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Hepatitis B and its Relationship With Oxidative Stress Featured

Despite the great breakthroughs we have witnessed in the last 50 years in the prevention, diagnosis, and treatment of hepatitis B, we are still far from eradicating or even curing the disease. Achieving further progress in controlling this disease will not be possible without discovering the exact pathogenesis behind it. One prime suspect in the pathogenesis of various diseases is oxidative stress. This review will exclusively explore hepatitis B in the context of oxidative stress to obtain a more comprehensive clinical perspective on its pathogenesis and eventual medical therapy.

Evidence Acquisition:: We systematically searched PubMed, Google Scholar, Web of Science, EMBASE, and Scopus using an extensive list of keywords in the following three categories: 1) Hepatitis B and oxidation 2) Hepatitis B and antioxidant system 3) Effects of approved anti-hepatitis B drugs on redox status. All relevant articles were obtained and reviewed carefully after the exclusion criteria were deployed.

Results: There is great evidence indicating extensive oxidative stress occurs in hepatitis B. This oxidative stress takes place on multiple levels, including lipid peroxidation, DNA oxidation, protein oxidation, and reactive oxygen and nitrogen species production. However, there are also conflicting results with regard to antioxidant therapy and antioxidant status in hepatitis B, some of which may be explained by the concept of “compensatory gaps.” Nevertheless, further studies are indicated to reach a more thorough judgment.

Conclusions: Despite the presence of vast oxidative stress in hepatitis B, antioxidant therapy is not always effective as a treatment strategy, especially considering that antioxidants can act as “double-edged swords” or antioxidants; if not used at the right time or place or in the right combination, these substances can easily become pro-oxidants. Therefore, several studies will be needed to determine suitable antioxidant therapies. We propose the “2-step Combined Antioxidant Adjuvant Therapy for hepatitis B (2CAAT Hep B)” as a new strategy for antioxidant adjuvant therapy. We also suggest developing an international platform and database for antioxidant adjuvant therapy in hepatitis B (IPAATH and IDAATH) to canalize this field of research in a standardized direction, especially when complexity is a problem.

(Alavian SM, Showraki A (2016). Hepatitis B and its Relationship With Oxidative Stress. Hepatitis Monthly. 16(9): e37973)

1. Context

Although it has been 50 years since the discovery of the Australian Antigen (i.e., HBsAg) by Nobel Prize Laureate, Professor Baruch Samuel Blumberg (1925 - 2011) (1), the hepatitis B virus still affects approximately 350 million individuals around the world (2) and is responsible for the deaths of about one million people annually (3). We have seen great progress in the prevention, diagnosis, and treatment of hepatitis B in the past few decades; however, we are far from eradicating or even eliminating the disease (4). The production of the first hepatitis B vaccine in 1983, which was called the first anti-cancer vaccine by the world health organization (WHO) (4), offered hope in controlling and preventing the disease. The outlook was further enhanced by the production and development of the first antiviral drugs in later years. With the implementation of new treatment strategies, some achievements have been made in controlling the disease, yet we are far from eradicating it. Hepatitis B remains the number one cause of liver cirrhosis globally (5). Moreover, hepatocellular carcinoma (HCC), which is the 5th most prevalent cancer and the 3rd highest cause of cancerrelated death, is one of hepatitis B’s major complications (6). Currently, only six drugs have been approved by the United States (US) food and drug administration (FDA) for the control and treatment of hepatitis B (7). These drugs include Interferon alpha (i.e., conventional INF-α 2a, conventional INF-α 2b, and peglayted INF-α 2a), Lamivudine, Adefovir, Entecavir, Telbivudine, and Tenefovir (7). Even though these drugs have been partly successful in decreasing liver cirrhosis and HCC, they cannot eradicate the virus from the host’s body and instead prevent its replication (8). In other words, the infection remained. In addition, facts such as medical costs, drug adverse effects, drug resistance, and treatment failure have made controlling hepatitis B more challenging (4). All currently available oral drugs must be consumed indefinitely, which carries significant costs and is associated with low patient compliance (4). Thus, there is a major need for the development of newer drugs and treatment strategies. However, this need cannot be met until we understand the exact pathogenesis of the disease. One topic that has attracted great attention in the pathogenesis of both infectious and non-infectious diseases is “oxidative stress.” This subject has gained such momentum that a new field of research called “Redox biology” has emerged (9). Normally, there is an equilibrium in the oxidationreduction system in all of our body’s cells that is crucial to the cells’ survival (10). If this equilibrium is somehow disrupted, either the oxidant levels increase or the antioxidant levels decrease, which is termed a state of “oxidative stress” (11). This condition is hazardous to the cell and will lead to vast injuries to various macro-molecules within the cell, such as DNA, proteins, and lipids (12, 13). As a result, oxidative stress is currently a major suspect in the pathogenesis of an extended spectrum of diseases and cancers (11). The investigation of the exact mechanisms of oxidative stress in different diseases could shed light on many unknowns and solve unanswered enigmas. This increase in our level of knowledge on hepatitis B’s pathogenesis will eventually lead to better and more effective treatments or even cures. The aim of this review was to clarify the role of oxidative stress in hepatitis B so that its results could contribute to a better understanding of the disease and its improved treatment or cure. We investigated the role of oxidative stress in the disease’ course and pathogenesis of hepatitis B from a clinical perspective using the information and data available in the literature in the following three categories: 1) Hepatitis B and oxidation status 2) Hepatitis B and the antioxidant system 3) The effects of approved anti-hepatitis B drugs on redox status.

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