1 40 2 Text A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text. URL Address <a href="http://doi.org/10.1016/j.bcp.2003.08.040" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.bcp.2003.08.040</a> Pages 337–351 Issue 2 Volume 67 Dublin Core The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/. Title A name given to the resource Cell cycle arrest and autoschizis in a human bladder carcinoma cell line following Vitamin C and Vitamin K3 treatment. Publisher An entity responsible for making the resource available Biochemical pharmacology Date A point or period of time associated with an event in the lifecycle of the resource 2004 2004-01 Subject The topic of the resource Antioxidants/*pharmacology; Ascorbic Acid/*pharmacology; Calcium/metabolism; Cell Cycle/*drug effects; Cultured; DNA; Flow Cytometry; Humans; Hydrogen Peroxide/metabolism; Male; Neoplasm/drug effects; Sulfhydryl Compounds/metabolism; Tumor Cells; Urinary Bladder Neoplasms/pathology; Vitamin K 3/*pharmacology Creator An entity primarily responsible for making the resource Jamison James M; Gilloteaux Jacques; Nassiri M Reza; Venugopal Meenakshi; Neal Deborah R; Summers Jack L Description An account of the resource Exponentially growing cultures of human bladder tumor cells (T24) were treated with Vitamin C (VC) alone, Vitamin K(3) (VK(3)) alone, or with a VC:VK(3) combination for 1, 2, or 4hr. Flow cytometry of T24 cells exposed to the vitamins for 1h revealed a growth arrested population and a population undergoing cell death. Cells in G(1) during vitamin treatment arrested in G(1) while those in S phase progressed through S phase and arrested in G(2)/M. DNA synthesis decreased to 14 to 21% of control levels which agreed with the percent of cells in S phase during treatment. Annexin V labeling demonstrated the majority of the cells died by autoschizis, but necrosis and apoptosis also were observed. Catalase treatment abrogated both cell cycle arrest and cell death which implicated hydrogen peroxide (H(2)O(2)) in these processes. Redox cycling of VC and VK(3) increased H(2)O(2) production and decreased cellular thiol levels and DNA content, while increasing intracellular Ca(2+) levels and lipid peroxidation. Feulgen staining of treated cells revealed a time-dependent decrease in tumor cell DNA, while electrophoresis revealed a spread pattern. These results suggest that Ca(2+) disregulation activates at least one DNase which degrades tumor cell DNA and induces tumor cell death. Identifier An unambiguous reference to the resource within a given context <a href="http://doi.org/10.1016/j.bcp.2003.08.040" target="_blank" rel="noreferrer noopener">10.1016/j.bcp.2003.08.040</a> Rights Information about rights held in and over the resource Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s). 2004 Antioxidants/*pharmacology Ascorbic Acid/*pharmacology Biochemical pharmacology Calcium/metabolism Cell Cycle/*drug effects Cultured DNA Flow Cytometry Gilloteaux Jacques Humans Hydrogen Peroxide/metabolism Jamison James M Male Nassiri M Reza Neal Deborah R Neoplasm/drug effects Sulfhydryl Compounds/metabolism Summers Jack L Tumor Cells Urinary Bladder Neoplasms/pathology Venugopal Meenakshi Vitamin K 3/*pharmacology Text A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text. URL Address <a href="http://doi.org/10.1016/s0006-2952(02)00904-8" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/s0006-2952(02)00904-8</a> Pages 1773–1783 Issue 10 Volume 63 Dublin Core The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/. Title A name given to the resource Autoschizis: a novel cell death. Publisher An entity responsible for making the resource available Biochemical pharmacology Date A point or period of time associated with an event in the lifecycle of the resource 2002 2002-05 Subject The topic of the resource Animals; Antioxidants/chemistry/*pharmacology/therapeutic use; Ascorbic Acid/chemistry/*pharmacology/therapeutic use; Cell Death/*physiology; Humans; Necrosis; Neoplasms/drug therapy/metabolism/*pathology; Oxidative Stress/*drug effects; Vitamin K/chemistry/*pharmacology/therapeutic use Creator An entity primarily responsible for making the resource Jamison James M; Gilloteaux Jacques; Taper Henryk S; Calderon Pedro Buc; Summers Jack L Description An account of the resource Vitamin C (VC) and vitamin K(3) (VK(3)) administered in a VC:VK(3) ratio of 100:1 exhibit synergistic antitumor activity and preferentially kill tumor cells by autoschizis, a novel type of necrosis characterized by exaggerated membrane damage and progressive loss of organelle-free cytoplasm through a series of self-excisions. During this process, the nucleus becomes smaller, cell size decreases one-half to one-third of its original size, and most organelles surround an intact nucleus in a narrow rim of cytoplasm. While the mitochondria are condensed, tumor cell death does not result from ATP depletion. However, vitamin treatment induces a G(1)/S block, diminishes DNA synthesis, increases H(2)O(2) production, and decreases cellular thiol levels. These effects can be prevented by the addition of catalase to scavenge the H(2)O(2). There is a concurrent 8- to 10-fold increase in intracellular Ca(2+) levels. Electrophoretic analysis of DNA reveals degradation due to the caspase-3-independent reactivation of deoxyribonuclease I and II (DNase I, DNase II). Redox cycling of the vitamins is believed to increase oxidative stress until it surpasses the reducing ability of cellular thiols and induces Ca(2+) release, which triggers activation of Ca(2+)-dependent DNase and leads to degradation of DNA. Recent experiments indicate that oral VC:VK(3) increases the life-span of tumor-bearing nude mice and significantly reduces the growth rate of solid tumors without any significant toxicity by reactivating DNase I and II and inducing autoschizis. This report discusses the mechanisms of action employed by these vitamins to induce tumor-specific death by autoschizis. Identifier An unambiguous reference to the resource within a given context <a href="http://doi.org/10.1016/s0006-2952(02)00904-8" target="_blank" rel="noreferrer noopener">10.1016/s0006-2952(02)00904-8</a> Rights Information about rights held in and over the resource Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s). 2002 Animals Antioxidants/chemistry/*pharmacology/therapeutic use Ascorbic Acid/chemistry/*pharmacology/therapeutic use Biochemical pharmacology Calderon Pedro Buc Cell Death/*physiology Gilloteaux Jacques Humans Jamison James M Necrosis Neoplasms/drug therapy/metabolism/*pathology Oxidative Stress/*drug effects Summers Jack L Taper Henryk S Vitamin K/chemistry/*pharmacology/therapeutic use