Background and Objectives: Helicobacter pylori (H. pylori) infection has been associated with increased production of reactive oxygen species, which leads to oxidative stress in the gastrointestinal ...mucosa. Nevertheless, the association of H. pylori infection and oxidative stress in erosive reflux disease (ERD) is still unclear. We sought to investigate the association between oxidative stress status and H. pylori infection in ERD. Materials and Methods: Eighty-three ERD patients (45 male/ 38 female; mean age: 40.4 ± 14.3 years) who had heartburn and/or regurgitation and erosion(s)-confirmed by endoscopy-in the distal esophagus were enrolled. Two antral biopsies were taken from the patients for rapid urease test. Blood samples were drawn for measurement of oxidative stress parameters, including malondialdehyde (MDA), ferric reducing antioxidant power (FRAP), superoxide dismutase (SOD) activity, and glutathione peroxidase (GPX) activity. Data were compared among H. pylori(+) and H. pylori(-) patients. Results : The overall prevalence of H. pylori infection was 71% (59/83). There was a significant increase in the levels of MDA in H. pylori(+) patients (0.98 ± 0.28 μmol/l) when compared with H. pylori(-) patients (0.84 ± 0.33 μmol/l; P = 0.048). However, the levels of FRAP in the H. pylori-infected patients were significantly lower than in those without infection (941 ± 211.8 vs. 1060.3 ± 216.6 μmol/l, respectively; P = 0.028). There were no significant differences in SOD activity, GPX activity, age, sex, and body mass index (BMI) of H. pylori(+) vs. H. pylori(-) patients (P > 0.05). Conclusion: Increased levels of MDA in H. pylori(+) patients showed association between oxidative stress and H. pylori infection in EDR patients. Also, considerable changes of antioxidant concentrations indicate a compensatory mechanism to cope with the increased oxidant status in H. pylori(+) patients. It may be concluded that oxidative stress increases in the presence of H. pylori in ERD patients, and antioxidant defense mechanisms, try to minimize oxidative stress damage.
Objectives: The aim of this study is to evaluate the potential effect of caffeic acid (CAF) on the growth of breast cancer cells, in addition to determining the contributing role of caspases, ...mitochondria, and oxidative status. Methods: MCF-7 and MDA-MB-468 breast cancer cells were exposed to varying concentrations of CAF for different periods of time. The potential cytotoxic effect was measured using the MTT assay. The activities of caspase 3 and caspase 8, as well as the cellular level of reactive oxygen species (ROS) and the level of mitochondrial membrane potential (Δψm), were evaluated in different groups of cells. Results: The findings showed that CAF decreased the percentage of MCF-7 and MDAMB-468 cells in a manner that depended on the dose and duration of exposure. The death of breast cancer cells induced by CAF was associated with an increase in ROS level in both cell lines. The decrease in mitochondrial membrane potential (Δψm) following CAF treatment suggests that mitochondrial dysfunction may be involved in the death of breast cancer cells induced by CAF. Importantly, the activity of caspase 8 increased after treatment, indicating the potential involvement of the extrinsic apoptosis pathway in the inhibition of breast cancer cell growth by CAF. The dosage of 20µm of CAF following 48 hours of incubation appeared to have the most significant impact on breast cancer cells. Conclusion: The study highlights the potential pro-apoptotic effect of CAF in both estrogen-positive and estrogen-negative breast cancer cells. This, in conjunction with other evidence, may lead to new insights for more effective therapeutic approaches in breast cancer
Breast cancer, the most common cancer in the women, is the leading cause of death. Necrotic signaling pathways will enable targeted therapeutic agents to eliminate apoptosis-resistant cancer cells. ...In the present study, the effect of shikonin on the induction of cell necroptosis or apoptosis was evaluated using the T-47D breast cancer cell line. The cell death modes, caspase-3 and 8 activities and the levels of reactive oxygen species (ROS) were assessed. Cell death mainly occurred through necroptosis. In the presence of Nec-1, caspase-3 mediated apoptosis was apparent in the shikonin treated cells. Shikonin stimulates ROS generation in the mitochondria of T-47D cells, which causes necroptosis or apoptosis. Induction of necroptosis, as a backup-programmed cell death pathway via ROS stimulation, offers a new strategy for the treatment of breast cancer.
A new facile method for thia-Fries rearrangement of arylsulfonates has been developed. A variety of arylsulfonates rearrange in excellent yields in the presence of Al
2
O
3
/MeSO
3
H as a new reagent ...without the use of any solvent.
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