Related Experiment Videos
Erdosteine against acetaminophen induced renal toxicity
Bunyamin Isik1, Reyhan Bayrak, Ali Akcay
1Department of Family Medicine, Division of Nephrology, Fatih University, Ankara, Turkey.
Molecular and Cellular Biochemistry
|March 15, 2006
Summary
Erdosteine, an antioxidant mucolytic agent, shows protective effects against acetaminophen-induced kidney damage in rats. It reversed key indicators of nephrotoxicity, suggesting a potential preventive role.
Area of Science:
- Pharmacology
- Toxicology
- Nephrology
Background:
- Acetaminophen (APAP) overdose is a significant clinical issue leading to severe kidney toxicity.
- Oxidative stress and inflammation are key mechanisms in APAP-induced nephrotoxicity.
- Erdosteine is a mucolytic agent with known antioxidant properties through its active metabolites.
Purpose of the Study:
- To investigate the potential protective effects of erdosteine against APAP-induced renal damage in a rat model.
- To evaluate the impact of erdosteine on oxidative stress markers and histological changes in the kidneys following APAP administration.
Main Methods:
- Female Wistar Albino rats were administered APAP (1 g/kg) alone or in combination with varying doses of erdosteine (150 or 300 mg/kg).
- Renal tissue was analyzed for lipid peroxidation, nitric oxide (NO) levels, and antioxidant enzyme activities (CAT, GSH-Px, SOD).
- Kidney histology was examined for signs of tubular damage, and blood urea nitrogen (BUN) and creatinine levels were measured.
Main Results:
- APAP treatment significantly increased lipid peroxidation and NO levels, while decreasing CAT and GSH-Px activities in renal tissue.
- Histopathological examination revealed tubular degeneration, vacuolization, and cell desquamation in APAP-treated rats, with elevated BUN and creatinine.
- Erdosteine treatment dose-dependently ameliorated these pathological changes, reducing oxidative stress and improving kidney morphology and function.
Conclusions:
- Erdosteine demonstrates significant protective effects against acetaminophen-induced nephrotoxicity in rats.
- Its antioxidant properties appear to mitigate the oxidative stress and cellular damage caused by APAP.
- Erdosteine may serve as a viable preventive therapeutic option for acetaminophen-induced kidney injury.
Related Concept Videos
01:11Renal Failure: Dose Adjustments
In patients with renal impairment, drugs undergo significant changes in their pharmacokinetics, which require dosage adjustments to ensure safe and effective therapy.
Reduced renal clearance and elimination rate are common outcomes of renal impairment. These alterations lead to a prolonged elimination half-life and an altered apparent volume of distribution for drugs. As a result, dosage adjustments are typically necessary to maintain optimal drug levels in the body.
However, dosage adjustments...
Reduced renal clearance and elimination rate are common outcomes of renal impairment. These alterations lead to a prolonged elimination half-life and an altered apparent volume of distribution for drugs. As a result, dosage adjustments are typically necessary to maintain optimal drug levels in the body.
However, dosage adjustments...
01:30Acute Kidney Injury IV: Diagnostic Studies and Prevention
Accurate diagnosis and effective prevention are critical in managing Acute Kidney Injury (AKI), which is linked to high mortality rates ranging from 10% to 80%. Timely recognition of at-risk patients and careful monitoring can significantly reduce the likelihood of kidney damage.Diagnostic Assessments:The diagnostic process starts with a comprehensive medical history to identify prerenal, intrarenal, and postrenal causes.Prerenal causes, such as dehydration, hypotension, or blood loss, should...
01:25Drug Dosing in Renal Diseases: Dose Adjustments Based on Drug Clearance and Elimination Rate Constant
In patients with renal disease, dosage adjustments are necessary to maintain therapeutic plasma drug concentrations and prevent toxicity or subtherapeutic exposure. Renal impairment alters drug pharmacokinetics, especially in conditions like uremia, where changes such as prolonged elimination half-life and altered apparent volume of distribution can significantly affect drug disposition. These changes require careful modification of the dosing regimen to achieve the desired clinical...
01:15Renal Drug Excretion: Overview
As primary excretory organs, the kidneys maintain homeostasis by removing waste substances from the bloodstream. They comprise over a million units called nephrons, which serve as the kidney's functional units.
A nephron consists of two primary structures: the renal corpuscle and the renal tubule. The renal corpuscle contains the glomerulus, a network of capillaries where the first step of renal excretion, glomerular filtration, occurs. Blood pressure forces water, ions, and small molecules out...
A nephron consists of two primary structures: the renal corpuscle and the renal tubule. The renal corpuscle contains the glomerulus, a network of capillaries where the first step of renal excretion, glomerular filtration, occurs. Blood pressure forces water, ions, and small molecules out...
01:28Drug Dosing in Renal Diseases: Estimation of Glomerular Filtration Rate Based on Serum Creatinine Concentration
Glomerular filtration rate (GFR) can be estimated from serum creatinine using the modification of diet in renal disease (MDRD) formula or the chronic kidney disease–epidemiology collaboration (CKD–EPI) equation. Both methods are widely used in clinical practice to assess kidney function and guide treatment decisions.The MDRD equation does not require weight or height measurements and is normalized to the body surface area of 1.73 m², considered the average adult surface area. This equation is...
01:28Renal Drug Excretion: Tubular Secretion
Active tubular secretion is a robust, energy-demanding process that utilizes carrier systems to transport drugs into renal tubules. The active renal secretion systems include the organic anion transporter (OAT) for weak acids and the organic cation transporter (OCT) for weak bases. Structurally similar drugs can compete for the same transporter, potentially leading to drug accumulation and toxicity. However, this principle can be exploited therapeutically. One example is probenecid (Probalan),...