Doxorubicin Induced Nephrotoxicity: Protective Effect of Nicotinamide

Introduction. Nephrotoxicity is one of the important side effects of anthracycline antibiotics. The aim of this study was to investigate the effects of nicotinamide (NAD), an antioxidant agent, against nephrotoxicity induced by doxorubicin (DXR). Methods. The rats were divided into control, NAD alone, doxorubicin (20 mg/kg, i.p.) and DXR plus NAD (200 mg/kg, i.p.) groups. At the end of the 10th day, kidney tissues were removed for light microscopy and analysis. The level of tissues' catalase (CAT), glutathione (GSH), glutathione peroxidase (GPx), inducible nitric oxide (iNOS) and endothelial nitric oxide (eNOS) activities were determined. Results. The activities of CAT, GPx, and GSH were decreased, and Po was increased in renal tissue of doxorubicin group compared with other groups. The tissue of the doxorubicin group showed some histopathological changes such as glomerular vacuolization and degeneration, adhesion to Bowman's capsule and thickening and untidiness of tubular and glomerular capillary basement membranes. Histopathological examination showed that NAD prevented partly DXR-induced tubular and glomerular damage. Conclusions. Pretreatment with NAD protected renal tissues against DXR-induced nephrotoxicity. Preventive effects of NAD on these renal lesions may be via its antioxidant and anti-inflammatory action

Partial load-bearing rabbit ulnar segmental defects are regenerated with biocompatible grafts with or without bone marrow-derived mesenchymal stem cells

BACKGROUND: The autologous bone grafts still have been used as the gold standard to initiate and facilitate bone healing in cases with bone defects. Because of some disadvantages of autologous bone grafts, the new biocomposite grafts have been researched. The purpose of the present study was to investigate whether the bone marrow-derived mesenchymal stem cells (BM-MSCs) loaded into a biocomposite scaffold enhance bone regeneration

The effects of beta-glucan on iron levels and lipid peroxidation in intra-abdominal sepsis in rats

Sepsis is defined as a systemic response of organisms to microorganisms and toxins. Sepsis is associated with the enhanced generation of reactive oxygen metabolites, leading to multiple organ dysfunctions. beta-glucan is accepted to be one of the most powerful immune response modifiers. The aim of this study was to investigate the putative protective effect of beta-glucan on changes of iron and malondialdehyde (MDA) levels in various tissue and blood after experimental sepsis in rats. Sepsis was induced by cecal ligation and perforation (CLP) in 32 male Wistar albino rat. To evaluate this, rats were divided into four groups as sham operated, beta-glucan treated sham operated, CLP and beta-glucan treated CLP. Sixteen hours after operation, rats were decapitated and MDA and iron levels were measured in the liver, kidney, heart, diaphragm tissues and blood. Also, whole tissue histopathology was evaluated by a light microscope. The results demonstrate that sepsis significantly decreased iron levels of all tissues and blood. The decrease in tissue iron levels and the increase MDA levels demonstrate the role of trace elements and free radicals in sepsis-induced tissue damage. Our results indicate that the given dose of beta-glucan was probably insufficient to prevent sepsis-induced organ injury

The effects of alpha lipoic acid on liver cells damages and apoptosis induced by polyunsaturated fatty acids

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Evaluation of effects of melatonin and caffeic acid phenethyl ester on acute potassium dichromate toxicity and genotoxicity in rats

Objective: The aim of this study is to investigate the possible protective effects of melatonin and caffeic acid phenethyl ester (CAPE) on potassium dichromate (K2Cr2O7)-induced nephrotoxicity and genotoxicity