Cartilage Viability After Repetitive Loading: A Preliminary Report
apoptosis; articular-cartilage; cartilage; cell death; chondrocyte; chondrocyte biosynthetic; dynamic compression; experimentally-induced osteoarthritis; explants; guinea-pigs; ii collagen; impact; load; local tissue strain; Orthopedics; repetitive load; responses; Rheumatology; signal-transduction
Lucchinetti E; Adams C S; Horton W E; Torzilli P A
Osteoarthritis and Cartilage
2002
2002-01
Journal Article or Conference Abstract Publication
<a href="http://doi.org/10.1053/joca.2001.0483" target="_blank" rel="noreferrer noopener">10.1053/joca.2001.0483</a>
Cell Death By Autoschizis In Tramp Prostate Carcinoma Cells As A Result Of Treatment By Ascorbate: Menadione Combination
ascorbate; autoschizis; carcinoma cells; cell death; combined vitamin-c; cultured-mammalian-cells; electron-microscopy; induced oxidative stress; kills cancer-cells; Microscopy; Microscopy; nuclease; Pathology; prostate; ribonucleoproteins; scanning electron; sodium ascorbate; synergistic antitumor-activity; TRAMP; transgenic adenocarcinoma; ultrastructural aspects
Gilloteaux J; Jamison J M; Neal D R
Ultrastructural Pathology
2005
2005-05
Journal Article or Conference Abstract Publication
<a href="http://doi.org/10.1080/01913120590951239" target="_blank" rel="noreferrer noopener">10.1080/01913120590951239</a>
Ultrastructural Aspects Of Autoschizis: A New Cancer Cell Death Induced By The Synergistic Action Of Ascorbate/menadione On Human Bladder Carcinoma Cells
2-methyl-1; 4-naphthoquinone; antitumor-activity; apoptosis; autoschizis; bladder tumor; cell death; combined vitamin-c; cultured-mammalian-cells; growth-invitro; induced oxidative stress; Microscopy; necrosis; Pathology; scanning electron-microscopy; T24 ultrastructure; tumor; vitamins
Gilloteaux J; Jamison J M; Arnold D; Taper H S; Summers J L
Ultrastructural Pathology
2001
2001-05
Journal Article or Conference Abstract Publication
<a href="http://doi.org/10.1080/019131201300343810" target="_blank" rel="noreferrer noopener">10.1080/019131201300343810</a>
In vivo reactivation of DNases in implanted human prostate tumors after administration of a vitamin C/K-3 combination
apoptosis; cancer; cancer-chemotherapy; carcinoma cells; Cell Biology; cell death; deoxyribonuclease-ii; DNASE; growth-invitro; identification; lines; necrobiology; pretreatment; programmed cell-death; Prostate cancer; synergistic antitumor-activity; vitamin C; vitamin K-3
Human prostate cancer cells (DU145) implanted into nude mice are deficient in DNase activity. After administration of a vitamin C/vitamin K-3 combination, both alkaline DNase (DNase I) and acid DNase (DNase II) activities were detected in cryosections with a histochemical lead nitrate technique. Alkaline DNase activity appeared 1 hr after vitamin administration, decreased slightly until 2 hr, and disappeared by 8 hr after treatment. Acid DNase activity appeared 2 hr after vitamin administration, reached its highest levels between 4 and 8 hr, and maintained its activity 24 hr after treatment. Methyl green staining indicated that DNase expression was accompanied by a decrease in DNA content of the tumor cells. Microscopic examination of 1-mum sections of the tumors indicated that DNase reactivation and the subsequent degradation of DNA induced multiple forms of tumor cell death, including apoptosis and necrosis. The primary form of vitamin-induced tumor cell death was autoschizis, which is characterized by membrane damage and the progressive loss of cytoplasm through a series of self-excisions. These self-excisions typically continue until the perikaryon consists of an apparently intact nucleus surrounded by a thin rim of cytoplasm that contains damaged organelles.
Taper H S; Jamison J M; Gilloteaux J; Gwin C A; Gordon T; Summers J L
Journal of Histochemistry & Cytochemistry
2001
2001-01
Journal Article
<a href="http://doi.org/10.1177/002215540104900111" target="_blank" rel="noreferrer noopener">10.1177/002215540104900111</a>
Mitochondrial dysfunction and tissue injury by alcohol, high fat, nonalcoholic substances and pathological conditions through post-translational protein modifications
Biochemistry & Molecular Biology; cell death; cytochrome-c-oxidase; hepatic ischemia-reperfusion; induced liver-injury; Mitochondrial dysfunction; Mitochondrial proteins; nadp(+)-dependent isocitrate dehydrogenase; nitric-oxide; Nitroxidative stress; oxidative stress; Post-translational modifications; rat-liver; Redox; synthase; targeted antioxidant mitoq; terminal kinase; Tissue injury
Mitochondria are critically important in providing cellular energy ATP as well as their involvement in anfi-oxiclant defense, fat oxidation, intermediary metabolism and cell death processes lt is well-established that mitochondrial functions are suppressed when living cells or organisms are exposed to potentially toxic agents including alcohol, high fat diets, smoking and certain drugs or in many pathophysiological states through increased levels of oxidative/nitrative stress. Under elevated nitroxidative stress, cellular macromolecules proteins, DNA, and lipids can undergo different oxidative modifications, leading to disruption of their normal, sometimes critical, physiological functions. Recent reports also indicated that many mitochondrial proteins are modified via various post-translation modifications (PTMs) and primarily inactivated. Because of the recently-emerging information, in this review, we specifically focus on the mechanisms and roles of five major PTMs (namely oxidation, nitration, phosphorylation, acetylation, and adduct formation with lipid-peroxides, reactive metabolites, or advanced glycation end products) in experimental models of alcoholic and nonalcoholic fatty liver disease as well as acute hepatic injury caused by toxic compounds. We also highlight the role of the ethanol-inducible cytochrome P450-2E1 (CYP2E1) in some of these PTM changes. Finally, we discuss translational research opportunities with natural and/or synthetic anti-oxidants, which can prevent or delay the onset of mitochondial dysfunction, fat accumulation and tissue injury. Published by Elsevier B.V.
Song B J; Akbar M; Abdelmegeed M A; Byun K; Lee B; Yoon S K; Hardwick J P
Redox Biology
2014
2014
Journal Article
<a href="http://doi.org/10.1016/j.redox.2014.10.004" target="_blank" rel="noreferrer noopener">10.1016/j.redox.2014.10.004</a>