Comparison of the effects of N-acetyl cysteine and erdosteine in rats with renal injury caused by paracetamol intoxication

2010 ◽  
Vol 30 (9) ◽  
pp. 1350-1358 ◽  
Author(s):  
Hayati Kandiş ◽  
Melih Engin Erkan ◽  
Ümran Yildirim ◽  
Harun Güneş ◽  
Mesut Erbaş ◽  
...  

Aim: The aim of the present study was to investigate the therapeutic and preventive effects of N-acetyl cysteine and erdosteine on renal injury associated with paracetamol (acetaminophen) intoxication. Materials and methods: Female albino Wistar rats were divided into six groups: control; paracetamol (1 g/kg, oral); paracetamol (1 g/kg, oral) + erdosteine (150 mg/kg/day, oral); paracetamol (1 g/kg, oral) + N-acetyl cysteine (140 mg/kg bolus, followed by 70 mg/kg, oral); N-acetyl cysteine control (140 mg/kg bolus, followed by 70 mg/kg, oral); and erdosteine control (150 mg/kg/day, oral). Potential renal injury was assessed using biochemical analyses, radionuclide imaging, and histopathological parameters. Results: In the paracetamol group, blood urea nitrogen and creatinine levels were significantly increased compared with controls. Histopathological examination showed tubular vacuolization, tubular necrosis, and remarkable interstitial inflammation. The excretion function was observed to be insufficient on radionuclide imaging. However, in the groups treated with erdosteine or N-acetyl cysteine after paracetamol, biochemical analyses, radionuclide imaging, and histopathological parameters showed significantly less evidence of renal toxicity than that observed in the group receiving paracetamol alone. Less renal toxicity was detected in rats receiving N-acetyl cysteine than in those receiving erdosteine. Conclusion: Renal injury may develop after paracetamol overdose. Erdosteine and N-acetyl cysteine are both effective in the prevention of renal injury when given in the early phase of paracetamol nephrotoxicity. N-acetyl cysteine is more protective than erdosteine.

2021 ◽  
pp. 096032712199190
Author(s):  
AA Dar ◽  
A Fehaid ◽  
S Alkhatani ◽  
S Alarifi ◽  
WS Alqahtani ◽  
...  

Methotrexate (MTX) is frequently used drug in treatment of cancer and autoimmune diseases. Unfortunately, MTX has many side effects including the hepato-renal toxicity. In this study, we hypothesized that Luteolin (Lut) exhibits protective effect against the MTX-induced hepato-renal toxicity. In order to investigate our hypothesis, the experiment was designed to examine the effect of exposure of male rats to MTX (20 mg/kg, i.p., at day 9) alone or together with Lut (50 mg/kg, oral for 14 days) compared to the control rats (received saline). The findings demonstrated that MTX treatment induced significant increases in the liver and kidney functions markers in serum samples including Aspartate transaminase (AST), Alanine transaminase (ALT), creatinine, urea and uric acid. MTX also mediated an oxidative stress expressed by elevated malondialdehyde (MDA) level and decreased level of reduced glutathione (GSH), antioxidant enzyme activities, and downregulation of the Nrf2 gene expression as an antioxidant trigger. Moreover, the inflammatory markers (NF-κB, TNF-α, and IL-1β) were significantly elevated upon MTX treatment. In addition, MTX showed an apoptotic response mediated by elevating the pro-apoptotic (Bax) and lowering the anti-apoptotic (Bcl-2) proteins. All of these changes were confirmed by the observed alterations in the histopathological examination of the hepatic and renal tissues. Lut exposure significantly reversed all the MTX-induced changes in the measured parameters suggesting its potential protective role against the MTX-induced toxicity. Finally, our findings concluded the antioxidative, anti-inflammatory and anti-apoptotic effects of Lut as a mechanism of its protective role against the MTX-induced hepato-renal toxicity in rats.


2014 ◽  
Vol 2014 ◽  
pp. 1-5 ◽  
Author(s):  
Qi Qu ◽  
Bingguang Dai ◽  
Bo Yang ◽  
Xuelian Li ◽  
Yimin Liu ◽  
...  

In the present study, we aimed to investigate the preventive effects of 4-hydroxychalcone (4HCH) on resistant hypertension. We used cryptochrome-null mice, which characteristically show high plasma aldosterone levels, inflammation, and renal injury. The cryptochrome-null mice received high-salt treatment and were treated orally with 4HCH 10 mg/kg, 4HCH 20 mg/kg, and 4HCH 40 mg/kg, respectively. The salt administration in cryptochrome-null mice is able to induce an increase in systolic pressure which is associated with hyperaldosteronism, inflammation, and kidney injury. Treatment with 40 mg/kg 4HCH reduced systolic hypertension, serum IL-1β, and TNF-αlevels and suppressed the activation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and renal injury. The impact of 4HCH on the hyperaldosteronism, inflammation, and kidney injury provides new insights for future development of therapeutic strategies in resistant hypertension.


Introduction: This study aimed to assess the effect of exposure to gasoline vapor (GV) on the histomorphology and biochemical markers of renal function in rats. Methods: Twenty-four mature Wistar Albino rats weighing 180–200 g were randomly divided into two groups (n = 12 per group). Animals in group 1 (G1) served as unexposed controls, while animals in group 2 (G2) were exposed to GV for 35 days. At the end of the exposure, the animals were sacrificed, and blood samples were collected for biochemical analysis while the kidneys were removed and processed for histopathological evaluation. Results: Serum biochemical markers of renal function in the exposed group differed significantly (p< 0.05) from the unexposed group in urea (45.16 ± 1.00mg/dl versus(vs) 13.20 ± 0.69 mg/dl), creatinine (1.16 ± 0.27mg/dl vs 0.38 ± 0.10mg/dl), uric acid (3.66 ± 0.82mmol/L vs 1.96 ± 0.08mmol/L), potassium (6.90 ± 0.27mmol/L vs 3.57 ± 0.26mmol/L), sodium (182.60 ± 3.21mmol/L vs 141.33 ± 10.46mmol/L), chloride (119.00 ± 1.58mmol/L vs 103.33 ± 2.07mmol/L), pH (6.82 ± 0.22 vs 7.38 ± 0.25), bicarbonate (16.60 ± 5.03mmol/L vs 26.50 ± 3.45mmol/L), and glucose (125.60 ± 16.23mg/ dl vs 83.33 ± 4.46mg/dl). Histopathological examination of kidney sections revealed areas of degenerative and necrotic changes in the glomerulus, tubules, and renal vasculature, particularly in the cortical portion of the kidney. Conclusion: Chronic exposure to gasoline compounds may be associated with significant structural and biochemical derangements in kidney function.


Author(s):  
Samar S Ibrahim ◽  
Alshaimaa M Said

Background: The present study was designed to evaluate the relative ameliorating efficacy of lycopene against the deleterious effects of boldenone, an androgenic steroid, on the rat testis and kidney.  Materials and Methods: 40 male albino rats were divided into four groups; control group received intramuscular (i.m) injection of olive oil once a week; lycopene (Lc) group received lycopene (10 mg/kg b.w p.o daily); boldenone (Bol) group received (5 mg/kg b.w i.m once a week); Bol + Lc group received boldenone (5 mg/kg b.w i.m once a week) and lycopene (10 mg/kg b.w p.o daily) all for four weeks. Results: intramuscular injection of boldenone significantly induced lipid peroxidation and DNA fragmentation as well as inhibited total antioxidant capacity (TAC) and catalase (CAT) activity in testis and kidney tissue. Additionally, up-regulation of Bax and down-regulation of Bcl-2 gene expression after Bol injection along with marked increase in serum inflammatory cytokines and decrease in serum testosterone. These alterations were confirmed by the histopathological examination of testis and kidney. On the other hand, lycopene oral administration attenuated the testicular and renal injuries induced by boldenone injection. Conclusion: administration of antioxidants as lycopene effectively ameliorated the adverse effects of boldenone on testis and kidney tissues. Key words: Boldenone undecylenate, lycopene, DNA fragmentation, interleukin-1β, tumor necrosis factor-α, apoptosis.


2020 ◽  
Vol 92 (4) ◽  
Author(s):  
Hasan Riza Aydin ◽  
Cagri Akin Sekerci ◽  
Ertugrul Yigit ◽  
Hatice Kucuk ◽  
Huseyin Kocakgol ◽  
...  

Aim: To date, various molecules have been investigated to reduce the effect of renal ischemia/reperfusion (I/R) injury. However, none have yet led to clinical use. The present study aimed to investigate the protective effect of cordycepin (C) on renal I/R injury in an experimental rat model. Materials and methods: Twenty-four mature Sprague Dawley female rat was randomly divided into three groups: Sham, I/R, I/R+C. All animals underwent abdominal exploration. To induce I/R injury, an atraumatic vascular bulldog clamp was applied to the right renal pedicle for 60 minutes (ischemia) and later clamp was removed to allow reperfusion in all rats, except for the sham group. In the I/R + C group, 10 mg/kg C was administered intraperitoneally, immediately after reperfusion. After 4 hours of reperfusion, the experiment was terminated with right nephrectomy. Histological studies and biochemical analyses were performed on the right nephrectomy specimens. EGTI (endothelial, glomerular, tubulointerstitial) histopathology scoring and semi-quantitative analysis of renal cortical necrosis were used for histological analyses and superoxide dismutase (SOD), catalase (CAT), malondialdehyde (MDA), total oxidant status (TOS) for biochemical analyses. Results: Histopathological examination of the tissue damage revealed that all kidneys in the sham group were normal. The I/R group had higher histopathological scores than the I/R + C group. In the biochemical analysis of the tissues, SOD, MDA, TOS values were found to be statistically different in the I/R group compared to the I/R + C group (p: 0.004, 0.004, 0.001 respectively). Conclusions: Intraperitoneal cordycepin injection following ischemia preserve renal tissue against oxidative stress in a rat model of renal I/R injury.


Author(s):  
Narges Abdoli ◽  
Issa Sadeghian ◽  
Khadijeh Mousavi ◽  
Negar Azarpira ◽  
Mohammad Mehdi Ommati ◽  
...  
Keyword(s):  

2020 ◽  
Vol 48 (8) ◽  
pp. 030006052092534
Author(s):  
Emmanuel Vandi Tizhe ◽  
Najume Dogon-Giginya Ibrahim ◽  
Mohammed Yakasai Fatihu ◽  
Suleiman Folorunsho Ambali ◽  
Ikechukwu Onyebuchi Igbokwe ◽  
...  

Objectives To assess the effects of zinc pretreatment on hepatorenal toxicity following chronic exposure to glyphosate-based herbicides in male rats. Methods Following zinc pretreatment (50 mg/kg and 100 mg/kg), 14.4 to 750 mg/kg of oral glyphosate (Bushfire® herbicide) was administered daily for 36 weeks. Thereafter, serum samples were obtained following jugular venipuncture. Liver and kidney samples were processed for histopathological examination. Results Serum aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase activity as well as levels of bicarbonate, calcium, creatinine were significantly increased following chronic exposure to Bushfire®. Serum levels of sodium, potassium, chloride, total protein, albumin, globulin and urea were unchanged. Moderate to severe coagulative necrosis of hepatocytes as well as glomerular and renal tubular necrosis were observed in herbicide-treated rats. Zinc pretreatment reduced the elevation of serum enzymes associated with hepatobiliary lesions, abrogated hypercalcemia and metabolic alkalosis, and mitigated serum accumulation of creatinine following Bushfire® exposure, but was ineffective in completely preventing histological lesions. Conclusion Chronic Bushfire® exposure in rats caused hepatorenal toxicity. The effects of exposure on serum parameters were ameliorated by zinc pretreatment, but the histopathological changes associated with toxicity persisted in milder forms in zinc-pretreated animals.


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