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Integrating Traditional and Complementary Medicine into National Health Care: Learning from the International Experience. Can Traditional Medicine Coexist with Modern Medicine in the Same Health Care System? Clinical Trials for Herbal Extracts. Herbal Medicine: Criteria for Use in Health and Disease. Effects of Phytochemicals in Chinese Functional Ingredients on Gut Health. Tea and Health. Ginkgo biloba: From Traditional Medicine to Molecular Biology. Ginger. Lingzhi Polyphorous Fungus (Ganoderma lucidum). Epimedium Species. Ligusticum chuanxiong Hort. Salvia miltiorrhiza. Schisandrin B and Other Dibenzocyclooctadiene Lignans. Spirulina: An Overview. Averrhoa bilimbi. Lentinus edodes: Shiitake Mushrooms. Cruciferous Vegetables and Chemoprevention: The Mechanisms of Isothiocyanate-Mediated Chemoprotection in Humans. Pharmacological and Chemopreventive Studies of Chrysanthemum. Andrographis paniculata and the Cardiovascular System. Rosemary. Crataegus (Hawthorn). Resveratrol: The Promise Therein. Pharmacological and Physiological Effects of Ginseng. Antioxidant Activities of Prickly Pear (Opuntia ficus indica) Fruit and Its Betalains: Betanin and Indicaxanthin. Antioxidant Activity and Antigenotoxicity of Cassia tora. Sho-saiko-to. Licorice Root Flavonoid Antioxidants Reduce LDL Oxidation and Attenuate Cardiovascular Diseases. Estrogen-Like Activity of Licorice Root Extract and Its Constituents. Protection of Oxidative Brain Injury by Chinese Herbal Medicine: Shengmai San as a Model Formula for the Antioxidant-Based-Compounds Therapy of Oxidative Stress-Related Diseases. Eurycoma longifolia Jack (Tongkat Ali). The Biological and Pharmacological Properties of Cordyceps sinesis, a Traditional Chinese Medicine That Has Broad Clinical Applications. Phytochemistry, Pharmacology, and Health Effects of Brandisia hancei. Ephedra. Echinacea and Immunostimulation. Medical Attributes of St. John's Wort (Hypericum perforatum). Therapeutic Potential of Curcumin Derived from Turmeric (Curcuma longa). Extracts from the Leaves of Chromolaena odorata: A Potential Agent for Wound Healing. Medicinal Properties of Eucommia Bark and Leaves. Systemic Reviews of Herbal Medicinal Products: Doing More Good Than Harm? Use of Silicon-Based Oligonucleotide Chip in Authentication of Toxic Chinese Medicine. Traditional Chinese Medicine: Problems and Drawbacks. Review of Adverse Effects of Chinese Herbal Medicine and Herb-Drug Interactions.
Radicals are species containing one or more unpaired electrons. The oxygen radical superoxide (O2-) and the non-radical oxidant hydrogen peroxide (H2O2) are produced during normal metabolism and perform several useful functions. Excessive production of O2- and H2O2 can result in tissue damage, which often involves generation of highly-reactive hydroxyl radical (.OH) and other oxidants in the presence of "catalytic" iron ions. A major form of antioxidant defence is the storage and transport of iron ions in forms that will not catalyze formation of reactive radicals. Tissue injury, eg. by ischaemia or trauma, can cause increased iron availability and accelerate free radical reactions. This may be especially important in the brain, since areas of this organ are rich in iron and cerebrospinal fluid cannot bind released iron ions. Oxidant stress upon nervous tissue can produce damage by several interacting mechanisms, including rises in intracellular free Ca2+ and, possibly, release of excitatory amino acids. Recent suggestions that iron-dependent free radical reactions are involved in the neurotoxicity of aluminium and in damage to the substantia nigra in Parkinson's disease are reviewed. Finally, the nature of antioxidants is discussed, it being suggested that antioxidant enzymes and chelators of iron ions may be more generally-useful protective agents than chain-breaking antioxidants.
Non-alcoholic fatty liver disease (NAFLD) is a common chronic liver disease. Iron, cholesterol, and oxidative damage are frequently suggested to be related to the progression of NAFLD, but the precise relationship between them remains unclear. Guinea pigs fed on a high cholesterol and fat diet (without oxidized lipids) generated a disease model of NAFLD with hallmark observations in liver histology and increased liver damage markers. Hepatic cholesterol and iron levels were found to be significantly elevated and directly correlated. Plasma hepcidin and transferrin levels were decreased. Plasma iron concentrations were found to be elevated, likely due to an increased intestinal iron absorption caused by the decrease in plasma hepcidin. However, hepatic transferrin receptor-2 levels were unchanged. No significant increase in hepatic lipid peroxidation was detected using F2-isoprostanes as a reliable biomarker, nor was there a rise in protein carbonyls, a general index of oxidative protein damage. Some increases in cholesterol oxidation products were observed, but largely negated after normalizing for the elevated hepatic cholesterol content. Indeed, increased hemosiderin deposition and unchanged ferritin levels in liver suggested that the excess iron mainly existed as hemosiderin, which is redox-inactive.
Early Markers in Parkinson's and Alzheimer's Diseases New Vistas in Drug Research, Volume 1 Eds. P. Dostert, P. Riederer, M.S. Benedetti and R. Roncuczi Springer Verlag, Vienna and New York, 310pp., 1990.
The question as to whether free radical reactions are a major cause of tissue injury in human disease, or merely an accompaniment to such injury, is very difficult to answer because of lack of adequate experimental techniques. New techniques that are becoming available are discussed, with specific reference to their use in humans.
In the presence of H2O2, ascorbate and phosphate buffer at pH 7.4, deoxyribose is degraded. Degradation is inhibited by catalase, mannitol, apotransferrin, apolactoferrin, or desferrioxamine. In the presence of sufficient apotransferrin to just inhibit deoxyribose degradation, reaction can be restored by adding more deoxyribose to the reaction mixture, but not by additional phosphate or ascorbate. It is suggested that deoxyribose degradation under our reaction conditions is achieved by a site-specific formation of hydroxyl radical using iron ions bound to the deoxyribose molecule. Spectrophotometric and kinetic evidence for the binding of iron ions to deoxyribose is presented.
Free radicals, such as superoxide, hydroxyl and nitric oxide, and other reactive oxygen species (ROS), such as hydrogen peroxide, are formed in vivo. Imbalance between production of ROS and anti-oxidant defence can result in oxidative stress, which may arise either from deficiencies of anti-oxidants (such as glutathione, ascorbate or α-tocopherol) and/or from increased formation of ROS. Oxidative stress can result in glutathione depletion, lipid peroxidation, membrane damage and DNA strand breaks as well as activation of proteases, nucleases and protein kinases. Some degree of oxidative stress occurs in most, if not all, human diseases, and the major question to be answered is whether it makes a significant contribution to the disease pathology. In the case of atherosclerosis, evidence from studies with the chain-breaking anti-oxidant probucol and from epidemiological work suggests that oxidative damage does indeed make an important contribution to plaque development.
Monograph on Free Radical Reactions (Environmental Health Perspectives, vol. 64, December 1985).Free Radicals, Aging, and Degenerative Diseases Modern Aging Research, Vol. 8, Eds. J.E. Johnson, Jr., R. Walford, D. Harman and J. Miquel, (Alan R. Liss, Inc., New York, 1986) 588 Pages. £93.00 p.“CRC Handbook of Methods for Oxygen Radical Research” Robert A. Greenwald, editor, CRC Press, Boca Raton, Florida, 1985. (447 pp)
