Current Search: Apoptosis -- Molecular aspects (x)
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- Title
- Anti-cancer activity of pomegranate (Punica granatum ) extracts in testicular cancer.
- Creator
- Brown, Jayann Marie, Florida Atlantic University, Kumi-Diaka, James
- Abstract/Description
-
Recent advancement in chemotherapy has resulted in higher and longer survival rates of testicular cancer patients. However the use of chemotherapeutic agents are not without serious, sometimes fatal side effects. This study investigated the potential therapeutic efficacy of pomegranate extracts in testis cancer cells, GC1-spg, in vitro. A battery of assays was used to determine the chemosensitivity of GC1-spg cells to two pomegranate extracts, S (seed) and P (pericarp), in single and...
Show moreRecent advancement in chemotherapy has resulted in higher and longer survival rates of testicular cancer patients. However the use of chemotherapeutic agents are not without serious, sometimes fatal side effects. This study investigated the potential therapeutic efficacy of pomegranate extracts in testis cancer cells, GC1-spg, in vitro. A battery of assays was used to determine the chemosensitivity of GC1-spg cells to two pomegranate extracts, S (seed) and P (pericarp), in single and combination treatments: MTS and LDH to determine post-treatment survival rate (growth inhibition) and cytotoxicity respectively; Acridine Orange/Ethidium Bromide fluorescent dye to assess treatment-induced apoptosis/necrosis; Annexin V-FITC and TUNEL assays for early and late apoptosis respectively. Results from the obtained data indicated that both extracts have significant cytotoxic effect on testicular cancer cells (GC1-spg) in single and combination treatments. The data revealed a dose and time dependency of chemosensitivity to both extracts; and that apoptosis was the major mechanism treatment-induced cell death. Synergism was also indicated in growth inhibition by combination treatment. These findings offer strong justification for further studies with pomegranate as potential phytotherapy.
Show less - Date Issued
- 2004
- PURL
- http://purl.flvc.org/fcla/dt/13154
- Subject Headings
- Testis--Cancer--Treatment, Generative organs, Male--Diseases--Treatment, Phytochemicals--Physiological effect, Cancer--Adjuvant treatment, Apoptosis--Molecular aspects
- Format
- Document (PDF)
- Title
- Mechanisms of protection against ischemic damage in the heart.
- Creator
- Moench, Ian, Charles E. Schmidt College of Science, Department of Biological Sciences
- Abstract/Description
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Heart disease including ischemic heart disease is the highest contributor to death and morbidity in the western world. The studies presented were conducted to determine possible pathways of protection of the heart against ischemia/reperfusion. We employed adenovirus mediated over-expression of Methionine sulfoxide reductase A (MsrA) in primary neonatal rat cardiac myocytes to determine the effect of this enzyme in protecting against hypoxia/reoxygenation. Cells transfected with MsrA encoding...
Show moreHeart disease including ischemic heart disease is the highest contributor to death and morbidity in the western world. The studies presented were conducted to determine possible pathways of protection of the heart against ischemia/reperfusion. We employed adenovirus mediated over-expression of Methionine sulfoxide reductase A (MsrA) in primary neonatal rat cardiac myocytes to determine the effect of this enzyme in protecting against hypoxia/reoxygenation. Cells transfected with MsrA encoding adenovirus and subjected to hypoxia/reoxygenation exhibited a 45% decrease in apoptosis as compared to controls. Likewise total cell death as determined by levels of Lactate Dehydrogenase (LDH) release was dramatically decreased by MsrA overexpression. The initial hypothesis that led to our testing sulindac was based on the fact that the S epimer of sulindac was a substrate for MsrA and that this compound might function as a catalytic anti-oxidant based on a reaction cycle that involved reductio n to sulindac sulfide followed by oxidation back to sulindac. To test this we examined the protective effect of sulindac in hypoxia re-oxygenation in both cardiac myocytes in culture and using a Langendorff model of myocardial ischemia. Using this model of myocardial ischemia we showed that pre-incubation of hearts with sulindac, or the S and R epimers of sulindac resulted in protection against cell death. We present several lines of evidence that the protective effect of sulindac is not dependent on the Msr enzyme system nor does it involve the well established role of sulindac as a Cyclooxygenase (COX) inhibitor. Numerous signaling pathways have been implicated in myocardial protective mechanisms, many of which require fluctuations in ROS levels as initiators or mediators., Sulindac shows very good potential as a preconditioning agent that could induce tissue protection against oxidative damage.Blocking of preconditioning pathways by administration of the PKC blocker chelerythine abrogated the ischemic protection afforded by sulindac. Secondly, an end-effector of preconditioning, inducible nitric oxide synthase (iNOS),was found to be induced by greater than 5 fold after 48 h prior feeding sulindac.
Show less - Date Issued
- 2008
- PURL
- http://purl.flvc.org/FAU/186291
- Subject Headings
- Biochemical markers, Diagnostic use, Cardiovascular system, Diseases, Diagnosis, Heart, Diseases, Molecular aspects, Medical care, Quality control, Coronary heart disease, Prevention, Apoptosis, Myocardial infarction, Prevention
- Format
- Document (PDF)