Published on March 11, 2014
Contents General properties Pathological damages FR Free radicals and cancer Free radicals and aging Drugs, foods, environment and free radicals Latest research
Other Sources Chemotherapeutic agents Doxorubicin, Cyclophosphamide, 5-fluorouracil, Methotrexate Vincristine
Cancer Carcinogens Chemotherapy Radiation Latest techniques Prevention
Chemotherapy Post-translational modifications (PTM) Protein oxidation Protein phosphorylation ER stress Calcium release Apoptosis ROS
Vitamin E 20 mg , 10 mg Scavenger Immune responses Nitrites to nitrosamines Oncogenes (H-ras and C-myc), and proliferation 50% oral cancer risk Breast cancer risk
Vitamin A Carotenoids and cancer risk Strongest b-carotene Cervix, lung and oral cavity Dietary antioxidants : stomach and breast cancer
….Vitamin A Communication Growth regulating signals from adjoining normal cells Tumor growth suppressed
Vitamin C Vitamin C : 1) hyaluronidase inhibitor system; 2) nitrosamines in the GIT 3) cytochrome P-450 system Selenium aerodigestive system
Hypertension & FRs Nitric oxide Antioxidants Glutathione Glutathione- depleted rats Vitamin E and C to the rats' diet
Hypertension AICR 400 and 800 gm per day Vitamins C, E, and b-carotene reduce : Coronary events, Reperfusion injury, Platelet aggregation, LDL oxidation
Drug Choices Univ of Florida Medical School, statin with ACE inhibitor, Decrease amounts of free radical Oxidization of LDL Endothelial cells Chelating agents Seresis Pharmaton
Diabetes & FRs Type 1 diabetes ß-cell destruction cytokines RNS ROS Ferritin Fenton reaction Low levels of antioxidant genes
Diabetes and FRs EUK-8 synthetic salen- manganese compounds Catalytic superoxide dismutase, Peroxidase, Catalase activity Inactivate superoxide and nitrogen oxides
EUK-8 EUK-8 to mice with established autoimmunity EUK-8 treatment and survival of islet allografts in newly diabetic mice
Down Syndrome Excess SO levels accumulation Antioxidant cellular function
Cell Types Cell type-specific responses to H2O2 responses RPE Corneal fibroblasts
Neurological Disorders Antioxidants slow the progression of certain neurological disorders Oxidation disorders of the nervous system. Vitamin C and E Parkinson's disease
Alzheimer Beta-amyloid and oxidative toxicity, Oxidative damage to neurons, Increases interneuronal calcium levels, damage due to free radicals. Carnosin
Treatment Vitamin E preventing or alleviating neurological disorders, Long-term Vitamin E deficiency progressive neurological syndrome
Melatonin Free radical scavenger and antioxidant Pineal gland, molecular damage Melatonin lowers tissue damage and dysfunction
Melatonin Melatonin absorbed any route Crosses all barriers, Enter all parts of every cell Preserves mitochondrial function, low toxicity Blood levels low, tissue levels higher, in bone marrow cells and bile
Cataract Oxidation, ultraviolet light, Damage to the proteins of the lens. The oxidized protein precipitates out and causes cloudiness of the lens.
….Cataract Antioxidants and antioxidant enzymes, remove the damaged portion, but the oxidation occurs at a faster rate With time, the damage becomes irreversible
Maculopathy Exposure to light, blue light, Age-related macular degeneration Vitamin E Carotenoids are said to decrease the risk of this disorder
Latest Uses Polymer, in pig sperm, enhance the lifespan of human sperm in fertility treatments Hybrid protein recognizes a molecule on the sperm's surface and the antioxidant vitamin E. Pig sperm live longer than untreated cells,
Glutamate Glutamate hippocampal cells of glutathione, incapable to reduce reactive oxygen species in cell death by oxidative stress. cells resistant to glutamate increased phosphorylation of (CREB) and decreased ERK1/2
Glutamate Increase in mRNA for receptors activated by the vasoactive intestinal peptide VIP and glutamate like the metabotropic glutamate receptor mGlu 1 Treating cells with VIP and glutamate led to the same changes in protein phosphorylation observed in resistant cells and induced the proto-oncogene Bcl-2.
Glutamate Bcl-2 overexpression protected by increasing the amount of intracellular glutathione and Bcl- 2 knockdown by small interfering RNAs (siRNA) increased glutamate susceptibility of resistant cells. Other receptors upregulated in this paradigm might represent useful targets in the treatment of neurological diseases associated with oxidative stress.
TBI and FRs Overactivation of ERK secondary cell death mechanisms in TBI. Fre radical scavenger S-PBN Neuroprotective properties in TBI Attenuates the early activation of ERK Resulted in less activation of caspase-3 Subsequent DNA fragmentation U0126 cortical atrophy at 2 weeks after trauma
Oxygenation therapy Disease is caused by absence of oxygen "good energy" metabolism, detoxification, and immune system function Oxygen therapies "good" energy, to "detoxify" metabolic poisons, and to kill invading organisms.
What's The Latest ? ROS mtDNA UV human hepatoma cell Alteres the ROS by MnSOD / catalase Results accumulation of hydrogen peroxide oxidative damage to mtDNA of UV-irradiated cells, and overexpression of both MnSOD and catalase reduces the mtDNA damage and blocks the growth inhibition by UV. Increased activity of MnSOD may lead to a toxic effect on mtDNA by UV- irradiation.
Cisplatin ROS, hydroxyl radicals, Cisplatin nephropathy Edarabone
Bibliography NCBI pubmed Ignata connect Science daily Grays cancer institution American institution for cancer research Univ. Florida Life extension magazine Net sources
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