Curcumin Improves Biomolecules Associated with Renal Function and Attenuates Oxidative Injury and Histopathological Changes in Potassium-Induced Toxicity in Rats' Kidney.

The protective effect of curcumin on potassium bromate (KBrO3)-induced renal damage was investigated in vivo. Treatment with KBrO3 (20 mg/kg bw) caused a significant increase in arginase and adenosine deaminase (ADA) activities in rats' kidney. However, oral administration of curcumin (20 mg/kg bw) caused a significant reduction in ADA and arginase activities in KBrO3 + CUR group. Furthermore, nitric oxide level was significantly low in KBrO3 group compared with the control. After treatment with curcumin in KBrO3 + CUR group, nitric oxide levels increased significantly (P < 0.05). Determination of some kidney biomarkers revealed elevated levels of creatinine, serum urea, and electrolytes (Na+ and Cl-) in KBrO3-treated rats. Curcumin effectively reduced the levels of these renal function parameters in KBrO3 + CUR groups and were not significantly different from the control. Antioxidant enzyme activities such as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPX) activities as well as glutathione (GSH) levels were significantly low with concomitant higher levels of malondialdehyde (MDA) after treatment with KBrO3. Curcumin caused a significant increase in SOD, CAT, and GPX activities including GSH levels with lower production of MDA in kidney homogenates of rats in KBrO3 + CUR. Curcumin ameliorated corpuscular degeneration in the kidney tissue and exhibited protection against tubular necrosis. These results revealed the protective effect of curcumin against KBrO3-induced renal toxicity by preventing degradation of ADA and arginine, improving antioxidant status and histopathological changes in rats' kidney.

Curcumin Administration Mitigates Cyclophosphamide-Induced Oxidative Damage and Restores Alteration of Enzymes Associated with Cognitive Function in Rats' Brain.

The use of chemotherapeutic drugs is associated with oxidative damage, cognitive dysfunction, and brain damage. This study sought to investigate the neuroprotective effect of curcumin against cognitive problems associated with treatment with cyclophosphamide via assessment of biomolecules associated with cognitive function in rats' brain homogenates. Rats were divided in to five groups: Control (vehicle), CUR (curcumin [20 mg/kg]), CPA (cyclophosphamide [150 mg/kg]), CUR1 + CPA (curcumin [20 mg/kg] and cyclophosphamide [150 mg/kg]), and CPA + CUR2 (cyclophosphamide [150 mg/kg] and curcumin [20 mg/kg]). After the treatment, cognitive behavior was assessed and enzymes [cholinesterases, purinergic enzymes, arginase, and angiotensin I-converting enzyme] associated with cognitive function were examined. Oxidative stress parameters [total thiol, non-protein thiol, malondialdehyde, and nitric oxide] including the expression of caspase-3 were also assessed in rats' brain. Our results showed that curcumin improved cognitive behavior, attenuated cholinergic deficit as revealed by the inhibition of cholinesterases, and improved purinergic signaling in cyclophosphamide-treated rats. Furthermore, curcumin reduced angiotensin-I-converting enzyme and arginase activities before and after treatment with cyclophosphamide. Curcumin also improved redox balance and showed protection against cyclophosphamide-induced oxidative damage to rats' brain via an increase in protein and non-protein thiols and nitric oxide levels as well as a significant reduction in malondialdehyde levels. Curcumin also prevented neuronal degeneration in different brain regions and reduced caspase-3 expression. Hence this study suggests that pre and post-treatment with curcumin improved neurobehavior, modulates some biomarkers associated with cognitive function and exhibit neuroprotection against cyclophosphamide-induced neurotoxicity in rats.

Mortality, oxidative stress and hepatotoxicity in juvenile African catfish, Clarias gariepinus Burchell, exposed to lead and cypermethrin.

In this study, juvenile catfish (Clarias gariepinus) were exposed to 2 mg/L Pb, 0.5 µg/L cypermethrin, or both for 96 h. Survival ranged from 100% in both treatments without cypermethrin, to 50% in fish exposed to cypermethrin only or the mixture. There were significant decreases in liver lysozyme, γ-glutamyl transpeptidase, and alanine aminotransferase activities in fish exposed to cypermethrin or the mixture. Liver aspartate aminotransferase activity (AST) showed a significant reduction after exposure to Pb or cypermethrin alone, and the effect of the mixture on AST was additive or potentially synergistic. Liver lipid peroxidation (LPO) was increased in fish exposed to the mixture compared to those exposed to cypermethrin only, indicating that Pb presence enhanced LPO caused by cypermethrin. Our study demonstrates the potential for toxic interaction between Pb and cypermethrin in fish and suggests that due to the varying responses to contaminant mixtures in our study, researchers should consider using a variety of biomarkers.