Nephrotoxicity In Male Albino Rats Research Articles

Ameliorative effect of selenium nanoparticles and fish oil on cisplatin and gamma irradiation-induced nephrotoxicity in male albino rats

Cisplatin (CP) is a major antineoplastic drug for the treatment of solid tumors, however, its clinical utility is limited by nephrotoxicity. Also, radiotherapy is an important treatment modality for many malignancies. The present studies were performed to test whether fish oil (FO) and/or selenium nanoparticles (SeNPs) administration have an ameliorative effect on CP and γ-irradiation induced nephrotoxicity. FO and/or SeNPs were administered to male albino rats daily for 12 days before being intraperitoneally injected with a single dose of CP (10 mg/kg body weight) and whole body exposed to a single dose of γ-radiation (0.7 Gy). Biochemical analysis and histopathological examination were performed. Pretreatment with FO and/or SeNPs before the administration of CP and exposure to γ-radiation significantly reduced CP- and γ-radiation-induced high levels of serum urea and creatinine and renal tumor necrosis factor-α, caspase-3 and cyclooxygenase-2, also they significantly prevented renal total antioxidant capacity levels decrease and ameliorated the levels of most studied trace elements. The histopathological results supported the biochemical findings of this study. The administration of FO and/or SeNPs might be useful for preventing nephrotoxicity which can be caused by CP and radiotherapy during the treatment of various malignancies.

The Protective Effect of Acacia senegal gum against Gentamicin-Induced Nephrotoxicity In Albino Rats

Introduction: Acacia senegal gum is commonly known as Arabic gum or gum Arabic(GA) which obtained from the branches and stems of the trees as a dried gummy exudates. It is widely used in food and pharmaceutical industries as emulsifier and suspending agent. It has many pharmacologic effects including gastrointestinal effects such as increasing the short chain fatty acids and enhance water and electrolytes intestinal absorption but variable effects on lipid metabolism. In chronic renal failure patients, gum arabic reduces serum urea nitrogen. It is a potent superoxide scavenger so that it have a good protective activity against acetaminophen-induced hepatotoxicity and doxorubicin-induced cardiotoxicity in rats. The Aim of study: In the present study, we investigated the protective effect of Acacia senegal gum against gentamicin (GM)-induced nephrotoxicity in male albino rats. Materials and Method: The animals were divided into three groups A (Control), B (GM-only treated rats, 80mg/Kg, IM for 7days) and C (GA 10g/100ml water, orally for 4weeks prior to GM treatment). The nephrotoxicity was evaluated biochemically by determination level of serum Creatinine (Crea), Urea (Urea) and Uric acid (UA) level and histologically by microscopic examination the degree of proximal tubular damage. Results: The results showed significant increase in the level of Crea, Urea and UA in animals treated with GM only. In group (C), the level of Crea was high significant compared with the control but the level of Urea was significantly decreased compared with the control and the level of UA was significantly decreased compared with group B but higher than the control. Conclusion: These results suggest that Acacia senegal gum has some nephroprotective in rats, may be due to its antioxidant activities of GA.

The possible protective effect of L-arginine against 5-fluorouracil-induced nephrotoxicity in male albino rats.

5-fluorouracil (5-FU) is a potent antineoplastic agent used for the treatment of various malignancies. The L-arginine nitric oxide (NO) pathway involved in the pathogenesis of chemotherapy induced kidney damage. This work investigated the beneficial mechanism of L-arginine supplementation in 5-FU induced nephropathy. Eighty male Wistar rats were divided into four equal groups: control group; L-arginine group (378 mg/rat/day for 4 weeks); 5-FU group (189 mg/rat/week for 4 weeks) and L-arginine for 1 week before and 4 weeks concomitant with 5-FU group. At the end of experiment, the kidney functions were assessed and kidneys specimens were processed for paraffin sections and stained with haematoxylin and eosin (H&E), Masson's trichome (MT) and periodic acid-Schiff (PAS) stains. Other sections were processed for immunohistochemical demonstration of caspase-3 and inducible NO synthase (iNOS). Image analyser was used to analyse the results morphometrically and statistically. L-arginine administration to 5-FU treated animals elicited significant reduction in serum urea and creatinine levels, urine volume, urinary protein excretion and kidney/body weight ratio in comparison to fluorouracil treated group. L-arginine improved glomeruloscelerosis, degeneration of convoluted tubules and interstitial fibrosis in 5-FU treated animals. L-arginine attenuated effectively some biochemical and histological changes in 5-FU nephrotoxicity.

Curcumin ameliorates diclofenac sodium-induced nephrotoxicity in male albino rats.

Exposure to drugs often results in toxicity in the kidney which represents the major control system maintaining homeostasis of the body and thus is especially susceptible to xenobiotics. Nephrotoxicity is a life-threatening side-effect of nonsteroidal anti-inflammatory drugs (NSAIDs). Diclofenac is one of the most frequently prescribed NSAIDs and have been reported to cause multiple organs damage. Curcumin (CUR) exhibits nephroprotective properties. Therefore, rats were divided into four groups; rats of groups 3 and 4 received diclofenac (100mg/kg, i.m.), whereas rats of groups 2 and 4 received CUR (100mg/kg, p.o.) for 3 days. Diclofenac revealed a significant increase in urea and creatinine levels and malondialdehyde concentration and marked reduction in catalase activity and reduced glutathione concentration. Histopathologically, diclofenac produced fatty changes and eosinophilic casts were detected in the renal tubules, those were attenuated by administration of CUR prior diclofenac.

Selenium nanoparticles with low-level ionizing radiation exposure ameliorate nicotine-induced inflammatory impairment in rat kidney.

Occupational exposure to low-level ionizing radiation (<1Gy) was shown to enhance cell protection via attenuating an established inflammatory process. Nicotine, a major toxic component of cigarette smoke, is responsible for smoking-mediated renal dysfunction. The present study was therefore aimed to investigate the protective impact of ginger Zingiber officinale selenium nanoparticles (SeNPs) with whole-body low-dose gamma radiation (γ-R) against nicotine-induced nephrotoxicity in male albino rats. Nicotine intoxication was induced with 0.5mg/kg BW. Rats received 0.1mg SeNPs/kg BW by gastric gavage concomitant with 0.5 Gy γ-R over 4weeks. Characterization studies showed the formation of spherical SeNPs with a size ranged from 10 to 30nm in diameter with a thin film encapsulating the nanoballs. Our data revealed that nicotine induced renal dysfunction manifested by significant abnormal levels of kidney function markers (creatinine, urea, sodium and potassium) accompanied by increased levels of malondialdehyde along with a reduction in glutathione level, glutathione peroxidase, and glutathione S-transferase activities. It is worthy to note that nicotine toxicity induced significant increments in serum inflammatory markers: tumor necrosis factor-α and vascular cell adhesion protein 1. Western blotting showed marked significant elevation in caspase-3 activities against nicotine. The mRNA gene expression of inducible cyclooxygenase-2 gene was highly increased with nicotine intoxication while that of cyclooxygenase-1 did not show any changes. Interestingly, our data demonstrated that SeNPs in synergistic interaction with γ-R are efficacious control against nicotine-induced nephrotoxicity via anti-oxidant-mediated anti-inflammatory activities. Thus, it is tempting to recommend dietary approaches with ginger SeNPs for smokers at workplaces exposed occupationally and regularly to low-level ionizing radiation.

Renoprotective effect of Mangifera indica polysaccharides and silymarin against cyclophosphamide toxicity in rats

The present study aims to evaluate the possible protective role of polysaccharides extracted from the Egyptian mango Mangifera indica L. (MPS) and silymarin against cyclophosphamide (CP) nephrotoxicity in male albino rats. Male rats were randomly divided into, control group (administered distilled water orally for 10days) and MPS (500, 1000mg/kg, p.o.) and/or silymarin (150mg/kg, p.o.) treated groups for 10days. In the last 5days of treatment rats were administered CP (150mg/kg, i.p). The MPS revealed significant prophylactic effect against kidney injury induced by CP as demonstrated by enhancement of the kidney function via decreasing serum creatinine, urea and uric acid. Treatment of rats with MPS extract and/or silymarin significantly increased the level of reduced glutathione (GSH) and superoxide dismutase (SOD) activity while decreased the level of total malondialdehyde (MDA) and glutathione-S-transferase (GST). Also, histopathological examinations confirmed the protective efficacy of MPS and/or silymarin against CP nephrotoxicity. In conclusion, the obtained results of the present study support the protective antioxidant role of MPS and/or silymarin against CP-induced kidney disorder in rats.

Hepato- and nephrotoxicity in male albino rats exposed to malathion and spinosad in stored wheat grains.

Adult male albino rats were fed on stored wheat grains (Triticum aestivum L.) treated with malathion and spinosad at both 8 and 16 ppm for 90 consecutive days to evaluate their hepatic and renal toxicity. The activity of serum acetylcholinesterase (AChE) was decreased in rats treated with the higher concentration of both tested pesticides. Biochemical parameters of liver functions [i.e., aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), acid phosphatase (ACP) activity, as well as total protein, albumin, bilirubin and cholesterol levels] were severely affected especially at higher concentration. Malathion and spinosad elevated the activity of ALT, AST, ALP and ACP in rats treated with the higher concentration. Also, total and direct bilirubin levels increased in rats treated with the higher concentration of both pesticides. On the contrary, both pesticides decreased total protein and albumin levels in treated rats in a concentration-dependent manner. Furthermore, malathion was found to be hyperglycemic. Kidney function parameters (i.e., urea and creatinine levels) were increased in treated rats in a concentration-dependent manner. The above mentioned effects were supported by histopathological examination of liver and kidney tissues. The obtained results indicated also that malathion was able to cause a more pronounced hepato- and renal toxicity in rats than spinosad.

Hepato and Nephrotoxicity in Male Albino Rats Exposed to Malathion and Spinosad in Stored Wheat Grains

Adult male albino rats were fed on stored wheat grains (Triticum aestivum L.) treated with malathion and spinosad at both 8 and 16 ppm for 90 consecutive days to evaluate their hepatic and renal toxicity. The activity of serum acetylcholinesterase (AChE) was decreased in rats treated with the higher concentration of both tested pesticides. Biochemical parameters of liver functions [i.e., aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), acid phosphatase (ACP) activity, as well as total protein, albumin, bilirubin and cholesterol levels] were severely affected especially at higher concentration. Malathion and spinosad elevated the activity of ALT, AST, ALP and ACP in rats treated with the higher concentration. Also, total and direct bilirubin levels increased in rats treated with the higher concentration of both pesticides. On the contrary, both pesticides decreased total protein and albumin levels in treated rats in a concentration-dependent manner. Furthermore, malathion was found to be hyperglycemic. Kidney function parameters (i.e., urea and creatinine levels) were increased in treated rats in a concentration-dependent manner. The above mentioned effects were supported by histopathological examination of liver and kidney tissues. The obtained results indicated also that malathion was able to cause a more pronounced hepato- and renal toxicity in rats than spinosad.

Sarah A. Vogel. Is It Safe? BPA and the Struggle to Define the Safety of Chemicals. xxi + 304 pp., illus., index. Berkeley: University of California Press, 2013.

Previous articleNext article No AccessBook ReviewsSarah A. Vogel. Is It Safe? BPA and the Struggle to Define the Safety of Chemicals. xxi + 304 pp., illus., index. Berkeley: University of California Press, 2013.Michael EganMichael Egan Search for more articles by this author PDFPDF PLUSFull Text Add to favoritesDownload CitationTrack CitationsPermissionsReprints Share onFacebookTwitterLinkedInRedditEmail SectionsMoreDetailsFiguresReferencesCited by Isis Volume 105, Number 1March 2014 Publication of the History of Science Society Article DOIhttps://doi.org/10.1086/676809 Views: 147Total views on this site Citations: 4Citations are reported from Crossref © 2014 by The History of Science Society. All rights reserved.PDF download Crossref reports the following articles citing this article:Shaimaa M. M. Saleh, A. Bakr Mahmoud, M. Bassam Al-Salahy, Fatma Ahmed Mohamed Moustafa Morphological, immunohistochemical, and biochemical study on the ameliorative effect of gallic acid against bisphenol A-induced nephrotoxicity in male albino rats, Scientific Reports 13, no.11 (Jan 2023).https://doi.org/10.1038/s41598-023-28860-1Eslam M. Hamed, Sam F.Y. Li Molecularly imprinted polymers-based sensors for bisphenol-A: Recent developments and applications in environmental, food and biomedical analysis, Trends in Environmental Analytical Chemistry 35 (Sep 2022): e00167.https://doi.org/10.1016/j.teac.2022.e00167Okunola A. Alabi, Kehinde I. Ologbonjaye, Adewale A. Sorungbe, Olutayo S. Shokunbi, Oyinkansola I. Omotunwase, Gbemisola Lawanson, Oluwafemi G. Ayodele Bisphenol A-induced Alterations in Different Stages of Spermatogenesis and Systemic Toxicity in Albino Mice ( Mus musculus ), Journal of Health and Pollution 11, no.2929 (Feb 2021).https://doi.org/10.5696/2156-9614-11.29.210307 Current Bibliography of the History of Science and Its Cultural Influences, 2014, Isis 105, no.S1S1 (Jul 2015): i–301.https://doi.org/10.1086/680345

Silymarin prevents adriamycin-induced cardiotoxicity and nephrotoxicity in rats

Adriamycin is a potent anticancer agent, its clinical use is limited for its marked cardiotoxicity and nephrotoxicity. The present study aimed to investigate the possible protective role of the natural antioxidant silymarin on ADR-induced heart and kidney toxicity. Studies were performed on four groups of rats. 1 – control group, 2 – silymarin group (50 mg/kg), 3 – adriamycin group (10 mg/kg), 4 – adriamycin + silymarin group. On the third day after ADR injection, plasma was separated for determination of LDH, CPK, cholesterol and total lipids. 30 days after ADR injection, plasma was separated for determination of creatinine and urea levels. Frozen heart specimens (72 h) and frozen kidney specimens (30 days) were used for estimation of lipid peroxides and GSH contents. Histopathological examinations of heart and kidney sections were also done. Pretreatment of ADR-treated rats with silymarin resulted in a significant decrease in the plasma CPK, LDH, creatinine and urea. On the other hand silymarin pretreatment did not change ADR-induced hyperlipidemia. Silymarin pretreatment significantly decreased the myocardial MDA contents. In addition, silymarin pretreatment normalized renal tissue contents of MDA and GSH. Histopathological examination of heart and kidney sections revealed that ADR caused only mild myocardial injury in silymarin pretreated rats. Also, silymarin pretreatment inhibited ADR-induced renal tubular damage in rats. These results have suggested that, silymarin ameliorated ADR-induced cardiotoxicity and protected against ADR-induced nephrotoxicity in male albino rats. The mechanisms of silymarin induced protection against ADR-induced toxicities were proved to be due to inhibition of lipid peroxidation and protection against GSH depletion.