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      A Role of Gallic Acid in Oxidative Damage Diseases: A Comprehensive Review

      1 , 1 , 1 , 2
      Natural Product Communications
      SAGE Publications

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          Abstract

          Gallic acid is a trihydroxybenzoic acid of plant metabolites widely spread throughout the plant kingdom. It has characteristics of the strong antioxidant and free radical scavenging activities, and can protect biological cells, tissues, and organs from damages caused by oxidative stress. This review aims to summarize the protective roles of gallic acid and the underlying pharmacological mechanisms in the pathophysiological process of the oxidative damage diseases, such as cancer, cardiovascular, degenerative, and metabolic diseases. The studies reviewed herein showed that the main therapeutic effects of gallic acid were attributed to its antioxidant properties. It modulated various signaling pathways through a wide range of inflammatory cytokines, and enzymic and nonenzymic antioxidants. However, the available data were limited to few studies assessing the treatment effects of gallic acid in human subjects to confirm its therapeutic outcomes. Therefore, the clinical trials were urgently needed to investigate the safety and efficacy of gallic acid treatment on human beings. The scientific data summarized in this review highlighted the therapeutic potentials of gallic acid for oxidative damage diseases. It could be developed as versatile adjuvant or therapeutically lead compound in future.

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              Reactive oxygen species (ROS) are an unenviable part of aerobic life. Their steady-state concentration is a balance between production and elimination providing certain steady-state ROS level. The dynamic equilibrium can be disturbed leading to enhanced ROS level and damage to cellular constituents which is called "oxidative stress". This review describes the general processes responsible for ROS generation in aquatic animals and critically analyses used markers for identification of oxidative stress. Changes in temperature, oxygen levels and salinity can cause the stress in natural and artificial conditions via induction of disbalance between ROS production and elimination. Human borne pollutants can also enhance ROS level in hydrobionts. The role of transition metal ions, such as copper, chromium, mercury and arsenic, and pesticides, namely insecticides, herbicides, and fungicides along with oil products in induction of oxidative stress is highlighted. Last years the research in biology of free radicals was refocused from only descriptive works to molecular mechanisms with particular interest to ones enhancing tolerance. The function of some transcription regulators (Keap1-Nrf2 and HIF-1α) in coordination of organisms' response to oxidative stress is discussed. The future directions in the field are related with more accurate description of oxidative stress, the identification of its general characteristics and mechanisms responsible for adaptation to the stress have been also discussed. The last part marks some perspectives in the study of oxidative stress in hydrobionts, which, in addition to classic use, became more and more popular to address general biological questions such as development, aging and pathologies. Copyright © 2010 Elsevier B.V. All rights reserved.
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                Author and article information

                Journal
                Natural Product Communications
                Natural Product Communications
                SAGE Publications
                1934-578X
                1555-9475
                August 29 2019
                August 2019
                August 29 2019
                August 2019
                : 14
                : 8
                : 1934578X1987417
                Affiliations
                [1 ]School of Chemical Engineering and Pharmaceutics, Henan University of Science and Technology, Luoyang, China
                [2 ]School of Clinical Medicine, Henan University of Science and Technology, Luoyang, China
                Article
                10.1177/1934578X19874174
                88a1875f-a58f-450d-a3af-e71d8bcaffb4
                © 2019

                http://journals.sagepub.com/page/policies/text-and-data-mining-license

                History

                Quantitative & Systems biology,Biophysics
                Quantitative & Systems biology, Biophysics

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