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Antioxidants in Health and Diseases

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Bioactives and Nutraceuticals".

Deadline for manuscript submissions: 20 October 2024 | Viewed by 8414

Special Issue Editors


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Guest Editor
Division of Antioxidant Research, Gifu University, Gifu, Japan
Interests: oxidative stress; antioxidants; regulation of redox; cancer metastasis; Alzheimer’s disease; diabetes mellitus; COVID-19 infection

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Guest Editor
Department of Otolaryngology-Head and Neck Surgery, Kyoto Prefectural University of Medicine, Kyoto, Japan
Interests: oxidative stress

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Guest Editor
Hospital Director Koji Abe, National Center of Neurology and Psychiatry, Tokyo, Japan
Interests: oxidative stress; Alzheimer’s disease; ALS

Special Issue Information

Dear Colleagues,

Numerous studies have shown that excessive oxidative stress is detrimental to human health and the source of many diseases. In recent years, COVID-19 infection and its vaccine sequelae have caused a wide variety of symptoms and diseases due to excessive oxidative stress. On the other hand, there are growing evidences that appropriate administration of antioxidants to humans can improve health and prevent disease. In this special issue, we call for papers on the effects of antioxidants not only in improving health, but also in preventing and treating many diseases such as cancer, dementia, diabetes, atherosclerosis, allergic diseases, and infectious diseases. Basic research on the prevention of diseases and infections by suppressing oxidative stress is also highly encouraged. There are scattered papers on antioxidants' harmful effects on cancer metastasis and health, mostly in animal studies with single or large doses of antioxidants. Manuscripts showing that the right dose of antioxidants is critical for positive effects are also welcome.

Dr. Haruhiko Inufusa
Prof. Dr. Shigeru Hirano
Dr. Koji Abe
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • antioxidants
  • oxidative stress
  • inflammation
  • mitochondria
  • health promotion
  • disease prevention and treatment

Published Papers (4 papers)

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Research

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13 pages, 1403 KiB  
Article
Tocotrienols Prevent the Decline of Learning Ability in High-Fat, High-Sucrose Diet-Fed C57BL/6 Mice
by Yugo Kato, Junhyoku Ben, Atsuto Noto, Shuntaro Kashiwaya, Yoshinori Aoki, Nobuo Watanabe, Hiroki Tsumoto, Yuri Miura and Koji Fukui
Int. J. Mol. Sci. 2024, 25(6), 3561; https://doi.org/10.3390/ijms25063561 - 21 Mar 2024
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Abstract
Obesity has been increasing worldwide and is well-known as a risk factor for cognitive decline. It has been reported that oxidative stress in the brain is deeply involved in cognitive dysfunction in rodent models. While there are many studies on oxidation in the [...] Read more.
Obesity has been increasing worldwide and is well-known as a risk factor for cognitive decline. It has been reported that oxidative stress in the brain is deeply involved in cognitive dysfunction in rodent models. While there are many studies on oxidation in the liver and adipose tissue of obese mice, the relationship between obesity-induced cognitive dysfunction and brain oxidation has not been elucidated. Here, we show that obesity induced by a high-fat, high-sucrose diet (HFSD) alters cognitive function in C57BL/6 male mice, and it may involve the acceleration of brain oxidation. Tocotrienols (T3s), which are members of the vitamin E family, can prevent HFSD-induced cognitive changes. To elucidate these mechanisms, respiratory metabolism, locomotor activity, temperature around brown adipose tissue, and protein profiles in the cerebrum cortex were measured. Contrary to our expectation, respiratory metabolism was decreased, and temperature around brown adipose tissue was increased in the feeding of HFSD. The proteins that regulate redox balance did not significantly change, but 12 proteins, which were changed by HFSD feeding and not changed by T3s-treated HFSD compared to control mice, were identified. Our results indicated that HFSD-induced obesity decreases mouse learning ability and that T3s prevent its change. Additionally, feeding of HFSD significantly increased brain oxidation. However, further study is needed to elucidate the mechanisms of change in oxidative stress in the brain by obesity. Full article
(This article belongs to the Special Issue Antioxidants in Health and Diseases)
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0 pages, 2963 KiB  
Article
A Blended Vitamin Supplement Improves Spatial Cognitive and Short-Term Memory in Aged Mice
by Koji Fukui, Fukka You, Yugo Kato, Shuya Yuzawa, Ayuta Kishimoto, Takuma Hara, Yuki Kanome, Yoshiaki Harakawa and Toshikazu Yoshikawa
Int. J. Mol. Sci. 2024, 25(5), 2804; https://doi.org/10.3390/ijms25052804 - 28 Feb 2024
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Abstract
Although many types of antioxidant supplements are available, the effect is greater if multiple types are taken simultaneously rather than one type. However, it is difficult to know which type and how much to take, as it is possible to take too many [...] Read more.
Although many types of antioxidant supplements are available, the effect is greater if multiple types are taken simultaneously rather than one type. However, it is difficult to know which type and how much to take, as it is possible to take too many of some vitamins. As it is difficult for general consumers to make this choice, it is important to provide information based on scientific evidence. This study investigated the various effects of continuous administration of a blended supplement to aging mice. In 18-month-old C57BL/6 mice given a blended supplement ad libitum for 1 month, spatial cognition and short-term memory in the Morris water maze and Y-maze improved compared with the normal aged mice (spontaneous alternative ratio, normal aged mice, 49.5%, supplement-treated mice, 68.67%, p < 0.01). No significant differences in brain levels of secreted neurotrophic factors, such as nerve growth factor and brain-derived neurotrophic factor, were observed between these two groups. In treadmill durability tests before and after administration, the rate of increase in running distance after administration was significantly higher than that of the untreated group (increase rate, normal aged mice, 91.17%, supplement-treated aged mice, 111.4%, p < 0.04). However, training had no reinforcing effect, and post-mortem serum tests showed a significant decrease in aspartate aminotransferase, alanine aminotransferase, and total cholesterol values. These results suggest continuous intake of a blended supplement may improve cognitive function and suppress age-related muscle decline. Full article
(This article belongs to the Special Issue Antioxidants in Health and Diseases)
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Review

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17 pages, 3722 KiB  
Review
Oxidative Stress and Bio-Regulation
by Toshikazu Yoshikawa and Fukka You
Int. J. Mol. Sci. 2024, 25(6), 3360; https://doi.org/10.3390/ijms25063360 - 15 Mar 2024
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Abstract
Reactive oxygen species (ROS) and free radicals work to maintain homeostasis in the body, but their excessive production causes damage to the organism. The human body is composed of a variety of cells totaling over 60 trillion cells. Each cell performs different functions [...] Read more.
Reactive oxygen species (ROS) and free radicals work to maintain homeostasis in the body, but their excessive production causes damage to the organism. The human body is composed of a variety of cells totaling over 60 trillion cells. Each cell performs different functions and has a unique lifespan. The lifespan of cells is preprogrammed in their genes, and the death of cells that have reached the end of their lifespan is called apoptosis. This is contrary to necrosis, which is the premature death of cells brought about by physical or scientific forces. Each species has its own unique lifespan, which in humans is estimated to be up to 120 years. Elucidating the mechanism of the death of a single cell will lead to a better understanding of human death, and, conversely, the death of a single cell will lead to exploring the mechanisms of life. In this sense, research on active oxygen and free radicals, which are implicated in biological disorders and homeostasis, requires an understanding of both the physicochemical as well as the biochemical aspects. Based on the discussion above, it is clear to see that active oxygen and free radicals have dual functions of both injuring and facilitating homeostasis in living organisms. Full article
(This article belongs to the Special Issue Antioxidants in Health and Diseases)
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12 pages, 1631 KiB  
Review
Update on Antioxidant Therapy with Edaravone: Expanding Applications in Neurodegenerative Diseases
by Toru Yamashita and Koji Abe
Int. J. Mol. Sci. 2024, 25(5), 2945; https://doi.org/10.3390/ijms25052945 - 3 Mar 2024
Viewed by 975
Abstract
The brain is susceptible to oxidative stress, which is associated with various neurological diseases. Edaravone (MCI-186, 3-methyl-1 pheny-2-pyrazolin-5-one), a free radical scavenger, has promising effects by quenching hydroxyl radicals (∙OH) and inhibiting both ∙OH-dependent and ∙OH-independent lipid peroxidation. Edaravone was initially developed in [...] Read more.
The brain is susceptible to oxidative stress, which is associated with various neurological diseases. Edaravone (MCI-186, 3-methyl-1 pheny-2-pyrazolin-5-one), a free radical scavenger, has promising effects by quenching hydroxyl radicals (∙OH) and inhibiting both ∙OH-dependent and ∙OH-independent lipid peroxidation. Edaravone was initially developed in Japan as a neuroprotective agent for acute cerebral infarction and was later applied clinically to treat amyotrophic lateral sclerosis (ALS), a neurodegenerative disease. There is accumulating evidence for the therapeutic effects of edaravone in a wide range of diseases related to oxidative stress, including ischemic stroke, ALS, Alzheimer’s disease, and placental ischemia. These neuroprotective effects have expanded the potential applications of edaravone. Data from experimental animal models support its safety for long-term use, implying broader applications in various neurodegenerative diseases. In this review, we explain the unique characteristics of edaravone, summarize recent findings for specific diseases, and discuss its prospects for future therapeutic applications. Full article
(This article belongs to the Special Issue Antioxidants in Health and Diseases)
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