME treatment is used to induce vascular lesions in experimental animal models. METHODS: We determined the effects of statins on protein carbonyl (PCO), lipid hydroperoxides (LHP), oxidized low-density lipoproteins (ox-LDL) and antioxidants such as paraoxonase 1 (PON1) and total thiols (T-SH) in long-term L-NAME-treated rats. Adult male Wistar rats were divided into three groups, namely, control, L-NAME-treated (1 mg/mL in drinking water for three weeks), and atorvastatin plus L-NAME-treated (4 mg/kg/day atorvastatin for 1 week during the third week of L-NAME treatment) groups. RESULTS: In the L-NAME group, the ox-LDL, LHP and PCO were higher and the PON1 and T-SH were lower than the concentrations observed for the controls. When compared with the L-NAME group, the L-NAME plus atorvastatin group had significantly lower ox-LDL and LHP and higher PON1 activities. Additionally, the elevated total cholesterol (TC) and low-density lipoprotein-C (LDL-C) in the L-NAME group were decreased by atorvastatin administration. TC and LDL-C were positively correlated with ox-LDL and LHP and negatively correlated with PON1 in all groups. High-density lipoprotein-C (HDL-C) was negatively correlated with ox-LDL. CONCLUSION: PON1 prevents LDL oxidation and inactivates LDL-derived oxidized phospholipids; its activity showed a pronounced decrease in the L-NAME treatment group and was increased in the atorvastatin group. Based on our findings, we concluded that the atorvastatin had HDL-related antioxidant activity as well as lipid-lowering properties.

Effects of curcumin on proinflammatory cytokines and tissue injury in the early and late phases of experimental acute pancreatitis.

BACKGROUND & AIMS: Acute pancreatitis (AP) varies from mild to severe necrotizing changes with high mortality. The objective of the current study was to investigate the effects of curcumin on tissue injury and proinflammatory cytokines in the early and late phases of AP. METHODS: AP was induced by sodium taurocholate in rats (n = 140). First group was left untreated. Group II received 100 mg/kg curcumin daily starting 20 days before AP induction. The rats were allocated into 7 sub-groups (n:5) and were sacrificed at 2, 6, 12, 24, 72, 144 and 288 h following the induction of AP. Blood and pancreatic tissue samples were collected for biochemical and histopathologic evaluations and the assessment of protein and mRNA levels, as well. RESULTS: Curcumin decreased total histopathologic scores in comparison with those of the taurocholate group (P < 0.05). Curcumin increased Caspase-3 activity and decreased trypsin activity, while inhibited nuclear factor-κ (NF-κB) at all time points (P < 0.05) and moreover reduced activator protein-1 (AP-1). Curcumin decreased chemokine (except for 288 h), TNF-α (except for 2 and 24 h), IL-6 (except for 2, 6 and 288 h) and iNOS (except for 144 and 288 h) mRNA levels (P < 0.05). Curcumin serum nitric oxide (NO) (except for 144 and 288 h) levels were reduced, as well. CONCLUSIONS: In conclusion, curcumin reduced tissue injury, trypsin activation and inhibited NF-κB and AP-1. However TNF-α, IL-6 and iNOS and NO were not inhibited at all time points. Therefore no direct correlation was detected in the subgroups between tissue injury, proinflammatory cytokines and oxidative enzymes.

The effects of hyperbaric oxygen application against cholestatic oxidative stress and hepatic damage after bile duct ligation in rats.

BACKGROUND: The aim of this study was to evaluate the preventive and therapeutic potential of hyperbaric oxygen therapy (HBO) on the liver tissue against bile duct ligation (BDL)-induced oxidative damage and fibrosis in rats. MATERIALS AND METHODS: We divided 32 adult male Sprague Dawley rats into four groups: sham, sham plus HBO, BDL, and BDL plus HBO; each group contained eight animals. We placed the sham plus HBO and BDL plus HBO groups in an experimental hyperbaric chamber in which we administered pure oxygen at 2.5 atmospheres absolute 100% oxygen for 90 min on 14 consecutive days. RESULTS: The application of BDL clearly increased the tissue malondialdehyde level, myeloperoxidase activity, and hydroxyproline content and decreased the antioxidant enzymes (superoxide dismutase and catalase activities) and glutathione level. Hyperbaric oxygen therapy treatment significantly decreased the elevated tissue malondialdehyde level, myeloperoxidase activity, and hydroxyproline content and increased the reduced superoxide dismutase and catalase activities and glutathione level in the tissues. The changes demonstrating the bile duct proliferation and fibrosis in expanded portal tracts include the extension of proliferated bile ducts into lobules, mononuclear cells, and neutrophil infiltration into the widened portal areas were observed in BDL group. Treatment of BDL with HBO attenuated alterations in liver histology. Alpha smooth muscle actin, cytokeratin-positive ductular proliferation, and the activity of terminal deoxynucleotidyl transferase 2'-deoxyuridine, 5'-triphosphate nick end labeling in the BDL decreased with HBO treatment. CONCLUSIONS: The data indicate that HBO attenuates BDL-induced oxidative injury, hepatocytes damage, bile duct proliferation, and fibrosis. The hepatoprotective effect of HBO is associated with antioxidative potential.

Melatonin ameliorates oxidative damage in hyperglycemia-induced liver injury.

PURPOSE: Melatonin (N-acetyl-5-methoxy-tryptamine) is synthesized mainly by the pineal gland and its antioxidant properties have been demonstrated both in short and long term studies. Our aim was to clarify the effects of hyperglycemia and to administer melatonin on lipid peroxidation, protein oxidation and oxidative DNA damage in rat. METHODS: Malondialdehyde (MDA), protein carbonyl (PCO) and total thiol (T-SH) levels were determined in plasma and liver tissue, glutathione (GSH) levels in erythrocyte and liver tissue, and 8-hydroxy-2-deoxyguanosine (8-OHdG) levels in plasma and liver. Thirty-eight male Wistar rats were divided into four groups: 1--injected with saline (n = 8), 2--injected with melatonin (n = 10), 3--injected with STZ (65 mg/kg, i.p.) (diabetic group) (n = 10) and 4--injected with melatonin (10 mg/kg/day, i.p.) and STZ (65 mg/kg, i.p.) (n = 10) for 8 weeks (diabetic+ melatonin group). Colorimetric methods were used to determine the level of the oxidative stress markers. 8-OhdGwas measured using ELISA. RESULTS: MDA, PCO and 8-OHdG levels in the plasma and the liver homogenates of diabetic rats were higher than controls and were significantly reduced after melatonin treatment. T-SH and GSH levels in samples were markedly reduced in untreated diabetic rats compared with control rats; however, these parameters were increased in diabetic rats following melatonin treatment. CONCLUSION: Our findings showed that melatonin administration partially ameliorated oxidative damage in liver injury in STZ-induced diabetic rats. The present study suggests that melatonin functions as a potent antioxidant agent in diabetes. Melatonin, a nutritional supplement, may be a good therapeutic option for diabetic patients.

Preventive effects of hyperbaric oxygen treatment on glycerol-induced myoglobinuric acute renal failure in rats.

Myoglobinuric acute renal failure (ARF) is a uremic syndrome caused by traumatic or non-traumatic skeletal muscle breakdown and intracellular elements that are released into the bloodstream. We hypothesized that hyperbaric oxygen (HBO) therapy could be beneficial in the treatment of myoglobinuric ARF caused by rhabdomyolysis. A total of 32 rats were used in the study. The rats were divided into four groups: control, control+hyperbaric oxygen (control+HBO), ARF, and ARF+hyperbaric oxygen (ARF+HBO). Glycerol (8 ml/kg) was injected into the hind legs of each of the rats in ARF and ARF+HBO groups. 2.5 atmospheric absolute HBO was applied to the rats in the control+HBO and ARF+HBO groups for 90 min on two consecutive days. Plasma urea, creatinine, sodium, potassium, calcium, aspartate aminotransferase, alanine aminotransferase, lactic dehydrogenase, creatinine kinase and urine creatinine and sodium were examined. Creatinine clearance and fractional sodium excretion could then be calculated. Superoxide dismutase, catalase, glutathione and malondialdehyde (MDA) levels were assessed in renal tissue. Tissue samples were evaluated by Hematoxylin-eosin, PCNA and TUNEL staining histopathologically. MDA levels were found to be significantly decreased whereas SOD and CAT were twofold higher in the ARF+HBO group compared to the ARF group. Renal function tests were ameliorated by HBO therapy. Semiquantitative evaluation of histopathological findings indicated that necrosis and cast formation was decreased by HBO therapy and TUNEL staining showed that apoptosis was inhibited. PCNA staining showed that HBO therapy did not increase regeneration. Ultimately, we conclude that, in accordance with our hypothesis, HBO could be beneficial in the treatment of myoglobinuric ARF.

Effects of Ganoderma lucidum on obstructive jaundice-induced oxidative stress.

OBJECTIVE: Obstructive jaundice develops after occlusion of the common bile duct. Direct hyperbilirubinaemia, which occurs secondary to the condition, causes various life-threatening pathologies. Cytoprotective effects of Ganoderma lucidum (GL) have previously been shown. In this study, the effects of GL on oxidative stress and oxidant DNA damage in experimental obstructive jaundice were evaluated. METHODS: Sixty Wistar albino adult female rats were randomly divided into six weight-matched equal groups: sham group, bile duct ligated group (BDL); after sham operation 250 mg/kg/d of GL administered group, after sham operation 500 mg/kg/d of GL administered group, after bile duct ligation 250 mg/kg/d of GL administered (GL1BDL) group, and after bile duct ligation 500 mg/kg/d of GL administered (GL2BDL) group. GL polysaccharide was orally administered to the rats via gavage tube once a day for 14 days after bile duct ligation. RESULTS: The plasma malondialdehyde levels of the GL1BDL and GL2BDL groups were significantly lower than those of the BDL group (p < 0.01). The plasma 8-hydroxy-2'-deoxyguanosine levels of the GL1BDL and GL2BDL groups were significantly lower than those of the BDL group (p < 0.001). The liver tissue Cu-Zn superoxide dismutase level of the GL2BDL group was significantly higher than that of the BDL group (p < 0.05). CONCLUSION: GL protected against DNA and liver tissue damage by reducing oxidative stress in obstructive jaundice.

Effect of vitamin C on oxidative liver injury due to isoniazid in rats.

BACKGROUND: The aim of the present study was to investigate the effect of different doses of vitamin C on oxidative liver injury due to isoniazid (INH) in rats. METHODS: Rats were divided into four subgroups, each containing 10 rats. Group 1 was the control group; group 2, INH 50 mg/kg per day; group 3, INH 50 mg/kg per day + low-dose vitamin C (100 mg/kg per day); group 4, INH 50 mg/kg per day + high-dose vitamin C (1000 mg/kg per day). INH and vitamin C were administered into their stomachs through an oral tube. After 21 days, measurements were made in both serum and homogenized liver tissues. The levels of glutathione (GSH), superoxide dismutase (SOD) and other biochemical variables were measured. Malondialdehyde (MDA), glutathione peroxidase (GSH-px) and vitamin C were measured using commercial kits. RESULTS: Aspartate amino transferase and alanine aminotransferase in group 2 were higher than those in groups 1, 3 and 4 (P < 0.008 for both). Serum and tissue levels of MDA in group 2 were higher than that in groups 1 and 3 (P < 0.008 for both). There was no difference in the SOD levels between the four groups (P= 0.095). Erythrocyte and tissue GSH in group 2 were higher than that in groups 1 and 3 (P < 0.008 for both). Interestingly, erythrocyte and tissue GSH in group 4 were lower than those in group 1 (P < 0.008 for both). Erythrocyte level of GSH-px in group 2 was higher than that in groups 1 and 3 (P < 0.008 for both). CONCLUSIONS: INH-induced liver injury is associated with oxidative stress, and co-administration of low-dose vitamin C may reduce this damage effectively in a rat model. The antioxidant effect of high-dose vitamin C does not seem more potent compared to the low dose.

Donor heart preservation with iloprost supplemented St. Thomas Hospital cardioplegic solution in isolated rat hearts.

This study was designed to assess the influence of St. Thomas Hospital cardioplegic solution (St. Th.) on heart preservation in rat hearts subjected to 6h ischemia when supplemented with iloprost. In the control group (n=8), nothing was added to St. Th., whereas 10 or 1000 nmol L(-1) iloprost was added in the second (n=7) and third (n=8) groups, respectively. Mechanical contraction parameters, cardiac tissue damage and oxidative stress markers were evaluated. The 10 nmol/L iloprost group peak systolic pressure (71.0+/-30.9 versus 41.0+/-9.4 mm Hg) and -dp/dtmax (1103.8+/-94.3 versus 678.6+/-156.8 mm Hg s(-1)) were significantly higher than control group at 30 min of reperfusion (p<0.05). Iloprost supplemented groups had higher GSH and catalase levels of coronary perfusate at reperfusion, in comparison with initial values (p<0.05). AST, CK, CK-MB values increased at 0 min of reperfusion and cTnI values at 45 min of reperfusion (p<0.05) in all groups with no difference between groups. According to our results, iloprost supplementation had mild but significant improvement in postischemic values in mechanical and oxidative stress parameters, resulting in better heart preservation.

Tumour preventive effect of Aloe vera leaf pulp lectin (Aloctin I) on Ehrlich ascites tumours in mice.

In this study, the prophylactic effect of the main lectin present in Aloe vera leaf pulp extract (Aloctin I) was assayed against Ehrlich ascites tumours in mice. The lectin administered prophylactically before tumour implantation regressed tumour size, however, this activity was less potent than that of the A. vera leaf pulp extract previously shown in our laboratory. Accordingly, serum sialic acid and tumour necrosis factor alpha (TNFalpha) levels, chosen as tumour markers, were decreased significantly by the prophylactic administration of the lectin. The increase in spleen and thymus weights in the group given only Aloctin I, could be explained by the immunomodulatory and mitogenic effects of lectins. These findings, along with lymphoid hyperplasia observed in spleen and thymus, suggest that the tumour preventive effect of Aloctin I could be due to its immunomodulatory activity.

The effects of methylene blue on renal scarring due to pyelonephritis in rats.

The aim of this study was to evaluate the efficiency of methylene blue (MB) in preventing renal scar formation after the induction of pyelonephritis (PNP) in a rat model with delayed antimicrobial therapy. An inoculum of the K-12 strain of Escherichia coli was injected into both kidneys. Control groups received isotonic saline instead of bacterial solution. Four equal groups were then formed: the PNP group was untreated and the PNP ciprofloxacin (CIP) treated group was treated only with CIP intraperitoneally (i.p.) starting on the third day following bacterial inoculation. In the PNP (MB)-treated group, MB was given i.p., and in the PNP MB + CIP-treated group, MB + CIP were administered i.p.. In the sixth week following bacterial inoculation, all rats were sacrificed, and both kidneys of the rats in all groups were examined biochemically and histopathologically for renal scarring. Renal scar was significant in the groups treated with MB alone or MB + CIP combination compared with untreated or antibiotic only groups. Delayed treatment with antibiotics had no effect on scarring. These results suggest that the addition of MB to the delayed antibiotic therapy might be beneficial in preventing PNP-induced oxidative renal tissue damage.

Effect of Aloe vera leaf pulp extract on Ehrlich ascites tumours in mice.

Among the various known therapeutic effects of Aloe vera (L.) Burm. fil., a few recent studies have shown that preparations of the plant leaves can prevent or regress the growth of certain tumours. In this study, undertaken with A. vera leaf pulp extract against Ehrlich ascites tumours in mice, the animals were separated into five groups: I - healthy control, II - tumour control, III - experiment 1 (extract given before tumour inoculation), IV - experiment 2 (extract given with tumour inoculation) and V - experiment 3 (extract given after tumour inoculation). Ehrlich ascites tumours (0.33 ml) were injected subcutaneously into groups II-V. Aloe extract was injected at 55 mg protein/kg, twice a week for 21 days. Tumour size, thymus and spleen weights were measured, as well as leucocyte count, tumour necrosis factor-alpha and sialic acid as tumour markers. The best inhibitory effect on tumour growth was obtained with the extract given prophylactically before tumour implantation (experiment 1), although Aloe extract also regressed tumour sizes when given simultaneously with (experiment 2), or therapeutically after (experiment 3), tumour implantation. Accordingly, serum sialic acid and tumour necrosis factor-alpha levels, chosen as tumour markers, which were raised in the tumour control group, were significantly decreased by the prophylactic administration of the extract. The increase in leucocyte count seen in experiment 1 and 2 groups, along with lymphoid hyperplasia observed in spleen and thymus necroscopy, lead us to think that the tumour preventive effect of Aloe could be due to its immunomodulatory activity. According to our results, A. vera could be proposed as a prophylactic for cancer prevention.