The effect of doxorubicin on rats that received toxic and carcinogenic benzo(a)pyrene.

Benzo(a)pyrene (B(a)P) is a polycyclic aromatic hydrocarbon with carcinogenic and toxic effects. Doxorubicin is a DNA-interacting drug widely used in chemotherapy. In the present study we investigated the effects of doxorubicin on rats that received benzo(a)pyrene. Sprague-Dawley male rats, 3-4 months old, were divided into 5 groups (n=9 per group). Group 1 (controls) received normal saline intraperitoneally (i.p.) and intragastrically (i.g.), Group 2 (controls) similarly received corn oil i.p. and i.g., Group 3 received corn oil soluble benzo(a)pyrene (10mg/kg b.wt every 10 days for 40 days), Group 4 received doxorubicin (4 mg i.p. on 3 consecutive days), Group 5 received doxorubicin for 3 days (as in group 4) followed by benzo(a)pyrene as in group 3. After twenty-four hours urine samples were collected, heart blood, liver and kidney tissue samples were obtained. Biochemical data were evaluated on urine and blood; liver and kidney tissue samples were investigated histologically. Uric acid, urine creatinine, creatine clearance, urea nitrogen, serum creatinine values, serum glutamic oxaloacetic transaminase (SGOT, AST), serum glutamic pyruvic transaminase (SGPT, ALT), alkaline phosphatase (ALP, AP), superoxide dismutase (SOD), catalase (CAT) activities and malondialdehyde (MDA) levels were significantly different in the 3rd group compared with control groups. Most of the parameters group 5 were statistically similar to control values. Histological appearance of the liver and the kidney tissue samples supported the improvement in the 5th group. The result of our study indicated that liver and kidney functions impaired with benzo(a)pyrene may be partially restored by doxorubicin

The effect of paclitaxel on rats following benzo(a)pyrene treatment

Objective: To observe the effects of paclitaxel on rats that received benzo(a)pyrene

Erythropoietin prevents nitric oxide and cathepsin-mediated neuronal death in focal brain ischemia

We examined the preventive effect of human recombinant erythropoietin (HrEPO) on nitric oxide (NO)-mediated toxicity to neurons and cysteine protease release into cytoplasm, which is attributed to neuronal death in brain ischemia. Focal cerebral ischemia was induced by permanent occlusion of middle cerebral artery in two sets of rat. The first set was used to monitor NO concentration and cathepsin activity, while the second was used for histological examination with hematoxylin and eosin, and TUNEL staining. A group in both set was administered human recombinant erythropoietin (HrEPO). NO content, cathepsins B and L activity increased significantly in the post-ischemic cerebral tissue (p 0.05). A significant increase in the number of necrotic and apoptotic neurons was observed in the post-ischemic cerebral cortex (p < 0.05). HrEPO treatment was markedly lowered both of these (p < 0.05). It is concluded that HrEPO prevents neuronal death by protecting neuronal liposomes from NO-mediated toxicity and suppressing the release of cathepsins. (C) 2010 Elsevier B.V. All rights reserved