Oxidative Damage In Kidney Research Articles

The protective effect of menhaden oil in the oxidative damage and renal necrosis due to dietary choline deficiency

Weanling rats fed a choline-deficient diet develop kidney oxidative damage, tubular and cortical kidney necrosis, renal failure and animal death. The effect of dietary menhaden oil was assayed on the mentioned sequence correlating oxidative stress with renal structure and function. Rats were fed ad libitum 4 different diets: (a) a choline-deficient diet with corn oil and sunflower hydrogenated oil as a source of fatty acids; (b) the same diet supplemented with choline; (c) a choline-deficient diet with menhaden oil as a source of fatty acids; and (d) the previous diet supplemented with choline. Animals were sacrificed at days 0, 2, 4 and 7. The histopathological study of the kidneys showed that renal necrosis was only observed at day 7 in choline-deficient rats receiving the vegetable oil diet, simultaneously with increased creatinine plasma levels. Homogenate chemiluminescence (BOOH-initiated chemiluminescence) and phospholipid oxidation indicate the development of oxidative stress and damage in choline-deficient rats fed vegetable oils as well as the protective effect of menhaden oil. Rats fed with the fish oil diet showed that oxidative stress and damage develop later, as compared with vegetable oil, with no morphological damage during the experimental period.

Oxidative Damage of Liver, Kidney and Serum Proteins with Apoptosis of above Tissues in Guinea Pigs Fed on Carbonated Soft Drink

Oxidative Damage of Liver, Kidney and Serum Proteins with Apoptosis of above Tissues in Guinea Pigs Fed on Carbonated Soft Drink

Protective effects of vitamin C and selenium supplementation on methomyl-induced tissue oxidative stress in adult rats

Methomyl (MET) is used worldwide in agriculture and health programs. Besides its advantages in the agriculture, it causes several toxic effects. The objective of this study was to examine the potential ability of vitamin C and/or selenium (Se), to alleviate the oxidative damage parameters, against MET-induced changes in blood biochemical markers and oxidative damage in liver and kidney of male Wistar rats. The animals were randomized into five groups of eight each: group I served as control rats; group II received MET (8mg/kgbody weight (BW)) in drinking water; group III received both MET and vitamin C (200mg/kg BW; by intraperitoneal injection); group IV received both MET and Se (0.6mg/100gBW). Animals of group V were treated with MET, vitamin C and Se. A significant increase in the levels of hepatic markers enzymes (alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase and lactate dehydrogenase) was determined. Furthermore, renal markers such as urea and creatinine were increased in MET-treated rats. Additionally, serum cholesterol and triglycerides were significantly enhanced. Exposure of rats to MET caused significant increase in malondialdehyde levels, thus causing a drastic alteration in antioxidant defense system, particularly in the activities of catalase and glutathione-S-transferase and glutathione peroxidase. However, simultaneous supplementation with vitamin C and Se restored these parameters partially. In conclusion, the results of the current study revealed that MET-induced toxicity caused perturbations of some biochemical parameters, lipid peroxidation and alterations in the antioxidant enzymes in liver and kidney homogenates. Administration of vitamin C and Se exhibited protective effect by inhibiting MET-induced toxicity in liver and kidney.

The protective effects of Prunus armeniaca L (apricot) against methotrexate-induced oxidative damage and apoptosis in rat kidney

This study was conducted to evaluate a possible protective role of apricot in apoptotic cell death induced by methotrexate (MTX) and renal damage by different histological and biochemical parameters. Twenty-eight rats were divided into four groups, control, apricot, methotrexate, and apricot + methotrexate. Methotrexate induced renal failure, as shown by significant serum creatinine and urea elevation. Additionally, the results indicated that methotrexate significantly induced lipid peroxidation and reduced antioxidant activities in rats. In contrast, apricot significantly prevented toxic effects of methotrexate via increased catalase, superoxide dismutase, and glutathione levels but decreased formation of malondialdehyde. Also, it was determined that exposure to methotrexate leads to significant histological damage in kidney tissue such as glomerulosclerosis and apoptosis. On the other hand, these effects can be eliminated with apricot diet. These data indicate that apricot may be useful in preventing undesirable effects of MTX such as nephrotoxicity.

Testing the efficacy of quercetin in mitigating bisphenol A toxicity in liver and kidney of mice

Quercetin (3,5,7,3',4'-pentahydroxy flavone) is a potent antioxidant found in various fruits and vegetables. The present investigation was an attempt to evaluate the mitigatory effect of quercetin on the damage caused by bisphenol A (BPA; 2,2-bis (4-hydroxyphenyl) propane), a well-known xenoestrogen, on liver and kidney of mice. Swiss strain adult male albino mice were orally administered with 120 and 240mg/kg body weight (bw)/day BPA with or without quercetin (60mg/kg bw/day) for 30days. On the completion of the treatment period, animals were killed; organs were isolated and used for the study. Results revealed that oral administration of BPA for 30days caused significant and dose-dependent decrease in body weight. Absolute and relative organ weights, total lipid and cholesterol contents were significantly increased in liver and kidney of mice when compared with vehicle control. BPA treatment also caused, when compared with vehicle control, a statistically significant reductions in the activities of catalase, superoxide dismutase, glutathione peroxidase, glutathione reductase and glutathione-S-transferase as well as in glutathione and total ascorbic acid contents; however, significant increase was found in malondialdehyde (MDA) levels. Histopathological studies revealed hepatocellular necrosis, cytoplasmic vacuolization and decrease in hepatocellular compactness in liver as well as distortion of the tubules, increased vacuolization, necrosis and disorganization of glomerulus in the kidney of BPA-treated mice. All these effects were dose-dependent. Co-treatment with quercetin (60mg/kg bw) and BPA (low dose and high dose) alleviates the changes in body weight, as well as absolute and relative organ weights of mice. It also ameliorates the oxidative stress created by BPA by lowering MDA levels and by increasing enzymatic and nonenzymatic antioxidants as well as it brings back the normal histoarchitecture of liver and kidney of mice. The present results revealed that graded doses of BPA caused oxidative damage in liver and kidney of mice, which is mitigated by quercetin.

Angiotensin II causes oxidative stress and DNA damage in mouse kidneys via the angiotensin II type 1 receptor

Angiotensin II causes oxidative stress and DNA damage in mouse kidneys via the angiotensin II type 1 receptor

N-acetilcisteína e deferoxamina protegem contra insuficiência renal aguda induzida por isquemia/reperfusão em ratos

Antioxidants are widely used in animal models to prevent renal injury after ischemia/reperfusion, but it is unknown if the benefits of antioxidants are additive. In this study, we aimed to investigate the protective effects of N-acetylcysteine plus deferoxamine in an animal model of kidney ischemia/reperfusion injury. Bilateral kidney ischemia was mastintained for 45 minutes. N-acetylcysteine, deferoxamine or both were administered into the aorta above the renal arteries immediately prior to induction of ischemia. Five rats from each group were sacrificed 1, 6 or 12 hours after reperfusion for the determination of blood creatinine, kidney oxidative damage parameters and myeloperoxidase activity. The combination of N-acetylcysteine and deferoxamine, but not their isolated use, prevented the increase in creatinine after ischemia/reperfusion. This prevention was followed by a consistent decrease in myeloperoxidase activity and oxidative damage parameters both in the kidney cortex and medulla. Treatment with N-acetylcysteine and deferoxamine was superior to the isolated use of either compound in an animal model of kidney ischemia/reperfusion.

Oxidative Stress and DNA Damage in Mice Kidneys Exposed to Cadmium Chloride

Background: Cadmium is one of the most toxic heavy metals in our environments having a very strong ability to accumulate in body organs especially in kidney. Our aim of this study is to determine of the genotoxicity and cytotoxicity in mice kidneys exposed to cadmium. Material and Method: In this study we sacrificed 30 male mice and randomly divided into 2 different groups (control& case). Every 5 mice remained in one cage at the same standard conditions. After a week, the mice were exposed to Cd (300µm/Kg.b.wt) on 0, 6, 12, 24, 48 hrs by peritoneal injections. After 24hrs from the latest injection, the mice were killed and obtained their kidneys, and then the oxidative stress markers (malondialdehide (MDA), glutathione (GSH) and superoxide dismutase (SOD)) were assayed on homogenized kidneys in order to study of cytotoxicity, genotoxicity and DNA damage. We used Comet assay on separated kidney cells. Finally, for analyzing statistical data, we used T-test and ANOVA using SPSS15 software. Results: In treated group, MDA and GSH concentration and also SOD (ρ<0.05) activity significantly increased in comparison with control group. Conclusion: The comet assay results obviously showed DNA breakage stimulated by Cd in treated group it was not seen in the control group.

Protective effect of ω-3 polyunsaturated fatty acids (PUFAs) on sodium nitroprusside–induced nephrotoxicity and oxidative damage in rat kidney

Sodium nitroprusside (SNP) a nitric oxide (NO) donor has proven toxic effects. Dietary ω-3 polyunsaturated fatty acid (PUFA) has been shown to reduce the severity of numerous ailments. Present study examined whether intake of fish oil (FO)/flaxseed oil (FXO, Omega Nutrition, St Vancouver, Canada) would have protective effect against SNP-induced toxicity. Male Wistar rats (150 ± 10 g) were used in this study. Initially animals were divided into two groups: one fed on normal diet and the other on 15% FO/FXO for 15 days. On the 16th day, SNP (1.5 mg/kg body weight) was administered intraperitoneally for 7 days daily. After 7 days animals were killed, kidneys were harvested for further analysis. SNP induced nephrotoxicity by increasing serum creatinine and blood urea nitrogen, SNP significantly decreased malate dehydrogenase, glucose-6-phosphatase, fructose-1,6-bisphosphatase and malic enzyme but increased lactate dehydrogenase and glucose-6-phosphate dehydrogenase. Brush border membrane enzymes such as alkaline phosphatase, γ-glutamyl transpeptidase and leucine amino peptidase were also decreased. The activity of catalase and glutathione peroxidase decreased concomitantly with increased lipid peroxidation, indicating that the significant kidney damage has been inflicted by SNP. Feeding of FO and FXO with SNP ameliorated the changes in various parameters caused by SNP. The results of the present study suggest that ω-3 PUFA-enriched FO and FXO from seafoods and plant sources, respectively, are similarly effective in reducing SNP-induced nephrotoxicity and oxidative damage. Thus, vegetarians who cannot consume FO can have similar health benefits from plant-derived ω-3 PUFA.

Protective effect of ω-3 polyunsaturated fatty acids onL-arginine-induced nephrotoxicity and oxidative damage in rat kidney

L-Arginine (ARG), an essential amino acid, is the endogenous source of the deleterious nitric oxide. Dietary ω-3 polyunsaturated fatty acid (PUFA)-enriched fish oil (FO) has been shown to reduce the severity of certain types of cancers, cardiovascular disease, and renal disease. Present study examined whether feeding of FO/flaxseed oil (FXO) would have protective effect against ARG-induced nephrotoxicity. ARG-induced nephrotoxicity was recorded by increased serum creatinine and blood urea nitrogen. ARG significantly altered the activities of metabolic and brush border membrane (BBM) enzymes. ARG caused significant imbalances in the antioxidant system. These alterations were associated with increased lipid peroxidation (LPO) and altered antioxidant enzyme activities. Feeding of FO and FXO with ARG ameliorated the changes in various parameters caused by ARG. Nephrotoxicity parameters lowered and enzyme activities of carbohydrate metabolism, BBM and inorganic phosphate (32Pi) transport were improved to near control values. ARG-induced LPO declined and antioxidant defense mechanism was strengthened by both FO and FXO alike. The results of the present study suggest that ω-3 PUFA-enriched FO and FXO from seafoods and plant sources, respectively, are similarly effective in reducing ARG-induced nephrotoxicity and oxidative damage. Thus, vegetarians who cannot consume FO can have similar health benefits from plant-derived ω-3 PUFA.

Amelioration of kidney function markers by Sonchus asper butanolic extract against KBrO3-induced toxicity in rat

The protective effects of Sonchus asper butanol extract against KBrO3- induced oxidative damage in kidney of rat were determined in this study. 24 Sprague-Dawley male rats (180 to 200 g) were divided into 4 groups. Group I was given saline (1 ml/kg b.w., 0.85% NaCl) and DMSO (1 ml/kg b.w.); group II was treated with KBrO3 (20 mg/kg b.w., i.p.); group III and IV administered with KBrO3 and after 48 h with Sonchus asper butanolic extract (SBE) (100; 200 mg/kg b.w.). All the treatments were given twice a week for five weeks. The results revealed that KBrO3 induced oxidative stress as evidenced by the significant alteration in physical and serum marker of kidney which were restored with SBE dose dependently revealed that S.asper butanol extract can protect the kidney against KBrO3 mediated oxidative damage. Key words: Sonchus asper, KBrO3, oxidative stress, physical analysis, serum markers.

Protective effects of Chrysanthemi Flos extract against streptozotocin-induced oxidative damage in diabetic mice

The present study was aimed to evaluate the protective role of Chrysanthemi Flos extract (CFE) against free radical-mediated oxidative damage in liver and kidney of streptozotocin (STZ) - induced diabetic mice. Chrysanthemi Flos was extracted with methanol. Male ICR mice (n = 24) were divided into four groups. Diabetes was induced by STZ injection (ip) at a dose of 100 mg/kg. Animals of treated groups were given CFE and gliclazide (1000 and 50 mg kg −1 body weight) for 30 days. The results revealed that oral administration of CFE and gliclazide inhibited the increase in lipid peroxidation, aspartate transaminase (AST), alanin transaminase (ALT) and alkaline phosphatase (ALP) activities caused by STZ. Besides, a significant amelioration in antioxidant enzymes like superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) was observed. On the other hand, non enzymic antioxidant such as reduced glutathione (GSH) and ascorbic acid level was significantly increased while α-tocopherol level was decreased. Furthermore, CFE caused significant restoration in DNA fragmentation induced by STZ. These findings suggest that CFE has protective effects against STZ induced oxidative damage in liver and kidney of diabetic mice.

Oxidative stress mediated cytotoxicity of TiO2 nano anatase in liver and kidney of Wistar rat

This study examined the adverse effects of TiO2 nanoparticle (nano-TiO2) on the kidney and liver of Wistar rats. Changes of serum biochemical parameters and pathological lesions indicated that liver and kidney were significantly affected in animals treated with 50 mg kg−1 of nano-TiO2. The inverse relationship between the level of reactive oxygen species and the activities of superoxide dismutase, catalase, and glutathione peroxidase indicates that nano-TiO2 induces oxidative stress. A significant increase in the apoptosis of liver and kidney in a dose-dependent manner was also observed. The ultrastructural observations confirmed the internalization of nano-TiO2 and their direct involvement in the mitochondria-mediated cytotoxicity. Data indicated that nano-TiO2 induce oxidative stress which produces genotoxicity such as oxidative DNA damage, micronuclei (MN) induction, and cell apoptosis in liver and kidney.

Radio-protective response on the environmental pollutant induced oxidative stress

The purpose of this study was to investigate the protective effect of low dose radiation on TCE induced oxidative damage in rats. The oxidative damage of both liver and kidney was assessed by serum alkaline phosphatase (ALP), Gamma Glutamyl Trans-Peptidase (GGTP), Alanine and Aspartate Amino Transferase (ALT & AST) activities in addition concentrations of cholesterol, high density lipoprotein-cholesterol (HDL-c), low density lipoprotein-cholesterol (LDL-c), Triacyglycerols (TGs), urea and creatinine were analyzed. Liver lipid peroxidation (MDA), Nitric Oxide (NO), reduced glutathione (GSH) levels, and activities of both Super-Oxide Dismutase (SOD) and Glutathione Peroxidase (GSH-Px) were measured. Results: TCE administration increase serum ALP, GGTP, ALT, AST activities, cholesterol, triacylglycerols, LDL-c, urea and creatinine concentrations, besides liver MDA and NO, whereas it decreased SOD, GSH-Px activities, GSH level in liver, HDL-c in serum. Low dose of gamma rays (0.5 Gy) exposure significantly improved lipid peroxidation and oxidative injury induced by TCE. Conclusion: The study indicates that treatment with low dose of gamma rays ameliorate harmful effects induced by TCE taking in consideration the effect of gamma radiation as a stimulant of radical detoxification.

Effects of melatonin on partial unilateral ureteral obstruction induced oxidative injury in rat kidney

Aim:This experimental study was designed to produce ischemia-reperfusion injury in rat kidney by performing partial unilateral ureteral obstruction (PUUO) and investigated the effects of melatonin on the levels of oxidative injury parameters.Materials and Methods:Twenty-four adult male rats were randomly divided into three groups as follows; control group (Group 1); only nephrectomy and blood (5 ml) drawn from vena cava inferior, PUUO group (Group 2); PUUO (10 days)+ipsilateral nephrectomy after recovery of PUUO+blood from vena cava inferior VCI, melatonin treated group (Group 3); PUUO (10 days)+melatonin (1/2 hr before release, 50 mg/kg, ip)+ipsilateral nephrectomy after recovery of PUUO+blood from VCI. The left ureter was embedded into the psoas muscle to create PUUO. After 10 days, PUUO was recovered and ipsilateral nephrectomies were performed for biochemical analysis of superoxide dismutase (SOD), catalase (CAT), malondialdehyde (MDA), glutathione peroxidase (GSH-Px), and protein carbonyl (PC) in the tissues and blood was drawn from inferior vena cava to study the same parameters in systemic circulation. The results were compared statistically.Results:The blood levels of MDA, NO, and PC were increased in the PUUO group in comparison to the sham-operated group (P<0.05). Melatonin treatment reduced MDA, NO, and PC levels in blood after PUUO recovery, but statistically significance consisted only for MDA and NO (P<0.05). The antioxidant enzyme activities (SOD, GSH-Px) were increased in the PUUO group (P<0.05). Melatonin treatment reduced SOD and GSH-Px activities in comparison with the sham-operated control group (P<0.05). Similarly, renal tissue levels of MDA, NO, and PC were increased in the PUUO group in comparison with the sham-operated group (P<0.05). Melatonin treatment ameliorated MDA, NO, and PC levels in renal tissue after PUUO recovery only MDA was statistically significant (P<0.05). Antioxidant enzyme activities (SOD, CAT, and GSH-Px) were increased in the PUUO group. Melatonin treatment caused reduction in SOD, CAT, and GSH-Px activities in comparison to the sham-operated control group (P<0.05).Conclusion:The results of this study showed that experimentally induced PUUO caused oxidative stress in rat kidney and melatonin treatment reduced oxidative stress and therefore may have a preventive effect on PUUO induced oxidative kidney damage in rats.

Effect of erdosteine on cyclosporine induced chronic nephrotoxicity.

Dear Editor, Drugs and exogenous toxins, including aminoglycosides, amphotericin B, cisplatin, and radiocontrast media, may cause acute kidney injury (1). The manifestations which indicate that damage is occurring are a sudden increase in kidney injury biomarkers (NGAL [neutrophil gelatinase-associated lipocalin], KIM-1 [kidney injury molecule-1], etc.) and kidney failure (creatinine, cystatin C). This implies a requirement for close monitoring of kidney function with eventual dose reduction or even the interruption of drug administration. However, it may eventuate that, even if the source of the damage is stopped, it could still result in permanent kidney failure. One of the major causes of kidney injury driven by different compounds is an increase in the production of reactive oxygen species (ROS), activation of stress kinases and thus apoptosis (2, 3). In their study “Protective effect of erdosteine on cyclosporine induced chronic nephrotoxicity in rats,” Uz et al. discuss the role of cyclosporine (CsA) in nephrotoxicity. CsA therapy causes dose and time related deterioration of kidney functions by inducing an increase in free radical production (4). The authors describe erdosteine, a mucolytic and anti-inflammatory agent used for the treatment of chronic pulmonary diseases, as having protective effects against CsA-induced nephropathy. This was assessed by evaluating changes in the levels of antioxidant enzymes and nitric oxide (NO) and by the study of kidney morphology through immunohistochemistry. Erdosteine has an antioxidant activity thanks to the presence of two blocked sulfhydryl groups. Erdosteine induced a marked decrease in proximal tubule degenerative changes compared with the CsA group. Moreover, the activity of the anti-oxidant enzyme glutathione peroxidase (GSHPx), increased after CsA + erdosteine treatment. Also increments of malondialdehyde (MDA) and nitric oxide (NO) levels in the rats’ kidneys were prevented by its administration. Recently the activity of other mucolitics has been proven to result in a reduction of kidney oxidative damage. Our studies have demonstrated that N-acetylcysteine (NAC), a thiol compound classically known as a mucolytic agent, is a potent antioxidant that scavenges a wide variety of oxygen-derived free-radicals and may be capable of preventing acute kidney injury (5, 6). Our in vitro data, using kidney cells, confirmed that NAC may be effective due to its antioxidant properties by preventing contrast-induced renal cell apoptosis. This effect was dose-dependent: indeed, the greater the dose, the larger the cellular benefit. Although still controversial, the protective effects of NAC in preventing contrast-induced acute kidney injury have been observed in several clinical studies and meta-analyses (6, 7). In conclusion, mucolytic agents seem to be effective in preventing drug–induced nephrotoxicity. Additional studies are however, warranted in order to clarify whether these drugs should be included in our clinical practice.

Eucommia ulmoides Bark Protects Against Renal Injury in Cadmium-Challenged Rats

Eucommia ulmoides Oliver is a perennial woody plant distributed widely in China. To characterize some major compounds in E. ulmoides bark extract, six compounds were identified via high-performance liquid chromatography qualitative analysis. E. ulmoides bark extract protects against cadmium-induced oxidative damage in rat kidneys. Two compounds of E. ulmoides bark extract, geniposide and genipin, which were identified both in serum and in kidney tissue, showed inhibitory effects on nitric oxide production. This study provides biological evidence supporting the usefulness of E. ulmoides bark against cadmium-induced toxic oxidative stress in rat kidney tissue.

The Effect of Rooibos ( Aspalathus Linearis) Supplementation On Tert-Butylhydroperoxide-Induced Oxidative Damage in Liver and Kidney of Rats

The Effect of Rooibos ( Aspalathus Linearis) Supplementation On Tert-Butylhydroperoxide-Induced Oxidative Damage in Liver and Kidney of Rats

Impaired Nrf2-ARE pathway contributes to increased oxidative damage in kidney of spontaneously hypertensive rats: Effect of antioxidant (honey)

Impaired Nrf2-ARE pathway contributes to increased oxidative damage in kidney of spontaneously hypertensive rats: Effect of antioxidant (honey)

Resveratrol ameliorates oxidative DNA damage and protects against acrylamide-induced oxidative stress in rats

Acrylamide (ACR), used in many fields from industrial manufacturing to laboratory personnel work is also formed during the heating process through interactions of amino acids. Therefore ACR poses a significant risk to human health. This study aimed to elucidate whether resveratrol (RVT) treatment could modulate ACR-induced oxidative DNA damage and oxidative changes in rat brain, lung, liver, kidney and testes tissues. Rats were divided into four groups as control (C); RVT (30mg/kg i.p. dissolved in 0.9% NaCl), ACR (40mg/kg i.p.) and RVT+ACR groups. After 10days rats were decapitated and tissues were excised. 8-hydroxydeoxyguanosine (8-OHdG) is a biomarker of oxidative DNA damage. 8-OHdG content in the extracted DNA solution was determined by enzyme-linked immunosorbent assay method. Malondialdehyde (MDA), glutathione (GSH) levels and myeloperoxidase activity (MPO) were determined in tissues, while oxidant-induced tissue fibrosis was determined by collagen contents. Serum enzyme activities, cytokine levels, leukocyte apoptosis were assayed in plasma. As an indicator of oxidative DNA damage, 8-OHdG levels significantly increased in ACR group and this was reversed significantly by RVT treatment. In ACR group, GSH levels decreased significantly while the MDA levels, MPO activity and collagen content increased in the tissues suggesting oxidative organ damage. In RVT-treated ACR group, oxidant responses reversed significantly. Serum enzyme activities, cytokine levels and leukocyte late apoptosis which increased following ACR administration, decreased with RVT treatment. Therefore supplementing with RVT can be useful in individuals at risk of ACR toxicity.