Ulcerative colitis increases oxidative damage accompanied by production of free oxygen radicals. Selenium (Se) and vitamin E are two natural antioxidants. The present study was undertaken to investigate the possible protective role of Se and vitamin E combination in experimental colitis induced by acetic acid (AA) in rats. This study was carried out on three groups, namely the first (control), the second (experimental colitis group, 2 ml 5% acetic acid), and the third groups (2 ml 5% acetic acid, vitamin E (100 mg/kg body weight (bw)) plus Se (0.2 mg/kg bw)). The activities of catalase (CAT), prolidase (PRS), myeloperoxidase (MPO), total antioxidant capacity (TAC), total oxidant status (TOS), oxidative stress index (OSI), total thiol (T-SH) were determined in plasma and colon samples. Macroscopic and microscopic damages in colon were increased by AA treatment (p < 0.01 and p < 0.01, respectively), whereas they were decreased by selenium and vitamin E treatment (p < 0.05 and p < 0.01, respectively). The activities of CAT and PRS in the plasma and colon were significantly affected (p < 0.05 and p < 0.01) by treatment of AA, Se, and vitamin E. MPO activity in colon was increased (p < 0.01) by AA treatment and decreased (p < 0.05) by Se and vitamin E administration. The values of TOS and OSI in plasma were increased (p < 0.5) by AA. The TAC and T-SH in colon were decreased (p < 0.05) by AA and increased (p < 0.05) by Se and vitamin E. Based upon these results, Se and vitamin E may play an important role in preventive indication of the oxidative damage associated by acetic acid caused inflammation.
The present investigation was designed to determine the protective effects of melatonin against bleomycin (BLM)-induced oxidant lung toxicity. Wistar-albino rats were divided into four groups: saline (SA, 0.4 mL/animal), 1% ethanol-saline (ALC, 0.4 mL/animal), bleomycin sulphate (BLM, 10 mg/kg), or bleomycin sulphate + melatonin (BLM, 10 mg/kg + MLT, 10 mg/kg). All injections were given intraperitoneally (i.p.), twice weekly for a period of 3 wk (a total of seven injections for each group). Twenty-five days after BLM treatment, pulmonary fibrosis was assessed as hydroxyproline content in lung homogenates. Findings show that BLM-induced pulmonary injury resulted in increases in bronchoalveolar lavage fluid (BALF) biomarkers including total protein, lactate dehydrogenase (LDH), glutathione-peroxidase (GSH-Px), superoxide dismutase (SOD), and catalase (CAT). Additionally, the levels of thiobarbituric acid reactive substances (TBARS), an index of lipid peroxidation (LPO), were also increased in BALF. Conversely, the level of glutathione (GSH) was reduced in BALF of BLM-treated rats. Melatonin provided protection against BLM-induced pulmonary fibrosis by suppressing oxidative stress. It abolished BLM-stimulated LPO and reversed the imbalance between oxidants and antioxidants in the BALFs. Results thus indicate that melatonin inhibits BLM-induced lung toxicity associated with oxidative damage.
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