Superoxide Dismutase Activity In Kidney Research Articles

Vitamin C reduces vancomycin-related nephrotoxicity through the inhibition of oxidative stress, apoptosis, and inflammation in mice.

BackgroundVancomycin (VCM) is an antibiotic widely used to treat a range of serious bacterial infections; however, it is associated with nephrotoxicity. Vitamin C (VC) is a classical antioxidant that can alleviate various organ injuries and inflammatory responses by reducing inflammation and oxidative stress. This study aimed to examine the effect of VC on VCM-related nephrotoxicity in mice.MethodsMice were randomized into four groups: control, VCM (400 mg/kg/day), VCM (400 mg/kg/day) + VC (200 mg/kg/day), and VC (200 mg/kg/day) groups. Both VCM and VC were administered via intraperitoneal injection for 7 d, after which kidney and blood samples were collected and evaluated. Creatinine (Cr), blood urea nitrogen (BUN), superoxide dismutase (SOD), malondialdehyde (MDA), interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF)-α, and nuclear factor-κB (NF-κB) were measured.ResultsIn the VCM group, kidney index, renal injury score, cell apoptosis, serum Cr and BUN, and kidney Cr, BUN, MDA, IL-1β, IL-6, TNF-α, and NF-κB were higher compared to the control group (all P<0.05), while body weight and kidney SOD activity were lower (both P<0.05). By contrast, no differences were observed between the control and VC groups (VC and VCM + VC groups) for all these indicators.ConclusionsThe antioxidant VC reduces VCM-related renal injury by reducing oxidative stress, cell apoptosis, and inflammation.

The potential protective role of folic acid against acetaminophen-induced hepatotoxicity and nephrotoxicity in rats.

Folic acid (FA), is a group B vitamin, has high reactive oxygen radicals quenching ability, resulting in protection against oxidative damage in aerobic cell. Acetaminophen (N-acetyl-p-aminophenol, APAP) is a nonsteroidal anti-inflammatory drug, and can promote oxidative damage in liver and kidney tissues. The aim of this study was to investigate whether folic acid has protective effects on oxidative liver and kidney injury caused by experimental APAP toxication. Forty female Sprague dawley rats were divided into 5 groups; control, APAP, FA, APAP+FA, and APAP+N-acetylcysteine (NAC) groups. APAP toxication was induced by oral gavage (3 g/kg bodyweight). FA (20 mg/kg bodyweight) and NAC (150 mg/kg bodyweight) were given by oral gavage to the specified groups. Oxidant and antioxidant parameter were determined in liver and kidney tissues. In addition, the liver and kidney tissues were histological evaluated. When compared with APAP group, superoxide dismutase (SOD) and catalase activities and glutathione levels were statistically higher, malondialdehyde (MDA) level and myeloperoxidase activity (except liver tissue) were statistically lower in both APAP+FA and APAP+NAC. Liver and kidney MDA level and kidney SOD activity were significantly lower in APAP+NAC group compared with APAP+FA group. Co-administration of NAC with APAP was found to provide protection, but hepatic cords were defective in some places and some glomerular tubules also had dilatation. Necrotic areas was reduced in the liver and the glomerular structure was in good condition in the APAP+FA group. As a result, FA might have a protective effect against APAP-induced hepato-nephrotoxicity and oxidative stress in rat.

Alterations in Peripheral Organs following Combined Hypoxemia and Hemorrhagic Shock in a Rat Model of Penetrating Ballistic-Like Brain Injury.

Polytrauma, with combined traumatic brain injury (TBI) and systemic damage are common among military and civilians. However, the pathophysiology of peripheral organs following polytrauma is poorly understood. Using a rat model of TBI combined with hypoxemia and hemorrhagic shock, we studied the status of peripheral redox systems, liver glycogen content, creatinine clearance, and systemic inflammation. Male Sprague-Dawley rats were subjected to hypoxemia and hemorrhagic shock insults (HH), penetrating ballistic-like brain injury (PBBI) alone, or PBBI followed by hypoxemia and hemorrhagic shock (PHH). Sham rats received craniotomy only. Biofluids and liver, kidney, and heart tissues were collected at 1 day, 2 days, 7 days, 14 days, and 28 days post-injury (DPI). Creatinine levels were measured in both serum and urine. Glutathione levels, glycogen content, and superoxide dismutase (SOD) and cytochrome C oxidase enzyme activities were quantified in the peripheral organs. Acute inflammation marker serum amyloid A-1 (SAA-1) level was quantified using western blot analysis. Urine to serum creatinine ratio in PHH group was significantly elevated on 7–28 DPI. Polytrauma induced a delayed disruption of the hepatic GSH/GSSG ratio, which resolved within 2 weeks post-injury. A modest decrease in kidney SOD activity was observed at 2 weeks after polytrauma. However, neither PBBI alone nor polytrauma changed the mitochondrial cytochrome C oxidase activity. Hepatic glycogen levels were reduced acutely following polytrauma. Acute inflammation marker SAA-1 showed a significant increase at early time-points following both systemic and brain injury. Overall, our findings demonstrate temporal cytological/tissue level damage to the peripheral organs due to combined PBBI and systemic injury.

Comparative and Interactive Biochemical Effects of Sub-Lethal Concentrations of Cadmium and Lead on Some Tissues of the African Catfish (Clarias gariepinus)

Cadmium is a strong toxic heavy metal which presents in paints and liquid wastes and causes oxidative stress in fish. On the other hand, lead is widely used for different purposes, e.g. lead pipes, it targets vital organs such as liver and kidney causing biochemical alterations. The present study evaluates the effects of 60 days exposure to Cd and Pb either single or combined together in African catfish. Sixty-four fishes were divided into 3 groups and exposed to CdCl2 (7.02 mg/L) or PbCl2 (69.3 mg/L) or a combination of them along with control group. Activities of acid phosphatase (ACP), lactate dehydrogenase (LDH) and glucose-6-phosphate dehydrogenase (G-6-PDH) were estimated. Moreover, gill, liver and kidney were assayed for activities of superoxide dismutase (SOD), catalase (CAT) and levels of glutathione (GSH) and malondialdehyde (MDA). Individual exposure showed that both Cd and Pb significantly decreased LDH activity and SOD activity in the kidney. Pb significantly increased G-6-PDH activity and decreased GSH level in the gill. CAT activity in liver and kidney elevated significantly on Cd exposure while lead caused a significant depletion in the liver and significant elevation in the kidney. Both Cd and Pb significantly increased MDA levels in liver and kidney while Pb increased its level in gills. The combined exposure resulted in normalization of LDH, G-6-PDH activity, and CAT activity in liver and kidney as well as GSH level in both tissues and MDA in gill and kidney. The combination increased SOD activity and MDA level in liver and decreased SOD activity in kidney and GSH level in gills. In conclusion, the antioxidant system of African catfish was adversely affected by prolonged exposure to Cd and Pb. The combined exposure caused less damage than individual exposure and returned most parameters to those of controls.

Effects of tebuconazole on cytochrome P450 enzymes, oxidative stress, and endocrine disruption in male rats.

The major objective of the present study was to determine the ability of a triazole fungicide tebuconazole to induce cytochrome P450-dependent monooxygenases, oxidative stress, and endocrine-disrupting activity using male rats treated with tebuconazole at 10, 25, and 50 mg/kg p.o. once daily for 28 days. In liver, tebuconazole dose-dependently increased microsomal contents of cytochrome P450 and cytochrome b5 and the activities of NADPH-cytochrome P450 reductase, 7-ethoxyresorufin O-deethylase, methoxyresorufin O-demethylase, pentoxyresorufin O-dealkylase, 7-ethoxycoumarin O-deethylase, aniline hydroxylase, and erythromycin N-demethylase. In kidney, tebuconazole increased 7-ethoxycoumarin O-deethylase activity without affecting other monooxygenase activities. In marked contrast to liver and kidney, tebuconazole decreased testicular 7-ethoxyresorufin O-deethylase, methoxyresorufin O-demethylase, 7-ethoxycoumarin O-deethylase, aniline hydroxylase, and erythromycin N-demethylase activities. The results of immunoblot analysis of liver microsomes of controls and tebuconazole-treated rats revealed that tebuconazole induced CYP1A1/2, CYP2B1/2, CYP2E1, and CYP3A proteins in liver. Additions of tebuconazole to liver microsomes inhibited microsomal 7-ethoxycoumarin O-deethylase activity in vitro (IC50 = 1.50-1.69 µM). Treatment of rats with tebuconazole decreased glutathione content and increased glutathione S-transferase, superoxide dismutase, catalase, and glutathione peroxidase activities in liver; increased superoxide dismutase activities in kidney and testis; but decreased glutathione S-transferase activity in testis. Treatments with tebuconazole decreased serum testosterone concentration and cauda epididymal sperm count. The present study demonstrates that tebuconazole induces a multiplicity of CYPs and oxidative stress in liver; inhibits testicular P450 and glutathione S-transferase activities; and produces anti-androgenic effects in male rats.

Possible protective effect of the algae spirulina against nephrotoxicity induced by cyclosporine A and/or gamma radiation in rats.

The present study was conducted to evaluate the possible protective role of the algae spirulina (Sp) against nephrotoxicity and oxidative stress which are the main secondary effects induced by the immunosuppressant drug CSA and/or ionizing radiation. In this study, male rats were given Sp (1g/kg) either for 15days before irradiation (6.5Gy) or 5days before and 10days concomitant with CSA (25mg/kg). Markers used to assess renal injury included serum creatinine, urea, glucose, albumin, protein, and lipid profile as well as kidney content of reduced glutathione (GSH); lipid peroxidation (thiobarbituric acid reactive substances (TBARS)); nitrite and superoxide dismutase (SOD) activity. In addition, some trace elements (Zn and Mg) were estimated in kidney. Apoptosis was assessed by immunohistochemical estimation of caspase-3 expression in addition to histopathological examination. Results revealed that gamma radiation and/or CSA induced elevation in urea, creatinine, lipids, and glucose while decreasing albumin and protein levels. There was a noticeable increase in kidney content of GSH, TBARS, and nitrite. Meanwhile, profound decrease in kidney SOD activity was observed. Treatment with Sp significantly reversed the changes induced by CSA and/or gamma radiation in renal function tests. Spirulina also ameliorated kidney oxidative stress through decreasing GSH, TBARS, and nitrite kidney content while increasing SOD activity. Histopathological examination further confirmed Sp protective efficacy. Moreover, kidney caspase-3 expression that was triggered by CSA and/or gamma radiation was decreased. In conclusion, spirulina can be regarded as a promising renoprotective natural agent against renal injury induced by CSA and/or gamma radiation.

Eruca sativa Essential Oil Protects upon Hyperthyroidism Induced Damages in Rat

The study was conducted to evaluate the protective effects of Eruca sativa oil upon hyperthyroidism induced damages to thyroid, kidney and brain of male Wistar rats. Our experimental conditions revealed an obvious increase in the serum FT4, creatinine, urea and calcium levels together with significant decrease in TSH, proteins and uric acid. In addition, hyperthyroidism treatment triggered an oxidative stress in thyroid, brain and kidney as revealed by an increased level of lipid peroxidation, an increase of superoxide dismutase activity in kidney and brain and a decrease of glutathione peroxidase and catalase activities in thyroid, kidney and brain functions. When Eruca sativa oil was added, all this parameter was significantly shifted to more normal values. In conclusion, Eruca sativa oil displays beneficial effects upon thyroid dysfunction, nephrotoxicity, neurotoxicity and oxidative stress in hyperthyroidism treated animals. This property could be attributed to the presence of antioxidant components determined by GC-MS. The experimental protocol was performed according to the European convention for the protection of vertebrate animals used for experimental and other scientific purposes (Council of Europe No 123, Strasbourg) and approved by the ethics committee for research on laboratory animal use of our institution.

Changes of Klotho protein and Klotho mRNA expression in a hydroxy-L-proline induced hyperoxaluric rat model.

Klotho protein is recognized as having a renoprotective effect and is used as a biomarker for kidney injury. We investigated the level of Klotho protein in hyperoxaluria-induced kidney injury and the effects of vitamin E (Vit E) and vitamin C (Vit C) supplementation. Hyperoxaluria was induced by feeding 2% (w/v) Hydroxy-L-proline (HLP) in the drinking water for 21 days. Rats were divided into 5 groups; control (Group 1, n=7), HLP treated rats that received nothing else (Group 2, n=7), Vit E (Group 3, n=6), Vit C (Group 4, n=6) and both Vit E and Vit C (Group 5, n=7). Vit E (200 mg/kg) was injected on days 1, 6, 11 and 16, while Vit C (500 mg/kg) was given intravenously on days 1 and 11. The Klotho protein levels and oxidative status were measured. The expression level of kidney Klotho protein expression was significantly reduced by HLP-treatment, while the mRNA expression was higher (P<0.05), the plasma and kidney malondialdehyde and kidney superoxide dismutase activities were increased, and the kidney reduced glutathione and urinary total antioxidant status were decreased (P<0.05). All of these changes were ameliorated by administration of Vit E, Vit C or especially the co-administration of both. In conclusion, HLP-induced hyperoxaluria reduced the kidney Klotho protein level, which could be restored by Vit E and/or Vit C.

Protective Effects of Onion Oil and Selenium against Cisplatin-Induced Nephrotoxicity and Oxidative Stress in Rats

Background: Nephrotoxicity is an inherent of certain anticancer drugs. Aim: This study aimed to assess the protective effect of onion oil and selenium against cisplatin-induced nephrotoxicity in male rats. Results: Cisplatin (5 mg/kg, i.p.) caused significant increases in serum sodium, blood urea nitrogen, serum creatinine, total sodium and potassium excreted in urine, urine volume and lipid peroxides measured as the malondialdehyde content of kidney, with significant decreases in serum total protein, creatinine clearance, reduced glutathione content of kidney and kidney superoxide dismutase activity as compared to the control group. On the other hand, administration of onion oil (100 mg/kg, p.o.) or selenium (1 mg/kg, p.o.) for 14 days with a single cisplatin dose on the 10th day ameliorated the cisplatin-induced nephrotoxicity as indicated by the restoration of kidney function and oxidative stress biomarkers. Conclusion: Onion oil and selenium showed protective effects against cisplatin-induced nephrotoxicity.

The Effect of Long Term Pre/postnatal Low/high Dose Nicotine Exposure on Tissue Oxidant/antioxidant Status and DNA Damage in Rats.

Most women do not stop smoking either during pregnancy or in the lactation period. This study was carried out to investigate the effect of long term per oral pre/postnatal low/high dose nicotine exposure on fetal plasma/tissue oxidant-antioxidant status in rats. The study groups were composed of pups whose parents used or did not use nicotine in pregnancy and lactation period. The pups were divided into 3 groups, each consisting of 10 rats; the control group (normal drinking water), low and high dose nicotine groups according to the dose of nicotine (0.4 mg/kg and 6.0 mg/kg BW/day, respectively) given per oral in drinking water. At the end of the 12(th) month, tissue/hemolysate/plasma oxidant-antioxidant status parameters and 8-hydroxy-2-deoxy-guanosine levels were measured. Plasma cotinine levels were higher in nicotine groups compared to controls (p<0.01). A significant increase in liver malonyldialdehyde levels (p<0.05) and a significant decrease in kidney superoxide dismutase activities (p<0.05) were determined in both nicotine groups compared to controls while no statistically significant difference was found in the other parameters. This investigation showed that long term nicotine exposure during-after pregnancy may have an adverse effect on vital organs of the offspring via impairing tissue oxidant/antioxidant balance. Liver and kidney seem to be the mostly affected organs possibly due to their major roles in nicotine metabolism.

Hesperidin and rutin, antioxidant citrus flavonoids, attenuate cisplatin-induced nephrotoxicity in rats.

This study aimed to assess the protective effect of hesperidin (HES) and rutin (RUT) against cisplatin-induced nephrotoxicity in male rats. Cisplatin (5 mg/kg, intraperitoneal) caused significant increases in serum sodium, blood urea nitrogen, serum creatinine, total sodium and potassium excreted in urine, urine volume, and lipid peroxides measured as the malondialdehyde content of kidney, with significant decreases in serum total protein, creatinine clearance, reduced glutathione content of kidney, and kidney superoxide dismutase activity as compared with the control group. On the other hand, administration of HES (200 mg/kg, per oral [p.o.]) or RUT (30 mg/kg, p.o.) for 14 days with a single cisplatin dose on the tenth day ameliorated the cisplatin-induced nephrotoxicity as indicated by the restoration of kidney function and oxidative stress biomarkers. Furthermore, the test drugs reduced the histopathological changes induced by cisplatin. In conclusion, HES and RUT showed protective effects against cisplatin-induced nephrotoxicity.

Celecoxib modulates nitric oxide and reactive oxygen species in kidney ischemia/reperfusion injury and rat aorta model of hypoxia/reoxygenation

ObjectiveThis study investigated the interaction between COX-2, NO and ROS after ischemia/reperfusion events in the kidney and vascular beds. Materials and methodsKidney IRI model in male Sprague–Dawley rats was used and various biochemical and histopathological parameters were examined. The isolated rat aortic rings served as model for hypoxia/reoxygenation. ResultsCelecoxib reduced serum creatinine and urea and kidney malonaldehyde levels, increased kidney superoxide dismutase activity and reduced glutathione level and histopathological scores at 24 and 48h after reperfusion compared to IRI group. This was associated with a significant increase in NO level to 0.70±0.03nmol/mg protein compared to 0.37±0.01nmol/mg protein for IRI group. Unexpectedly, celecoxib reduced COX-2 expression in the kidney. Celecoxib reversed the effect of hypoxia–reoxygenation on ACh and SNP-induced relaxation in aortic rings but failed to potentiate the SNP relaxations in the control rings. Hypoxia–reoxygenation significantly impaired celecoxib’s relaxation of aorta (12.69±2.69% vs. 35.84 ±0.84%) which was significantly inhibited in presence of L-NAME. ConclusionsCelecoxib beneficially affects the outcome of renal IRI by lowering the expression of COX-2 and hence reducing oxidative stress and increasing the bioavailability of NO. Direct interaction between celecoxib and NO in associated vascular beds may also be a contributing mechanism.

Effect of Curcumin on some Heavy Metals Induced Renal and Testicular Injuries in Male Rats

Back ground Toxic heavy metals in water, air and soil are global problems that are a growing threat to humanity. Heavy metals are widely distributed in the environment and some of them occur in food, water, air and tissues even in the absence of occupational exposure. The antioxidant and protective influences of curcumin on a mixture of some heavy metals (Pb, Hg and Cd) induced renal and testicular injuries in male rats were detected. Curcumin, a yellow pigment from Curcuma longa, is a major component of turmeric and is commonly used as a spice and food-coloring material. It exhibits anti-inflammatory, anti-tumor, and antioxidant properties. Aim The present study aims to evaluate the antioxidative activities and protective role of curcumin against some heavy metals induced renal and testicular injuries in male rats. Material and Method Male Swiss albino rats were orally administrated by curcumin (150 mg/kg B.W.) using suitable stomach tube (eight weeks) before receiving mixture of heavy metals (Pd, Hg and Cd) in drinking water for two weeks. Levels of plasma creatinine, urea, uric acid and serum testosterone concentration were measured, glutathione content and superoxide dismutase activities in kidney and testis tissues were estimated and also histological examinations for kidney and testis tissue were detected. Results The results revealed that mixture of heavy metals lead to significant increase in the level of plasma creatinine, urea and uric acid, Meanwhile, significant decrease in serum testosterone concentration. Glutathione content and superoxide dismutase activities in kidney and testis tissues were significantly decrease by using a mixture of heavy metals. But groups administrated with curcumin before administrated with mixture of heavy metals, exerted noticeable amelioration against their damage in most of the biochemical and histological tested parameters.

Protective effect of vitamin E and atorvastatin against potassium dichromate-induced nephrotoxicity in rats

Potassium dichromate, a Cr (VI) compound, is the most toxic form of Cr (VI) and has been demonstrated to induce nephrotoxicity associated with oxidative stress in humans and animals. The wide environmental distribution of Cr lead to an increased interest of its toxicity and biological effects. The present study was designed to investigate the protective effect of vitamin E and atorvastatin against potassium dichromate-induced nephrotoxicity in rats. A single injection of potassium dichromate (15 mg/kg) to rats induced renal tubule damage and an increase in the following markers of renal injury 2 days later; blood urea nitrogen and serum creatinine. In addition, potassium dichromate injection increased the following nitrosative and oxidative stress biomarkers in kidney; malondialdehyde (MDA), total nitrate/nitrite (Nox). This was associated with a significant reduction in kidney glutathione (GSH), metallothionein (MT) contents and superoxide dismutase (SOD) activity. Furthermore inflammatory mediators such as myeloperoxidase (MPO) and tumor necrosis alpha (TNF-α) were increased. Renal damaged was also evidenced by the change in the kidney histopathological picture. Two weeks pre-treatment with vitamin E or atorvastatin before dichromate administration markedly improved its toxicity as indicated by reduction of serum urea and creatinine as well as improvement of kidney histopathological changes. Oxidative stress biomarkers such as renal MDA and nitric oxide contents were also decreased. Kidney superoxide dismutase activity was restored after pre-treatment with vitamin E. Furthermore, atorvastatin significantly reduced TNF-α content and MPO activity while vitamin E reduced TNF-α content. It could be concluded that the ability of vitamin E as well as atorvastatin to ameliorate potassium dichromate-induced renal injury was associated with their antioxidant and anti-inflammatory properties.

Acute renal failure potentiates methylmalonate-induced oxidative stress in brain and kidney of rats

Tissue methylmalonic acid (MMA) accumulation is the biochemical hallmark of methylmalonic acidemia. The disease is clinically characterized by progressive neurological deterioration and kidney failure, whose pathophysiology is still unclear. In the present work we investigated the effects of acute MMA administration on various parameters of oxidative stress in cerebral cortex and kidney of young rats, as well as the influence of acute renal failure on MMA-elicited effects on these parameters. Acute renal failure was induced by gentamicin, an aminoglycoside antibiotic whose utilization over prolonged periods causes nephrotoxicity. The administration of gentamicin alone increased carbonyl content and inhibited superoxide dismutase (SOD) activity in cerebral cortex, as well as increased thiobarbituric acid-reactive substances (TBA-RS) and sulfhydryl levels and diminished glutathione peroxidase activity in kidney. On the other hand, MMA administration increased TBA-RS levels in cerebral cortex and decreased SOD activity in kidney. Furthermore, the simultaneous administration of MMA and gentamicin to the rats provoked an augment in TBA-RS levels and superoxide generation in cerebral cortex and in TBA-RS, carbonyl and sulfhydryl levels in kidney, while diminished SOD activity in both studied tissues. Finally, nitrate/nitrite content, reduced glutathione levels, 2’,7’-dihydrodichlorofluorescein oxidation and catalase activity were not affected by this animal treatment in either tissue. In conclusion, our present data are in line with the hypothesis that MMA acts as a toxin in brain and kidney of rats and suggest that renal injury potentiates the toxicity of MMA on oxidative stress parameters in brain and peripheral tissues.

Protective effect of alpha tocopherol on contrast-induced nephropathy in rats.

Contrast-induced nephropathy (CIN) is a prominent cause of in-hospital acute kidney injury occurring after the administration of intravenous radiocontrast medium. Oxidative stress has been proposed as one of the more important mechanisms in the pathogenesis of CIN. The aim of the present study has been to determine the effect of alpha tocopherol on the reduction of renal damage in a rat model of CIN. Male Sprague Dawley rats were subjected into six groups pretreated with alpha-tocopherol (250 or 500 mg/kg/day) or the vehicle tweeen80 for 5 days before the induction of CIN. Renal function and oxidative stress markers; level of malondialdehyde (MDA), total antioxidant capacity (TAC), superoxide dismutase (SOD) activity were determined. Kidney tissues were sectioned for pathohistological examination. In the contrast media (CM) group, an increase in serum urea and creatinine was found. Tubular necrosis and peritubular capillary congestion were demonstrated in this group. Also, an imbalance of oxidative stress markers; an increase in MDA and a decreased SOD activity in kidney were shown. On the contrary, in CIN-induced rats administrated with alpha-tocopherol group, a significant reduction of renal function and renal MDA, together with a significant increase of renal SOD, were observed. Interestingly, a reduction in MDA and an increase of TAC in serum, along with prevention of tubular injury, were demonstrated in this group, as compared to the CM group. This present study demonstrated that alpha tocopherol showed protective effect on the rat renal damage induced CIN. Therefore, this vitamin could be used as an antioxidant to attenuate the radiocontrast oxidative damage.

ROLE OF OCIMUM CANUM IN PREVENTION OF REPERFUSION-INDUCED RENAL ISCHEMIA IN WISTAR ALBINO RATS

Acute renal failure is defined as rapid loss of renal function and has been associated with a high mortality rate. Ischemia and reperfusion (I/R) injury of the kidney is the most prominent cause of intrinsic acute renal failure. Activation of reactive oxygen species is implicated in renal ischemia/reperfusion (I/R) injury. This study investigated the anti-ischemic effect of hydro-alcoholic leaf extract of Ocimum canum (OC) against renal I/R injury by its effect on reactive oxygen species. Wistar albino rats were administered different doses of hydro-alcoholic leaf extract of Ocimum canum (OC) before renal ischemia, followed by reperfusion for 24 hours. Serum creatinine, Serum Cystatin C, serum oxaloacetate transaminase (SGOT), serum pyruvate transaminase (SGPT), blood urea nitrogen (BUN) and Lactate dehydrogenase (LDH) were measured for renal dysfunction. Serum and tissue Malondialdehyde (MDA), reduced glutathione (GSH) levels, catalase (CAT), and superoxide dismutase (SOD) levels were measured. Renal sections were analyzed for histological grading of renal injury. Hydro-alcoholic leaf extract of Ocimum canum (OC) significantly reduced increased creatinine, Cystatin C, serum oxaloacetate transaminase (SGOT), serum pyruvate transaminase (SGPT), blood urea nitrogen (BUN) and Lactate dehydrogenase (LDH). Ocimum canum also increased kidney superoxide dismutase activity, catalase and reduced glutathione levels and reduced the malondialdehyde levels. Hydro-alcoholic leaf extract of Ocimum canum reduced histological renal damage. These results suggest that the hydro-alcoholic leaf extract of Ocimum canum reduces renal dysfunction and injury caused by renal I/R.

Grape Seed Proanthocyanidin Extract Reduces Renal Ischemia/Reperfusion Injuries in Rats

Activation of reactive oxygen species and inflammation are implicated in renal ischemia/reperfusion (I/R) injuries. This study investigated whether grape seed proanthocyanidin extract (GSPE) protects against renal I/R injury by its effect on reactive oxygen species and the inflammation pathway. Wistar rats were administered GSPE before renal ischemia, followed by reperfusion for 24 hours. Plasma concentrations of urea, creatinine and cystatin C were measured for renal dysfunction. Serum and tissue superoxide dismutase activity and glutathione peroxidase and malondialdehyde levels were measured. Renal sections were analyzed for histological grading of renal injury, and nuclear factor-κB activity was determined. GSPE significantly reduced increases in urea, creatinine and cystatin C; increased kidney superoxide dismutase activity and glutathione peroxidase levels and reduced malondialdehyde levels. GSPE reduced histological renal damage and nuclear factor-κB activity. These results suggest that GSPE reduces renal dysfunction and injury caused by renal I/R.

Protective effect of herbomineral formulation (Dolabi) on early diabetic nephropathy in streptozotocin-induced diabetic rats

The effect of a herbomineral formulation (HMF) on early diabetic nephropathy was investigated. Diabetes was induced in Wistar rats by administering streptozotocin (55 mg/kg, intraperitoneally). The occurrence of early diabetic nephropathy in rats was revealed by high plasma glucose and depleted liver glycogen, decreased glucose uptake by peripheral tissue, impaired renal function, increased antioxidants and lipid peroxidation in kidney. These changes were accompanied by elevated malondialdehyde, glutathione and superoxide dismutase activity in kidney. Furthermore, increased total urine volume, urinary albumin excretion rate, urinary albumin to creatinine ratio, increased relative kidney weight, decreased glomerular filtration rate (GFR) and urinary creatinine were also observed in diabetic nephropathy rats. HMF treatment significantly lowered blood glucose, glycosylated hemoglobin, creatinine, blood urea nitrogen, triglycerides, total cholesterol, serum albumin level, total urine volume, urinary albumin excretion rate, urinary albumin to creatinine ratio and relative kidney weight, and increased urinary creatinine and GFR. Altered levels of antioxidants, viz. lipid peroxidation, glutathione and superoxide dismutase (SOD), in kidney of diabetic nephropathy rats were restored. Histopathological findings indicated dense mesangial matrix in the glomeruli of diabetic nephropathy rats, which may be due to over-activation of matrix metalloproteinases and was reduced following HMF treatment. Our experimental findings clearly demonstrate that HMF has an ability to prevent the progression of early diabetic nephropathy. Such protective effect of HMF might be due to the presence of flavonoids (catechin, quercetin, rutin) and triterpene saponins (oleanolic acid and gymnemic acid) which are known to possess potent antioxidant properties.

Effect of pentylenetetrazole and sound stimulation induced single and repeated convulsive seizures on the MDA, GSH and NO levels, and SOD activities in rat liver and kidney tissues

Objectives The aim of our study was to evaluate the activity of superoxide dismutase (SOD) and the levels of glutathione (GSH), malondialdehyde (MDA), and nitric oxide (NO) in liver and kidney tissues in a rat model of convulsive seizure induced by single and repeated doses of pentylenetetrazole (PTZ) and sound stimulation with key ringing. Materials and methods Male Wistar adult rats ( n = 48), were used in the experiment. The animals were divided into six groups: (1) Single Seizure Control Group (SS-Control; n = 8), (2) Repeated Seizures Control Group (RS-Control; n = 8), (3) PTZ induced Single Seizure Group (SS-PTZ Group; n = 8), (4) PTZ induced Repeated Seizures Group (RS- PTZ Group; n = 8), (5) Key-Ringing Induced Single Seizure Group (SS-KEY Group; n = 8), (6) Key-Ringing Induced Repeated Seizures Group (RS-KEY Group; n = 8). Following injections rats were observed for seizure activity for 30 min. Animals were sacrificed 24 h after induced seizure (single or last seizure) or saline administration. MDA, NO, GSH levels and SOD activities were determined in liver and kidney tissues. Results There was no significant difference between SS-Control and RS-Control groups, SS-PTZ and SS-KEY groups, and RS-PTZ and RS-KEY groups ( p > 0.05) in none of the examined 4 parameters in liver and kidney tissues. The liver and kidney levels of MDA and NO in SS-PTZ group were found to be significantly higher than the SS-Control group ( p < 0.05). In SS-KEY group, the liver and kidney levels of MDA and NO were found to be significantly higher and GSH levels were significantly lower than the SS-Control group ( p < 0.05). While liver and kidney levels of MDA in RS-PTZ group and RS-KEY group were found to be significantly higher than the RS-Control group ( p < 0.05), liver and kidney GSH levels were significantly lower ( p < 0.05). The liver levels of NO in RS-PTZ group and RS-KEY group were found to be significantly higher than the RS-Control group ( p < 0.05). Kidney SOD activities in RS-PTZ group and RS-KEY group were found to be significantly lower than the RS-Control group ( p < 0.05). When RS-PTZ group is compared with the SS-PTZ group, the liver SOD activity and kidney NO level were found to be significantly lower in the RS-PTZ group ( p < 0.05). While the liver NO level and GSH level in RS-KEY group were significantly higher than the SS-KEY group, SOD activity was significantly lower in the RS-KEY group ( p < 0.05). When RS-KEY group was compared with SS-KEY group, the kidney NO level and SOD activity were found to be significantly lower in the RS-KEY group ( p < 0.05). Conclusion In conclusion, key-ringing or PTZ induced single and repeated seizures result in increased oxidative damage and lipid peroxidation, and decreased antioxidant defense mechanisms.