ABSTRACT
Las formulaciones disponibles actualmente para uso dermatológico, basadas en sustancias antioxidantes tales como vitaminas C y E, entre otras, abundan con promesas de revertir el envejecimiento cutáneo. En el presente trabajo se realiza una revisión de los sistemas antioxidantes cutáneos, de la relación entre envejecimiento y daño oxidativo, así como de la evidencia disponible en cuanto al tratamiento con antioxidantes. La intención de este artículo es que el dermatólogo comprenda las bases fisiológicas de acción de los antioxidantes, para poder juzgar su utilidad con una mirada crítica
Subject(s)
Humans , Animals , Ascorbic Acid/therapeutic use , Antioxidants , Reactive Oxygen Species , Skin , Skin Aging , Ultraviolet Rays , Vitamin E , Ascorbic Acid/pharmacology , Ascorbic Acid/physiology , Administration, Topical , Antioxidants , beta Carotene , Catalase , Clinical Trials as Topic , Cosmetics , Skin Physiological Phenomena , Glutathione Peroxidase/radiation effects , Glutathione Peroxidase/physiology , Glutathione Reductase/radiation effects , Glutathione Reductase/physiology , Glutathione Transferase/radiation effects , Glutathione Transferase/physiology , Interleukins , Ozone , Peroxidase , Skin , Sunlight , Superoxide Dismutase/radiation effects , Superoxide Dismutase/physiology , Ubiquinone , Vitamin EABSTRACT
Aerobic life is characterized by a steady generation of reactive oxygen species balanced by a similar rate of their consumption by antioxidants. To maintain homeostasis, there is a requirement for the continuous regeneration of antioxidant capacity, and if this is not met, oxidative stress occurs, resulting in pathophysiological events. Cellular protection against oxidative stress is organized at multiple levels. Defense strategies include prevention, interception, replacement, and repair. These mechanisms are coupled to the intermediary metabolism for a continuous supply of energy, reducing equivalents, and precursors, and depend on the dietary supply of metabolic fuels and essential molecules to allow an optimal cellular functioning
Subject(s)
Humans , Antioxidants/metabolism , Catalase/physiology , Glutathione Peroxidase/physiology , Oxidative Stress/physiology , Peroxidases/physiology , Reactive Oxygen Species/physiology , Superoxide Dismutase/physiology , Free Radicals/metabolismABSTRACT
The present study was devoted to investigate the effect of selenium chloride, N-ethyl maleimide [NEM] and N-nitro-L-arginine methylester [NAME] on ethanol-induced gastric lesions in rats. The ultimate aim was to explore further the possible role of endogenously formed glutathione and nitric oxide [NO] in the protection against ethanol-induced gastric mucosal injury in rats. All rats treated with 80 percent ethanol developed hemorrhagic ulceration. This was associated with a significant increase in lipid degradation products represented by increased levels of malondialdehyde; the degradation product of lipid peroxides, together with a significant decrease in gastric mucosal glutathione peroxidase [GSHPx] activity and mucosal glutathione [GSH]. Orally administered selenium chloride exerted significant protection against gastric mucosal injury induced by ethanol, possibly via increasing endogenous antioxidant reserve represented by increased GSHPx activity. This acts to scavenge oxygen free radicals produced during mucosal ischemia induced by ethanol with resultant decrease in rate of lipid peroxidation. Depletion of endogenous GSH by NEM had no potentially ulcerogenic effect in the control rats. However, when given before ethanol treatment, the ulcer index significantly increased. Lipid peroxides were not significantly affected in the control rats in spite of the significant depletion of GSH. However, when the mucosa was challenged during ethanol treatment in the presence of depleted GSH and decreased GSHPx activity, oxygen free radicals failed to be buffered and lipid peroxides increased more significantly. Blocking NO synthase activity by NAME during alcohol treatment exaggerated the mucosal lesions as revealed by a decrease of the preventive index. This supports the protective role of endogenous NO on the gastric mucosal injury induced by ethanol. The aggressive effect of NAME was accompanied with a significant decrease of GSHPx activity as well as of endogenous GSH. The lipid peroxides, however, were found to be reduced despite the decreased antioxidant activity. In conclusion, repletion of gastric GSHPx system by selenium chloride exerts cytoprotective effect while blockade of endogenous GSH via NEM or blockade of NO synthesis with NAME aggravated the alcohol-induced gastric lesions
Subject(s)
Animals, Laboratory , Gastric Mucosa/injuries , Ethanol/toxicity , Rats , Glutathione Peroxidase/physiologyABSTRACT
Orygen free radical is a highly toxic agent which is liberated during many metabolic processes. This toxic product is detoxified through the oxygen detoxifying enzyme system, superoxide dismutase [S.O.D.], catalase and glutathione peroxidase. The above mentioned enzymes were found to be elevated in the early stage of chronic renal failure and the activity decreased with the development of the disease. The early affected enzyme is glutathione peroxidase