Curcumin prevents oxidative renal damage induced by acetaminophen in rats

Expressions of Protein Oxidation Markers, Dityrosine and Advanced Oxidation Protein Products in Acetaminophen-Induced Liver Injury in Rats

“…Tubular cell death was observed in rats 24 hr after injection. These findings are consistent with the results of the previous study in which an overdose of APAP was administered to experimental animals [5,11]. APAP-induced nephrotoxicity is due to NAPQI produced as a result of the metabolic conversion of APAP by the microsomal P-450 enzyme system, similarly to liver injury [11,25,27].…”

“…APAP-induced nephrotoxicity is due to NAPQI produced as a result of the metabolic conversion of APAP by the microsomal P-450 enzyme system, similarly to liver injury [11,25,27]. Oxidative stress is reported to play a role in the pathogenesis of APAP-induced nephrotoxicity, as evidenced by an increase in the lipid peroxidation and depletion of intracellular glutathione, similarly to APAP-induced liver injury [5].…”

Antioxidant and Anti-inflammatory Effects of Curcumin Against Hepatorenal Oxidative Injury in the Experimental Sepsis Model Created in Rats

“…MDA measurement is used as an indicator of lipid peroxidation. [33] In an acetaminophen-induced renal injury model in rats, Cekmen et al [34] showed that renal tissue MDA levels were decreased with curcumin. Moreover, tissue MDA levels were also decreased with curcumin in a renal ischemia/ reperfusion model [35] and in a methotrexate-induced hepatic injury model.…”

Acetaminophen-induced nephrotoxicity in rats: Protective role ofCardiospermum halicacabum

“…Acute overdose of acetaminophen is known to cause hepatic and renal damage in both human and experimental animals (Ghosh & Sil, 2007). Nephrotoxicity is less common compared to hepatotoxicity in acetaminophen overdose, but renal damage and acute renal failure can occur even in the absence of liver injury and can even lead to death in humans and experimental animals (Cekmen et al, 2009;Palani et al, 2009). Hepatic-derived acetaminophen metabolites, particularly glutathione conjugates, play important role in nephrotoxicity.…”