Erdosteine Against Acetaminophen Induced Renal Toxicity

Abstract

Acetaminophen (APAP) induced toxicities have been a major problem in clinical practice. The aim of the present study was to demonstrate a possible protective role of erdosteine, a mucolytic agent having antioxidant properties via its active metabolites, on APAP induced renal damage in rats. Female Wistar Albino rats were divided into groups including control, erdosteine (150 mg/kg, oral), APAP (1 g/kg, oral) APAP+erdosteine (150 mg/kg, oral) and APAP+erdosteine (300 mg/kg, oral). APAP treatment caused lipid peroxidation as well as high NO level in renal tissue. Also, APAP treated rats had decreased activities of CAT and GSH-Px, but not SOD. In addition, tubular epithelial degeneration, vacuolization and cell desquamation were clearly observed in the APAP treated rats. The cellular debris in the proximal tubules and cortical interstitial congestions were prominent in the kidneys of APAP treated rats. BUN and creatinine levels were increased after APAP administration. All these pathological changes were reversed after erdosteine treatments. Erdosteine treated APAP groups showed milder tubular degeneration, epithelial vacuolization in the proximal tubules, lesser cellular desquamation and better morphology when compared with APAP groups. In conclusion, erdosteine may be a choice of preventive treatment against APAP induced nephrotoxicity.

Impact of Dehydroepiandrosterone in Prevention of Paracetamol Induced Nephrotoxicity in Rats

“…In this study, we demonstrated that the administration of Science Publications AMJ overdose PCM (750 mg kg −1 ) for 28 consecutive days was able to induce nephrotoxicity in rats, as demonstrated by the significantly increased level of plasma urea and creatinine and significant decreases in serum total proteins. These results are in agreement with that observed by Isik et al (2006) who noticed an elevation in serum urea and creatinine in rats after 1 g kg −1 b.w. of PCM administration.…”

Effects of medical ozone therapy on acetaminophen-induced nephrotoxicity in rats

“…Different studies have shown that APAP-induced renal damage is consistent with acute tubular necrosis. [1][2][3][22][23][24] Direct toxic effect of APAP on capillary wall may be responsible from APAP-induced acute tubular necrosis. The other histopathological findings of APAPinduced nephrotoxicity in rats are tubular epithelial degeneration, proximal tubular vacuolization, cell desquamation, necrosis and cellular debris in the proximal tubules, and cortical interstitial congestion.…”

“…Renal insufficiency occurs in approximately 1-2% of the patients with an overdose of APAP. [1][2][3][4] The main toxicity of APAP is the result of drug metabolism in the liver and other organs. At the pharmacologic doses, APAP is metabolized mostly to inactive compounds via Phase II reactions by conjunction by sulfate and glucuronide.…”

A case of acetaminophen (paracetamol) causing renal failure without liver damage in a child and review of literature

“…In another study, it is showed that acetaminophen increases reactive oxygen radicals such as nitric oxide and this also contributes to cell damage. 5,6 In our patient, nephrotoxicity without hepatotoxicity occurred after acetaminophen overdose. Some clinical situations such as alcohol ingestion, low protein diets, starvation, and inducing the P-450 enzymatic system with drugs (carbamazepine, phenobarbital, phenytoin, and so on) may enhance the nephrotoxicity of acetaminophen.…”