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      Free radicals, oxidative stress, and antioxidants in human health and disease

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          Abstract

          Free radicals and other reactive oxygen species (ROS) are constantly formed in the human body. Free-radical mechanisms have been implicated in the pathology of several human diseases, including cancer, atherosclerosis, malaria, and rheumatoid arthritis and neurodegenerative diseases. For example, the superoxide radical (O 2 ·−) and hydrogen peroxide (H 2O 2) are known to be generated in the brain and nervous system in vivo, and several areas of the human brain are rich in iron, which appears to be easily mobilizable in a form that can stimulate free-radical reactions. Antioxidant defenses to remove O 2 ·− and H 2O 2 exist. Superoxide dismutases (SOD) remove O 2 ·− by greatly accelerating its conversion to H 2O 2. Catalases in peroxisomes convert H 2O 2 into water and O 2 and help to dispose of H 2O 2 generated by the action of the oxidase enzymes that are located in these organelles. Other important H 2O 2-removing enzymes in human cells are the glutathione peroxidases. When produced in excess, ROS can cause tissue injury. However, tissue injury can itself cause ROS generation (e.g., by causing activation of phagocytes or releasing transition metal ions from damaged cells), which may (or may not, depending on the situation) contribute to a worsening of the injury. Assessment of oxidative damage to biomolecules by means of emerging technologies based on products of oxidative damage to DNA (e.g., 8-hydroxydeoxyguanosine), lipids (e.g., isoprostanes), and proteins (altered amino acids) would not only advance our understanding of the underlying mechanisms but also facilitate supplementation and intervention studies designed and conducted to test antioxidant efficacy in human health and disease.

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          Most cited references135

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          Effects of a combination of beta carotene and vitamin A on lung cancer and cardiovascular disease.

          Lung cancer and cardiovascular disease are major causes of death in the United States. It has been proposed that carotenoids and retinoids are agents that may prevent these disorders. We conducted a multicenter, randomized, double-blind, placebo-controlled primary prevention trial -- the Beta Carotene and Retinol Efficacy Trial -- involving a total of 18,314 smokers, former smokers, and workers exposed to asbestos. The effects of a combination of 30 mg of beta carotene per day and 25,000 IU of retinol (vitamin A) in the form of retinyl palmitate per day on the primary end point, the incidence of lung cancer, were compared with those of placebo. A total of 388 new cases of lung cancer were diagnosed during the 73,135 person-years of follow-up (mean length of follow-up, 4.0 years). The active-treatment group had a relative risk of lung cancer of 1.28 (95 percent confidence interval, 1.04 to 1.57; P=0.02), as compared with the placebo group. There were no statistically significant differences in the risks of other types of cancer. In the active-treatment group, the relative risk of death from any cause was 1.17 (95 percent confidence interval, 1.03 to 1.33); of death from lung cancer, 1.46 (95 percent confidence interval, 1.07 to 2.00); and of death from cardiovascular disease, 1.26 (95 percent confidence interval, 0.99 to 1.61). On the basis of these findings, the randomized trial was stopped 21 months earlier than planned; follow-up will continue for another 5 years. After an average of four years of supplementation, the combination of beta carotene and vitamin A had no benefit and may have had an adverse effect on the incidence of lung cancer and on the risk of death from lung cancer, cardiovascular disease, and any cause in smokers and workers exposed to asbestos.
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            Endothelium-derived relaxing factor produced and released from artery and vein is nitric oxide.

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              Vascular endothelial cells synthesize nitric oxide from L-arginine.

              Nitric oxide (NO) released by vascular endothelial cells accounts for the relaxation of strips of vascular tissue and for the inhibition of platelet aggregation and platelet adhesion attributed to endothelium-derived relaxing factor. We now demonstrate that NO can be synthesized from L-arginine by porcine aortic endothelial cells in culture. Nitric oxide was detected by bioassay, chemiluminescence or by mass spectrometry. Release of NO from the endothelial cells induced by bradykinin and the calcium ionophore A23187 was reversibly enhanced by infusions of L-arginine and L-citrulline, but not D-arginine or other close structural analogues. Mass spectrometry studies using 15N-labelled L-arginine indicated that this enhancement was due to the formation of NO from the terminal guanidino nitrogen atom(s) of L-arginine. The strict substrate specificity of this reaction suggests that L-arginine is the precursor for NO synthesis in vascular endothelial cells.
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                Author and article information

                Journal
                J Am Oil Chem Soc
                J Am Oil Chem Soc
                Journal of the American Oil Chemists' Society
                Springer-Verlag (Berlin/Heidelberg )
                0003-021X
                1558-9331
                1998
                : 75
                : 2
                : 199-212
                Affiliations
                GRID grid.13097.3c, ISNI 0000000123226764, OICA International, Saint Lucia, West Indies, and Pharmacology Group, , King’s College London, ; SW3 6LX London, Great Britain
                Article
                32
                10.1007/s11746-998-0032-9
                7101596
                32287334
                45e8fc68-c8da-4b2d-8ea8-0bb7551b846b
                © AOCS Press 1998

                This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic.

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                Custom metadata
                © AOCS Press 1998

                General chemistry
                antioxidants,atherosclerosis,dna damage,flavonoids,free radicals,8-hydroxydeoxyguanosine,isoprostanes,lipid peroxidation,oxidative protein damage,oxidative stress,phytochemicals

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