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      Theaflavin Chemistry and Its Health Benefits

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          Abstract

          Huge epidemiological and clinical studies have confirmed that black tea is a rich source of health-promoting ingredients, such as catechins and theaflavins (TFs). Furthermore, TF derivatives mainly include theaflavin (TF1), theaflavin-3-gallate (TF2A), theaflavin-3′-gallate (TF2B), and theaflavin-3,3′-digallate (TF3). All of these TFs exhibit extensive usages in pharmaceutics, foods, and traditional medication systems. Various indepth studies reported that how TFs modulates health effects in cellular and molecular mechanisms. The available literature regarding the pharmacological activities of TFs has revealed that TF3 has remarkable anti-inflammatory, antioxidant, anticancer, antiobesity, antiosteoporotic, and antimicrobial properties, thus posing significant effects on human health. The current manuscript summarizes both the chemistry and various pharmacological effects of TFs on human health, lifestyle or aging associated diseases, and populations of gut microbiota. Furthermore, the biological potential of TFs has also been focused to provide a deeper understanding of its mechanism of action.

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          Free radicals and antioxidants in normal physiological functions and human disease.

          Marian Valko, Dieter Leibfritz, Jan Moncol … (2007)
          Reactive oxygen species (ROS) and reactive nitrogen species (RNS, e.g. nitric oxide, NO(*)) are well recognised for playing a dual role as both deleterious and beneficial species. ROS and RNS are normally generated by tightly regulated enzymes, such as NO synthase (NOS) and NAD(P)H oxidase isoforms, respectively. Overproduction of ROS (arising either from mitochondrial electron-transport chain or excessive stimulation of NAD(P)H) results in oxidative stress, a deleterious process that can be an important mediator of damage to cell structures, including lipids and membranes, proteins, and DNA. In contrast, beneficial effects of ROS/RNS (e.g. superoxide radical and nitric oxide) occur at low/moderate concentrations and involve physiological roles in cellular responses to noxia, as for example in defence against infectious agents, in the function of a number of cellular signalling pathways, and the induction of a mitogenic response. Ironically, various ROS-mediated actions in fact protect cells against ROS-induced oxidative stress and re-establish or maintain "redox balance" termed also "redox homeostasis". The "two-faced" character of ROS is clearly substantiated. For example, a growing body of evidence shows that ROS within cells act as secondary messengers in intracellular signalling cascades which induce and maintain the oncogenic phenotype of cancer cells, however, ROS can also induce cellular senescence and apoptosis and can therefore function as anti-tumourigenic species. This review will describe the: (i) chemistry and biochemistry of ROS/RNS and sources of free radical generation; (ii) damage to DNA, to proteins, and to lipids by free radicals; (iii) role of antioxidants (e.g. glutathione) in the maintenance of cellular "redox homeostasis"; (iv) overview of ROS-induced signaling pathways; (v) role of ROS in redox regulation of normal physiological functions, as well as (vi) role of ROS in pathophysiological implications of altered redox regulation (human diseases and ageing). Attention is focussed on the ROS/RNS-linked pathogenesis of cancer, cardiovascular disease, atherosclerosis, hypertension, ischemia/reperfusion injury, diabetes mellitus, neurodegenerative diseases (Alzheimer's disease and Parkinson's disease), rheumatoid arthritis, and ageing. Topics of current debate are also reviewed such as the question whether excessive formation of free radicals is a primary cause or a downstream consequence of tissue injury.
          Article 0 comments Cited 1211 times – based on 0 reviews     Review now
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            Mitochondria, oxidants, and aging.

            Robert Balaban, Shino Nemoto, Toren Finkel (2005)
            The free radical theory of aging postulates that the production of intracellular reactive oxygen species is the major determinant of life span. Numerous cell culture, invertebrate, and mammalian models exist that lend support to this half-century-old hypothesis. Here we review the evidence that both supports and conflicts with the free radical theory and examine the growing link between mitochondrial metabolism, oxidant formation, and the biology of aging.
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              Oxidative stress sensor Keap1 functions as an adaptor for Cul3-based E3 ligase to regulate proteasomal degradation of Nrf2.

              Akira Kobayashi, Moon-Il Kang, Hiromi Okawa … (2004)
              Transcription factor Nrf2 is a major regulator of genes encoding phase 2 detoxifying enzymes and antioxidant stress proteins in response to electrophilic agents and oxidative stress. In the absence of such stimuli, Nrf2 is inactive owing to its cytoplasmic retention by Keap1 and rapid degradation through the proteasome system. We examined the contribution of Keap1 to the rapid turnover of Nrf2 (half-life of less than 20 min) and found that a direct association between Keap1 and Nrf2 is required for Nrf2 degradation. In a series of domain function analyses of Keap1, we found that both the BTB and intervening-region (IVR) domains are crucial for Nrf2 degradation, implying that these two domains act to recruit ubiquitin-proteasome factors. Indeed, Cullin 3 (Cul3), a subunit of the E3 ligase complex, was found to interact specifically with Keap1 in vivo. Keap1 associates with the N-terminal region of Cul3 through the IVR domain and promotes the ubiquitination of Nrf2 in cooperation with the Cul3-Roc1 complex. These results thus provide solid evidence that Keap1 functions as an adaptor of Cul3-based E3 ligase. To our knowledge, Nrf2 and Keap1 are the first reported mammalian substrate and adaptor, respectively, of the Cul3-based E3 ligase system.
              Article 0 comments Cited 296 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Chunhua Zhang:
                ORCID: https://orcid.org/0000-0001-9567-0987
                Chunpeng (Craig) Wan:
                ORCID: https://orcid.org/0000-0001-6892-016X
                Journal
                Journal ID (nlm-ta): Oxid Med Cell Longev
                Journal ID (iso-abbrev): Oxid Med Cell Longev
                Journal ID (publisher-id): OMCL
                Title: Oxidative Medicine and Cellular Longevity
                Publisher: Hindawi
                ISSN (Print): 1942-0900
                ISSN (Electronic): 1942-0994
                Publication date Collection: 2021
                Publication date (Electronic): 18 November 2021
                Volume: 2021
                Electronic Location Identifier: 6256618
                Affiliations
                1College of Agriculture and Forestry, Pu'er University, Pu'er 665099, China
                2Jiangxi Key Laboratory for Postharvest Technology and Nondestructive Testing of Fruits & Vegetables, College of Agronomy, Jiangxi Agricultural University, Nanchang 330045, China
                3Department of Physiology and Biochemistry, Cholistan University of Veterinary and Animal Sciences (CUVAS), Bahawalpur 63100, Pakistan
                4Research Center of Tea and Tea Culture, College of Agronomy, Jiangxi Agricultural University, Nanchang, Jiangxi, China
                Author notes

                Academic Editor: Lei Chen

                Author information
                https://orcid.org/0000-0002-6165-8258
                https://orcid.org/0000-0001-8873-1227
                https://orcid.org/0000-0003-3987-017X
                https://orcid.org/0000-0001-9567-0987
                https://orcid.org/0000-0001-6892-016X
                Article
                DOI: 10.1155/2021/6256618
                PMC ID: 8601833
                PubMed ID: 34804369
                SO-VID: d53b3d3b-4f08-4127-b0d3-086e68254f89
                Copyright © Copyright © 2021 Zhiguo Shan et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 15 September 2021
                Date revision received : 30 October 2021
                Date accepted : 2 November 2021
                Funding
                Funded by: Special Planning Project for Key Scientific Research of Pu'er College
                Award ID: 2020XJGH08
                Funded by: Young Backbone Teacher Training Project of Pu'er College
                Award ID: 2020GGJS005
                Funded by: Young Academic and Technical Leaders Reserve Talent Training Program of Pu'er College
                Award ID: QNRC20-02
                Funded by: Pu'er College Key Project
                Award ID: K2018012
                Funded by: Yunnan Provincial Education Department Science Research Fund Project
                Award ID: K2017058
                Award ID: 2018JS513
                Funded by: Pu'er tea processing engineering research center in Yunnan Province University, Pu'er College High-level Talents Research Initiation Project
                Award ID: K2015032
                Funded by: National Natural Science Foundation of China
                Award ID: 32160725
                Categories
                Subject: Review Article

                ScienceOpen disciplines: Molecular medicine
                Data availability:
                ScienceOpen disciplines: Molecular medicine

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