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1.
Polyphenols: Potential Beneficial Effects of These Phytochemicals in Athletes.
D'Angelo, S
Current sports medicine reports. 2020;(7):260-265
Abstract
An athlete's dietary requirements depend on several aspects, including the environment, the sport, and the athlete's goals. Although it is recognized that regular exercise improves muscle performance and energy metabolism, unaccustomed or excessive exercise may cause cell damage and impair muscle function by triggering tissue inflammation and oxidative stress. Supplement use among athletes is widespread and recently new attention has been applied to polyphenols. Polyphenols are a class of organic chemical compounds, mainly found in plants, characterized by the presence of multiples of phenol structural units, and over recent decades, special attention has been paid to the healthy role of fruit-derived polyphenols in the human diet. This article will summarize latest knowledge on polyphenolic compounds that have been demonstrated both to exert an effect in exercise-induced muscle damage and to play a biological/physiological role in improving physical performance.
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Mechanisms of sensing and response to proteotoxic stress.
Santiago, AM, Gonçalves, DL, Morano, KA
Experimental cell research. 2020;(2):112240
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Abstract
Cells are continuously subject to various stresses, battling both exogenous insults as well as toxic by-products of normal cellular metabolism and nutrient deprivation. Throughout the millennia, cells developed a core set of general stress responses that promote survival and reproduction under adverse circumstances. Past and current research efforts have been devoted to understanding how cells sense stressors and how that input is deciphered and transduced, resulting in stimulation of stress management pathways. A prime element of cellular stress responses is the increased transcription and translation of proteins specialized in managing and mitigating distinct types of stress. In this review, we focus on recent developments in our understanding of cellular sensing of proteotoxic stressors that impact protein synthesis, folding, and maturation provided by the model eukaryote the budding yeast, Saccharomyces cerevisiae, with reference to similarities and differences with other model organisms and humans.
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Cardioprotective Effects of Dietary Phytochemicals on Oxidative Stress in Heart Failure by a Sex-Gender-Oriented Point of View.
Komici, K, Conti, V, Davinelli, S, Bencivenga, L, Rengo, G, Filippelli, A, Ferrara, N, Corbi, G
Oxidative medicine and cellular longevity. 2020;:2176728
Abstract
Dietary phytochemicals are considered an innovative strategy that helps to reduce cardiovascular risk factors. Some phytochemicals have been shown to play a beneficial role in lipid metabolism, to improve endothelial function and to modify oxidative stress pathways in experimental and clinical models of cardiovascular impairment. Importantly, investigation on phytochemical effect on cardiac remodeling appears to be promising. Nowadays, drug therapy and implantation of devices have demonstrated to ameliorate survival. Of interest, sex-gender seems to influence the response to HF canonical therapies. In fact, starting by the evidence of the feminization of world population and the scarce efficacy and safety of the traditional drugs in women, the search of alternative therapeutic tools has become mandatory. The aim of this review is to summarize the possible role of dietary phytochemicals in HF therapy and the evidence of a different sex-gender-oriented response.
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Physical exercise: An inducer of positive oxidative stress in skeletal muscle aging.
Thirupathi, A, Pinho, RA, Chang, YZ
Life sciences. 2020;:117630
Abstract
Oxidative stress is the core of most pathological situations, and its attribution toward disease conversion is not yet well established. The adaptive capacity of a cell can overcome ROS-induced pathology. However, when a cell fails to extend its maximum adaptive capacity against oxidative stress, it could lead a cell to misbehave or defunct from its normal functions. Any type of physical activity can increase the cells' maximum adaptive capacity, but aging can limit this. However, whether aging is the initiating point of reducing cells' adaptive capacity against oxidative stress or oxidative stress can induce the aging process is a mystery, and it could be the key to solving several uncured diseases. Paradoxically, minimum ROS is needed for cellular homeostasis. Nevertheless, finding factors that can limit or nullify the production of ROS for cellular homeostasis is a million-dollar question. Regular physical exercise is considered to be one of the factors that can limit the production of ROS and increase the ROS-induced benefits in the cells through inducing minimum oxidative stress and increasing maximum adapting capacity against oxidative stress-induced damages. The type and intensity of exercise that can produce such positive effects in the cells remain unclear. Therefore, this review discusses how physical exercise can help to produce minimal positive oxidative stress in preventing skeletal muscle aging.
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Glycemic Variability and CNS Inflammation: Reviewing the Connection.
Watt, C, Sanchez-Rangel, E, Hwang, JJ
Nutrients. 2020;(12)
Abstract
Glucose is the primary energy source for the brain, and exposure to both high and low levels of glucose has been associated with numerous adverse central nervous system (CNS) outcomes. While a large body of work has highlighted the impact of hyperglycemia on peripheral and central measures of oxidative stress, cognitive deficits, and vascular complications in Type 1 and Type 2 diabetes, there is growing evidence that glycemic variability significantly drives increased oxidative stress, leading to neuroinflammation and cognitive dysfunction. In this review, the latest data on the impact of glycemic variability on brain function and neuroinflammation will be presented. Because high levels of oxidative stress have been linked to dysfunction of the blood-brain barrier (BBB), special emphasis will be placed on studies investigating the impact of glycemic variability on endothelial and vascular inflammation. The latest clinical and preclinical/in vitro data will be reviewed, and clinical/therapeutic implications will be discussed.
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Minireview Exploring the Biological Cycle of Vitamin B3 and Its Influence on Oxidative Stress: Further Molecular and Clinical Aspects.
Doroftei, B, Ilie, OD, Cojocariu, RO, Ciobica, A, Maftei, R, Grab, D, Anton, E, McKenna, J, Dhunna, N, Simionescu, G
Molecules (Basel, Switzerland). 2020;(15)
Abstract
Vitamin B3, or niacin, is one of the most important compounds of the B-vitamin complex. Recent reports have demonstrated the involvement of vitamin B3 in a number of pivotal functions which ensure that homeostasis is maintained. In addition, the intriguing nature of its synthesis and the underlying mechanism of action of vitamin B3 have encouraged further studies aimed at deepening our understanding of the close link between the exogenous supply of B3 and how it activates dependent enzymes. This crucial role can be attributed to the gut microflora and its ability to shape human behavior and development by mediating the bioavailability of metabolites. Recent studies have indicated a possible interconnection between the novel coronavirus and commensal bacteria. As such, we have attempted to explain how the gastrointestinal deficiencies displayed by SARS-CoV-2-infected patients arise. It seems that the stimulation of a proinflammatory cascade and the production of large amounts of reactive oxygen species culminates in the subsequent loss of host eubiosis. Studies of the relationhip between ROS, SARS-CoV-2, and gut flora are sparse in the current literature. As an integrated component, oxidative stress (OS) has been found to negatively influence host eubiosis, in vitro fertilization outcomes, and oocyte quality, but to act as a sentinel against infections. In conclusion, research suggests that in the future, a healthy diet may be considered a reliable tool for maintaining and optimizing our key internal parameters.
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Benefits and Adverse Effects of Histidine Supplementation.
Thalacker-Mercer, AE, Gheller, ME
The Journal of nutrition. 2020;(Suppl 1):2588S-2592S
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Abstract
Histidine is a nutritionally essential amino acid with many recognized benefits to human health, while circulating concentrations of histidine decline in pathologic conditions [e.g., chronic obstructive pulmonary disease (COPD) and chronic kidney disease (CKD)]. The purpose of this review is to examine the existing literature regarding the benefits of histidine intake, the adverse effects of excess histidine, and the upper tolerance level for histidine. Supplementation with doses of 4.0-4.5 g histidine/d and increased dietary histidine intake are associated with decreased BMI, adiposity, markers of glucose homeostasis (e.g., HOMA-IR, fasting blood glucose, 2-h postprandial blood glucose), proinflammatory cytokines, and oxidative stress. It is unclear from the limited number of studies in humans whether the improvements in glucoregulatory markers, inflammation, and oxidative stress are due to reduced BMI and adiposity, increased carnosine (a metabolic product of histidine with antioxidant effects), or both. Histidine intake also improves cognitive function (e.g., reduces appetite, anxiety, and stress responses and improves sleep) potentially through the metabolism of histidine to histamine; however, this relation is ambiguous in humans. At high intakes of histidine (>24 g/d), studies report adverse effects of histidine such as decreased serum zinc and cognitive impairment. There is limited research on the effects of histidine intake at doses between 4.5 and 24 g/d, and thus, a tolerable upper level has not been established. Determining tolerance to histidine supplementation has been limited by small sample sizes and, more important, a lack of a clear biomarker for histidine supplementation. The U-shaped curve of circulating zinc concentrations with histidine supplementation could be exploited as a relevant biomarker for supplemental histidine tolerance. Histidine is an important amino acid and may be necessary as a supplement in some populations; however, gaps in knowledge, which this review highlights, need to be addressed scientifically.
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Coenzyme Q10 Supplementation for the Reduction of Oxidative Stress: Clinical Implications in the Treatment of Chronic Diseases.
Gutierrez-Mariscal, FM, Arenas-de Larriva, AP, Limia-Perez, L, Romero-Cabrera, JL, Yubero-Serrano, EM, López-Miranda, J
International journal of molecular sciences. 2020;(21)
Abstract
Apart from its main function in the mitochondria as a key element in electron transport, Coenzyme Q10 (CoQ10) has been described as having multiple functions, such as oxidant action in the generation of signals and the control of membrane structure and phospholipid and cellular redox status. Among these, the most relevant and most frequently studied function is the potent antioxidant capability of its coexistent redox forms. Different clinical trials have investigated the effect of CoQ10 supplementation and its ability to reduce oxidative stress. In this review, we focused on recent advances in CoQ10 supplementation, its role as an antioxidant, and the clinical implications that this entails in the treatment of chronic diseases, in particular cardiovascular diseases, kidney disease, chronic obstructive pulmonary disease, non-alcoholic fatty liver disease, and neurodegenerative diseases. As an antioxidant, CoQ10 has proved to be of potential use as a treatment in diseases in which oxidative stress is a hallmark, and beneficial effects of CoQ10 have been reported in the treatment of chronic diseases. However, it is crucial to reach a consensus on the optimal dose and the use of different formulations, which vary from ubiquinol or ubiquinone Ubisol-Q10 or Qter®, to new analogues such as MitoQ, before we can draw a clear conclusion about its clinical use. In addition, a major effort must be made to demonstrate its beneficial effects in clinical trials, with a view to making the implementation of CoQ10 possible in clinical practice.
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Mechanisms of Co, Ni, and Mn toxicity: From exposure and homeostasis to their interactions with and impact on lipids and biomembranes.
Sule, K, Umbsaar, J, Prenner, EJ
Biochimica et biophysica acta. Biomembranes. 2020;(8):183250
Abstract
Anthropogenic activity has increased human exposure to metals and resulted in metal induced toxicity. Essential trace elements like cobalt (Co), nickel (Ni), and manganese (Mn) are best known for their roles as important cofactors in many enzymes involved in signalling, metabolism, and response to oxidative stress. However, deficiencies as well as long-term overexposure to these metals can result in negative health effects. Co has been associated with cardiomyopathy, lung disease, and hearing damage, while Ni is a known carcinogen, as well as a common sensitizing metal. Mn is best classified as a neurotoxicant that causes a disorder alike to idiopathic Parkinson's disease known as Manganism. Although the mechanisms of Co, Ni, and Mn toxicity are complex and have yet to be fully elucidated, research over the years has provided useful insights into understanding metal-induced detrimental effects at the cellular and molecular level. One area of research that has been explored in less detail are metal interactions with lipids and biological membranes, which are a potentially critical target as membranes are the first point of contact for cells. This review covers the current understandings of Co, Ni and Mn toxicity, in terms of human exposure, homeostasis and mechanisms of transport, potential cellular targets, and, of primary focus, metal interactions with lipid and biomembranes. A variety of effects like membrane rigidification, leakage affecting membrane potentials, lipid phase changes, alterations in lipid metabolism and changes of cellular morphology illustrate the vast potential for metal-based membrane effects contributing to their toxicity.
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10.
Proteostasis Failure in Neurodegenerative Diseases: Focus on Oxidative Stress.
Höhn, A, Tramutola, A, Cascella, R
Oxidative medicine and cellular longevity. 2020;:5497046
Abstract
Protein homeostasis or proteostasis is an essential balance of cellular protein levels mediated through an extensive network of biochemical pathways that regulate different steps of the protein quality control, from the synthesis to the degradation. All proteins in a cell continuously turn over, contributing to development, differentiation, and aging. Due to the multiple interactions and connections of proteostasis pathways, exposure to stress conditions may cause various types of protein damage, altering cellular homeostasis and disrupting the entire network with additional cellular stress. Furthermore, protein misfolding and/or alterations during protein synthesis results in inactive or toxic proteins, which may overload the degradation mechanisms. The maintenance of a balanced proteome, preventing the formation of impaired proteins, is accomplished by two major catabolic routes: the ubiquitin proteasomal system (UPS) and the autophagy-lysosomal system. The proteostasis network is particularly important in nondividing, long-lived cells, such as neurons, as its failure is implicated with the development of neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis. These neurological disorders share common risk factors such as aging, oxidative stress, environmental stress, and protein dysfunction, all of which alter cellular proteostasis, suggesting that general mechanisms controlling proteostasis may underlay the etiology of these diseases. In this review, we describe the major pathways of cellular proteostasis and discuss how their disruption contributes to the onset and progression of neurodegenerative diseases, focusing on the role of oxidative stress.