Kidney Of Male Wistar Rats Research Articles

Protective Effect of Vitamins A, E, and C on the Zinc Oxide Nanoparticles Induced Oxidative Stress Status in Kidney of Male Wistar Rats

Protective Effect of Vitamins A, E, and C on the Zinc Oxide Nanoparticles Induced Oxidative Stress Status in Kidney of Male Wistar Rats

Combined cerium and zinc oxide nanoparticles induced hepato-renal damage in rats through oxidative stress mediated inflammation

The toxicity profiles of nanoparticles (NPs) used in appliances nowadays remains unknown. In this study, we investigated the toxicological consequences of exposure to cerium oxide (CeO2) and zinc oxide (ZnO) nanoparticles given singly or in combination on the integrity of liver and kidney of male Wistar rats. Twenty (20) rats were allotted into four groups and treated as: Control (normal saline), CeO2NPs (50 μg/kg), ZnONPs (80 μg/kg) and [CeO2NPs (50 μg/kg) + ZnONPs (80 μg/kg)]. The nanoparticles were given to the animals through the intraperitoneal route, three times per week for four repeated weeks. Results revealed that CeO2 and ZnO NPs (singly) increased serum AST and ALT by 29% & 57%; 41% & 18%, and co-administration by 53% and 23%, respectively. CeO2 and ZnO NPs increased hepatic and renal malondialdehyde (MDA) by 33% and 30%; 38% and 67%, respectively, while co-administration increased hepatic and renal MDA by 43% and 40%, respectively. The combined NPs increased hepatic NO by 28%. Also, CeO2 and ZnO NPs, and combined increased BAX, interleukin-1β and TNF-α by 45, 38, 52%; 47, 23, 82% and 41, 83, 70%, respectively. Histology revealed hepatic necrosis and renal haemorrhagic parenchymal in NPs-treated rats. Summarily, CeO2 and ZnO NPs produced oxidative injury and induced inflammatory process in the liver and kidney of experimental animals.

Protective effect of cinnamon oil against ciprofloxacin toxicity on liver and kidney of male Wistar rats

Cinnamon zeylanicum is one of many herbal medications. This herb contains different materials like, cumarin, cinnamaldehyde and cinnamic acid. The plant plays a role as antiallergic, antiviral, antimicrobial, anti-inflammatory and antioxidant and other health conditions. This study focused on the therapeutic effect of cinnamon oil on hepatorenal toxicity induced by ciprofloxacin in male rats. Forty rats were housed in the animal house of the College of Pharmacy, University of Kerbala, Karbala city, Iraq. The animals were separated into four groups: Group 1. Control group (not taken drug nor cinnamon oil), Group 2. Ciprofloxacin group (drenched 250 mg/kg/day of ciprofloxacin for 30 days), Group 3. Cinnamon oil group (drenched 1ml/kg/day of cinnamon oil for 30 days) and Group 4. Cinnamon+ciprofloxacin group (drenched 1ml/kg/day of cinnamon + 250 mg/kg/day of ciprofloxacin for 30 days). Finally, 2ml of blood was collected from each rat and the serum was separated for estimating the biochemical parameters of the liver like, Aspartate transaminase (AST), alanine transaminase(ALT) and alkaline phosphatase(ALP) and the kidney (Creatinine, Urea and albumin) . The results proved that ciprofloxacin significantly elevates the parameters of the liver and kidney (p≤0.05). The results also proved the benefit of cinnamon oil in improving health by reducing the toxic effect of ciprofloxacin by lowering the elevated levels of (liver enzymes, creatinine, urea and albumin). The study showed that this oil reduced the toxic effect of ciprofloxacin on the kidney and liver.

Polyphenol-rich Spondias mombin leaf extract abates cerebral ischemia/reperfusion-induced disturbed glutamate-ammonia metabolism and multiorgan toxicity in rats

ABSTRACT Introduction: This study investigated the protective properties of Spondias mombin leaf extract (SML), in cerebral ischemia/reperfusion (I/R) mediated toxicity in the brain, liver, and kidney of male Wistar rats. Materials and methods: Animals were subjected to 30 min of bilateral common carotid artery occlusion followed by 24 h of reperfusion (BCCAO/R). The animals were divided into sham, I/R, and I/R treated with SML (25, 50 and 100 mg/kg) or quercetin (20 mg/kg) groups. Animals were sacrificed after 24 h of reperfusion and markers of organ toxicity (urea creatinine, glutamine synthetase (GS), glutaminase (GA), aspartate aminotransferase (AST), alanine aminotransferase (ALT), acetylcholinesterase (AChE)) were measured in the brain regions (cortex, striatum, and hippocampus), liver, and kidney. Results and discussion: BCCAO/R significantly (p < 0.0001) inhibited the glutamate-glutamine cycle and mediated toxicity in the cerebral cortex, striatum, hippocampus, liver, and kidney of rats. Post-treatment with SML significantly (p < 0.0001) reversed glutamate-glutamine cycle inhibition and ameliorated cerebrohepatorenal toxicity in ischemic rats. Conclusion: Cerebral I/R significantly mediated cerebral, hepatic, and renal toxicity through the inhibition of glutamate-ammonia detoxification in rats, and SML protected against this post-ischemic glutamate-ammonia mediated multiorgan toxicity.

Ivermectin ameliorate the toxic effect of dimethylhydrazine in male Wistar rats

Cancer is emerging as one of the most significant challenges to the human health. Ivermectin (IVM) is one of the most effective drugs in veterinary and human medicine. The purpose of this study was to evaluate the potential preventative effect of IVM against cytotoxicity induced by dimethylhydrazine (DMH) in Male Wistar rats. Three concentrations of IVM (0.25, 0.5 and 1 mg/kg) were utilized in this study. Liver function enzymes, inflammatory markers and histopathological alterations in liver and kidney tissues were investigated. Obtained data showed that the combination of DMH with each concentration of IVM increased the activity of liver enzymes (ALT, ALP, AST, and GGT) compared to control and DMH alone. RT-PCR findings showed upregulation in the level of INF-γ, IL-6, IL-1β, Cox1, and Cox2 genes compared to control. In contrast, IL-6 gene was down-regulated. The levels of genes expression were down-regulated with combined DMH with medium and high concentrations compared to DMH alone. Microscopic analysis demonstrated histological alterations in the liver and kidney of rats treated with DMH. Combinations of DMH either with medium or high concentration resulted in less pathological features in both liver and kidney tissues. In conclusion, this study showed that IVM mitigated the toxic effects of DMH on the liver and kidney of male Wistar rats.

Inhibitory effects of Indonesian temu kunci (Boesenbergia rotunda) rhizome extract on nitric oxide synthase production and on the kidneys of Wistar rats

Nitric oxide synthases (NOSs) are enzymes that function by generating nitric oxide (NO) from its substrate, L‑arginine, in human tissues. There are three known isoforms of NOS, eNOS (endothelial NOS), nNOS (neuronal NOS), and iNOS (inducible NOS). iNOS is released in response to inflammation. The human iNOS inhibitor, S‑ethylisothiourea (SEITU), has been found to attach to a Glu377 residue within the active‑site cavity of the enzyme. The discovery of iNOS inhibitors is always challenging. <em>Boesenbergia rotunda</em> (<em>B. rotunda</em>) has been reported to reduce inflammation in an animal model. The present study examined the inhibitory effects of <em>B. rotunda</em> rhizome ethanolic extract (BRE) on iNOS using the fluorometric method and investigated the histopathological effects of higher concentrations of BRE (1,000, 2,000 and 4,000 mg/kg body weight) on the kidneys of male Wistar rats. Molecular docking simulation of quercetin and kaempferol towards iNOS was also performed. The phytochemical screening of BRE indicated the presence of polyphenolics, flavonoids, triterpenoids, and saponins. The <em>in vitro</em> experiment confirmed that BRE reduced NO production with a half‑maximal inhibitory concentration value of 79.06 µg/ml. Both quercetin and kaempferol interacted with Glu377 by building hydrogen bonds. Furthermore, the animal experiment resulted in no mortality and no marked morphological changes in the rat kidneys at all concentrations, indicating the safety of BRE as regards this organ. Taken together, BRE may be further developed as a safe anti‑inflammatory drug candidate.

Effects of Fructose and Stress on Rat Renal Copper Metabolism and Antioxidant Enzymes Function.

The effects of a fructose-rich diet and chronic stress on copper metabolism in the kidneys are still understudied. We investigated whether fructose and/or chronic unpredictable stress modulate copper metabolism in a way that affects redox homeostasis, thus contributing to progression of metabolic disturbances in the kidney. We determined protein level of copper transporters, chaperones, and cuproenzymes including cytochrome c oxidase, as well as antioxidant enzymes function in the kidneys of male Wistar rats subjected to 20% liquid fructose supplementation and/or chronic stress. Liquid fructose supplementation increased level of copper chaperone of superoxide dismutase and decreased metallothionein level, while rendering the level of copper importer and copper chaperones involved in copper delivery to mitochondria and trans Golgi network unaffected. Stress had no effect on renal copper metabolism. The activity and expression of renal antioxidant enzymes remained unaltered in all experimental groups. In conclusion, fructose, independently of stress, decreased renal copper level, and modulated renal copper metabolism as to preserve vital cellular function including mitochondrial energy production and antioxidative defense, at the expense of intracellular copper storage.

Nephrotoxicity of nickel nano and microparticles in rat- a comparative, time dependent study with special reference to antioxidant defence system

A comparative and time dependent study on the effects of nickel oxide nano and nickel oxide microparticles (5 mg/kg body weight) each, has been performed in the kidney of male Wistar rats at two intervals of 15 and 30 days. Morphological, functional changes and effects on antioxidant enzymes in the kidney were studied. Exposure to both, NiONPs and NiOMPs significantly enhanced the generation of reactive oxygen species viz. malondialdehyde, hydrogen peroxide and nitric oxide in rat kidney. However, increase was higher in NiONPs treated rats than NiOMPs treated rats. Diminished values for reduced glutathione and enzymes, that is, superoxide dismutase, glutathione peroxidise and catalase confirmed the role of oxidative stress in NiONPs induced nephrotoxicity. Increased oxidative DNA damage and histopathological changes further supported this hypothesis. Present results suggest that nanoparticles of nickel are more toxic to kidney than nickel metal ions. Reactive oxygen species are a critical factor in NiONPs induced renal toxicity in rat.

Ameliorative Effect of Trevo Dietary Supplement Against Lead Acetate Nephrotoxicity

Background: Trevo is a nutritional supplement with numerous bioactive natural products, with detoxifying and antioxidant properties. The purpose of this study was to investigate the ability of Trévo to protect against oxidative stress induced by lead in the kidneys of male Wistar rats. Methods: Thirty-five healthy male Wistar rats were divided into five groups of seven rats each, using a randomized design. I=control; II=15 mg/kg of lead acetate (PbA); III=2 ml/kg of trevo+PbA; IV=5 ml/kg of trevo+PbA; V=5 ml/kg of trevo. Animals were treated with trevo for five days before co-administration with lead intraperitoneally for 10 consecutive days. Animals were sacrificed 24hr after the last administration, blood samples were collected via cardiac puncture, and processed for assessment of urea, creatinine, and uric acid (UA), while the kidney samples were excised and processed for the following biochemical assays: Malondialdehyde (MDA), Glutathione-S-Transferase (GST), Catalase (CAT), Superoxide Dismutase (SOD), and Reduced Glutathione (GSH). Results: Injection of PbA caused a significant increase in the serum levels of urea, creatinine, and uric acid, and a significant increase (P&lt;0.001) in the MDA concentration, and decreases in GSH concentration, CAT, SOD, and GST activities (P&lt;0.05) as compared to the controls. Pretreatment with trevo prevented the oxidative stress induced by lead acetate in the kidney tissue samples and improve the renal function. The protective effect was evident at 5 ml/kg of trevo. Conclusion: The results showed that trevo was nephroprotective against lead toxicity and the activity might be linked to the presence of numerous antioxidant phytochemicals present in trevo.

MiADMSA abrogates sodium tungstate-induced oxidative stress in rats

Tungsten (W) and its compounds have emerged as a relatively new area of environmental health concern in the last decade. Tungsten is environmentally benign due to its increasing use in armour-piercing munitions and as a replacement for lead in other ammunition. It has also been identified in various hazardous waste sites and therefore been proposed for inclusion in the Environmental Protection Agency National Priorities List. The major objective of this study was to evaluate the therapeutic efficacy of orally administered monoisoamyl 2, 3-dimercaptosuccinic acid (MiADMSA) against tungstate induced oxidative injury in blood, liver and kidneys of male Wistar rats. MiADMSA, a thiol chelator has gained wide recognition recently as a future chelating drug of choice specifically for arsenic and was chosen for this study as tungstate ions too have an affinity toward the –SH group thus, being less bioavailable in the body. We determined the effects of MiADMSA (50 mg/kg, p.o.) against sodium tungstate (500 ppm in drinking water, daily for 28 days) induced biochemical changes indicative of oxidative stress in blood, and other soft tissues of of male Wistar rats. Tungsten exposure led to an increased levels of Reactive Oxygen Species (ROS) in liver, kidney, spleen and blood accompanied also by an increase in TBARS levels. The GSH: GSSG ratio also showed a decrease on sodium tungstate intoxication. Treatment with MiADMSA restored most of the sodium tungstate-induced alterations in the biomarkers suggestive of oxidative stress. These preliminary results led us to conclude that sub-acute exposure to tungstate-induced oxidative stress could be effectively reduced by the administration of MiADMSA and thus might be a promising antidote for studying in detail its efficacy in reducing body tungstate burden and its excretion post tungstate exposure.

The potential protective role of apigenin against oxidative damage induced by nickel oxide nanoparticles in liver and kidney of male Wistar rat, Rattus norvegicus.

Nickel oxide nanoparticles (NiONPs) are involved in several applications but still have some adverse effects. Apigenin (APG) is a widespread natural product with antioxidative, anticancer, and anti-inflammatory properties. The present work aimed to study the protective role of APG against the NiONP-induced toxicity in male Wistar rats. Rats were randomly distributed to one control group and three treated groups. The treated groups were orally administered NiONPs (100mg/kg) alone, APG (25mg/kg) alone, or APG 1h before NiONPs, once daily for 28days. Blood, liver, and kidney were collected after 7, 14, and 28days of administration for Ni accumulation, hematological, biochemical, histological, and transmission electron microscopy (TEM) investigations. As compared to the controls, the administration of NiONPs alone significantly elevated the levels of Ni, malondialdehyde, total cholesterol, low-density lipoprotein cholesterol, creatinine, urea, blood urea nitrogen, and the activity of alanine and aspartate aminotransferases as well as the count of white blood cells. Besides, marked reductions in the activity of superoxide dismutase, and the levels of glutathione, high-density lipoprotein cholesterol, total proteins, albumin, globulin, hemoglobin, packed cell volume, and red blood cell count were reported. Histologically, the liver and kidney of rats administered NiONPs alone showed remarkable disturbances. According to TEM, subcellular alterations were observed in the liver and kidney of rats administered NiONPs alone. In contrast, APG administering before NiONPs substantially alleviated all the studied parameters. In conclusion, APG can ameliorate the NiONP-induced hepatotoxicity and nephrotoxicity in male Wistar rats.

Sub-acute oral toxicity study of aqueous extract of tobacco leaves (Nicotiana tabacum L.) on lipid profile, the tissue, and serum of the liver and kidney of male Wistar rats

Context Tobacco consumption may pose a very serious threat to the physiological state of the body; yet, fewer records have been documented in that regard. Objective We investigated the impact of aqueous extract of tobacco leaves on the lipid profile, the tissue, and serum levels of the liver and kidney of male Wister rats. Materials and methods Rats (n = 52; weight = 33 − 47 g; ∼ 2½ weeks old) were acclimatised for 7 days and administered aqueous extract of tobacco leaves at 100, 200, 400, 0 mg/kg of body weight (to group A, B, C, D) for 30 days. Results Compared with the control group, the kidney tissue and serum (i.e., urea and creatinine) were not influenced, in contrast, indices of the liver such as AST, ALT, and ALP, dose-dependently increased. Changes such as coagulative necrosis resulted in the infiltration of mononuclear inflammatory cells and the vacuolar degeneration of the liver. Beside the reduction in the high-density lipoprotein of the rats, there was an increase in the concentration of triglycerides, very low-density lipoprotein, low-density lipoprotein, and the total cholesterol. Conclusion Thus, extract of tobacco leaves can greatly influence the body lipid profile, beside the serum and tissues of the liver.

Assessment of the Anti-apoptotic Effects of Peganum harmala Leaf Extract on Type 2 Diabetes in the Kidney of Male Wistar Rats

Background: Growing evidence has shown that the apoptosis of cells plays an important role in the advancement of the Diabetic nephropathy (DN). Objectives: This study attempted to discover the therapeutic potential of Peganum harmala leaf extract in the apoptosis of diabetic kidney disease. Methods: In the present experimental research, 32 male Wistar rats were studied, and diabetes was induced by streptozotocin (STZ) (65 mg/kg). The animals were randomly divided into four groups (n=8, in each group) as follows: control, diabetic, control+leaf extract, diabetic+leaf extract. For our purposes, the methanolic extract of P. harmala leaves (150 mg/kg) was given by gavage for 28 days. Flow cytometry and real-time polymerase chain reaction (PCR) analyses were utilized to determine the percentages of apoptotic cells. Also, histological alterations and blood biochemical parameters were evaluated. Results: The P. harmala leaf extract has a high amount of flavonoids (25.84%), a lower percentage of alkaloids (0.14%), and some antioxidant properties. Serum urea (P&lt;0.001) and apoptosis (P&lt;0.05) significantly elevated in diabetic rats relative to the control ones. The mean of fasting blood creatinine, urea, and albumin level was not significantly changed in diabetic+leaf extract rats as compared to the diabetic ones. Histopathological results also displayed that diabetic complications in the kidney could not be improved following treatment by the leaf extract of P. harmala. In addition, the leaf extract could not significantly reduce the apoptosis and caspase-3 expression compared to diabetics in renal cells. Conclusion: Based on our findings, the leaf extract of P. harmala is unable to inhibit apoptosis in the diabetic kidney model.

Oxidative stress, DNA damage and apoptosis induced by tebuconazole in the kidney of male Wistar rat

Tebuconazole (TEB) is a broad-spectrum conazole fungicide that has been used in agriculture in the control of foliar and soil-borne diseases of many crops. The present study has investigated the adverse effects of subchronic exposure to TEB on the kidney of male rats. Animals were divided into four equal groups and treated with TEB at increasing doses 0.9, 9 and 27 mg/kg body weight for 28 consecutive days. The results showed that TEB induced oxidative stress in the kidney demonstrated by an increase in malondialdehyde (MDA), protein carbonyl (PC), advanced oxidation protein product (AOPP) levels and DNA damage, as compared to the controls. Furthermore, superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) activities were increased in the renal tissue of treated rats. Moreover, significant decrease in reduced glutathione (GSH) content in TEB-treated rats was observed, while oxidized glutathione (GSSG) levels were increased, thus a marked fall in GSH/GSSG ratio was registered in the kidney. Glutathione reductase (GR) activity showed a significant increase after TEB exposure. Moreover, TEB down-regulated the expression of Bcl2 and up-regulated the expression of Bax and caspase 3, which triggered apoptosis via the Bax/Bcl2 and caspase pathway. Also, TEB administration resulted in altered biochemical indicators of renal function and varying lesions in the overall histo-architecture of renal tissues. Taken together, our findings brought into light the renal toxicity induced by TEB, which was found to be significant at low doses.

Phosphorus Localization and Its Involvement in the Formation of Concentrated Uranium in the Renal Proximal Tubules of Rats Exposed to Uranyl Acetate.

Although the kidneys comprise a critical target of uranium exposure, the dynamics of renal uranium distribution have remained obscure. Uranium is considered to function physiologically in the form of uranyl ions that have high affinity for phosphate groups. The present study applied microbeam-based elemental analysis to precisely determine the distribution of phosphorus and uranium in the kidneys of male Wistar rats exposed to uranium. One day after a single subcutaneous injection of uranyl acetate (2 mg/kg), areas of concentrated phosphorus were scattered in the S3 segments of the proximal tubule of the kidneys, whereas the S3 segments in control rats and in rats given a lower dose of uranium (0.5 mg/kg) contained phosphorus without concentrated phosphorus. Areas with concentrated phosphorus contained uranium 4- to 14-fold more than the mean uranium concentration (126–472 vs. 33.1 ± 4.6 μg/g). The chemical form of uranium in the concentrated phosphorus examined by XAFS was uranium (VI), suggesting that the interaction of uranyl ions with the phosphate groups of biomolecules could be involved in the formation of uranium concentration in the proximal tubules of kidneys in rats exposed to uranium.

The Ameliorating Potential of Annona muricata on Sodium Fluoride-induced Toxicity on Liver and Kidney of Male Wistar Rats

The Ameliorating Potential of Annona muricata on Sodium Fluoride-induced Toxicity on Liver and Kidney of Male Wistar Rats

Renal damage induced by the pesticide methyl parathion in male Wistar rats

ABSTRACTLittle information is apparently available regarding the nephrotoxic effects induced by pesticides. The aim of this study was to examine the influence of low doses of methyl parathion (MP) on the structure and function of the kidney of male Wistar rats. A corn oil (vehicle) was administered to control rats, whereas treated rats received MP at 0.56 mg/kg orally (1/25 of LD50), every third day, for 8 weeks. At the end of each week following MP exposure, creatinine and glucose levels were measured in plasma, while glucose, inorganic phosphate, total proteins, albumin, and activity of γ-glutamyltranspeptidase (GGT) were determined in urine. Kidney histological study was also performed. Compared with control rats, MP significantly increased plasma glucose and creatinine levels accompanied by decreased urinary flow rate and elevated urinary excretion rates of glucose, phosphate, and albumin. Further, the activity of GGT in urine was increased significantly. The proximal cells exhibited cytoplasmic vacuolization, positive periodic acid Schiff inclusions, and brush border edge loss after 2 or 4 weeks following MP treatment. Finally, renal cortex samples were obtained at 2, 4, 6, and 8 weeks of MP treatment, and the concentrations of reduced glutathione (GSH) and glutathione peroxidase (GPx) activity were measured. The mRNA expression levels of BAX and tumor necrosis factor-α (TNF-α) were also determined (RT-PCR). MP significantly decreased renal GSH levels, increased GPx activity, as well as downregulated the mRNA expression of TNF-α and BAX. Densitometry analysis showed a significant reduction in TNF-α and BAX mRNA expression levels at 2 and 4 weeks following MP treatment. Low doses of MP produced structural and functional damage to the proximal tubules of male rat kidney.

Pre- and post- morphological evaluation of the kidneys of male Wistar rats inoculated with Rhipicephalus sanguineus (Latreille, 1806) (Acari: Ixodidade) salivary gland extract

Pre- and post- morphological evaluation of the kidneys of male Wistar rats inoculated with Rhipicephalus sanguineus (Latreille, 1806) (Acari: Ixodidade) salivary gland extract

Rescue effects of ginger extract on dose dependent radiation-induced histological and biochemical changes in the kidneys of male Wistar rats

Radiation is an essential modality in the management of cancer therapy, but its acute and chronic side effects on the normal organs limit the helpfulness of radiotherapy. The deleterious effects of radiation begin with oxidative stress and inflammatory reaction to radiolytic hydrolysis and formation of free radicals. The aim of the current study was to investigate the effect of dose dependent whole body radiation exposure on histological and biochemical alterations in rat kidney. It was also planned to find out whether ginger extract mitigated the deleterious effects of different doses of radiation in rat kidney. Male Wistar rats were exposed to three doses (2, 4, and 8Gy) of γ- ray with or without a 10day pretreatment with ginger extract. After 10days of whole body γ- ray exposure, the results revealed proliferation of glomerular and tubular cells, fibrosis in glomerular and peritubular and a significant increase in 8-OHdG, CRP, cystatin C (in 8Gy), plasma urea and creatinine levels, as well as a significant decrease in total antioxidant capacity of radiation groups compared to those of the control group. Ginger extract administration once daily for 10 consecutive days before exposure to 2–4–8Gy radiotherapy, which ameliorated histological and biochemical alterations in kidneys of the rats entirely or partially compared to those in the ethanol group rats. These findings indicate that whole body exposure to radiation induces kidney damage through oxidative DNA damage and inflammatory reactions, and that these effects can be alleviated using ginger pretreatment as an antioxidant and anti-inflammatory agent.

The para isomer of dinitrobenzene disrupts redox homeostasis in liver and kidney of male wistar rats

BackgroundPara-Dinitrobenzene (p-DNB) is one of the isomers of dinitrobenzene which have been detected as environmental toxicants. Skin irritation and organ toxicities are likely for industrial workers exposed to p-DNB. This study evaluated the effect of sub-chronic exposure of rats to p-DNB on cellular redox balance, hepatic and renal integrity. MethodsForty eight male Wistar rats weighing 160–180g were administered 50, 75, 1000 and 2000mg/kg b.wt (body weight) of p-DNB or an equivalent volume of vehicle (control) orally and topically for 14 days. After the period of treatment, the activities of kidney and liver catalase (CAT), alkaline phosphatase (ALP) and superoxide dismutase (SOD) as well as extent of renal and hepatic lipid peroxidation (LPO) were determined. Serum ALP activity and plasma urea concentration were also evaluated. ResultsCompared with control animals, p-DNB -administered rats showed decrease in the body and relative kidney and liver weights as well as increased renal and hepatic hydrogen peroxide and lipid peroxidation levels accompanied by decreased superoxide dismutase and catalase activities. However, p-DNB caused a significant increase in plasma urea concentration and serum, liver and kidney ALP activities relative to control. In addition, p-DNB caused periportal infiltration, severe macro vesicular steatosis and hepatic necrosis in the liver. ConclusionsOur findings show that sub-chronic oral and sub-dermal administration of p-DNB may produce hepato-nephrotoxicity through oxidative stress.