The present study was undertaken to evaluate the place of oxidative stress on breast cancer. Lipid peroxidation as evidenced by malondialdehyde (MDA) and the status of the antioxidants superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) were estimated in tissues of 10 fibroadenoma and 40 breast cancer patients. Lipid peroxidation in breast cancer tissues was enhanced compared to nonmalignant tissues (p < 0.001). Similarly, antioxidants SOD (p < 0.001) and GPx (p = 0.007) in tumor tissues significantly were increased. On the contrary, CAT activity was found significantly decreased (p < 0.001). We found that oxidant/antioxidant status was independent from any prognostic factors concerning breast cancer. The results of our study have shown higher oxygen-free-radical production and decreased CAT activity support the oxidative stress hypothesis in breast carcinogenesis.
Hydrocephalus causes damage to periventricular white matter at least in part through chronic ischemia. Emphasizing the periventricular ischemia/hypoxia in hydrocephalus, various authors indicated the secondary biochemical impairment and oxidative damage in experimentally induced and congenital hydrocephalic rat brain. (-)-Epigallocatechin gallate (EGCG), the main constituent of green tea polyphenols, has been shown to be of some protective value in various models of neurological injury as a free oxygen radical scavenger. In the present study the effects of EGCG were examined on the periventricular oxidative damage in experimental childhood-onset hydrocephalus. Hydrocephalus was induced in 3 weeks-old rat pups by kaolin injection into the cisterna magna. A single daily dose of 50 mg/kg of EGCG injected into the peritoneum of the rats for 15 days significantly reduced periventricular white matter malondialdehyde levels when compared to non-treated hydrocephalic animals. Our results indicate that EGCG may have a protective effect against periventricular white matter oxidative damage in hydrocephalus induced infantile rats.
Study Design: The e ect of epidural space perfusion with chilled saline solution (% 0.9 NaCl) on lipid peroxidation after experimental spinal cord injury in rats was evaluated. Objectives: The extent of lipid peroxidation is a useful parameter for evaluating the cellular disturbance caused by spinal cord trauma in experimental conditions. The protective e ects of hypothermia against neurological injury resulting from trauma or ischemia both in experimental and clinical situations have been demonstrated. Setting: Departments of Neurosurgery and Biochemistry, Cerrahpasa Medical School, Istanbul, Turkey. Methods: Twenty-®ve female Wistar Albino rats were used. There were ®ve rats in group I (sham-operated), seven rats in group II (trauma), and eight rats in group III (epidural cooling). The remaining ®ve rats were used for the pilot study to determine the spinal cord and body temperature. A clip compression method was used to produce acute spinal cord injury. In group III, 30 min after the trauma the injured spinal cord was cooled by perfusion of the epidural space with chilled saline solution (% 0.9 NaCl) with a¯ow rate of 5 ml/min for 30 min. At 2 h after trauma, all rats other than the ones used in the pilot study, were sacri®ced and the spinal cords were excised. The extent of lipid peroxidation in the spinal cord was assessed by measuring the tissue content of malonil dialdehyde (MDA). Results: The tissue MDA contents were 1.58 micromol MDA/gram wet weight (gww) in group 1 (sham-operated), 2.58 micromol MDA/gww in group 2 (trauma), and 1.77 micromol/ gww in group 3 (epidural cooling), the di erences being statistically signi®cant.
Conclusion:The results indicated that epidural cooling of traumatized spinal cord is e ective in preventing secondary damage due to the peroxidation of lipid membranes.
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