Free Radicals

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Information about Free Radicals
Health & Medicine

Published on March 11, 2014

Author: mahmoodi2000

Source: slideshare.net

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

Cancer 

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

www.mahmoodi.org

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