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Search for other papers by Nahom Teferi in
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Iron accumulation and ferroptosis have long been implicated in the pathogenesis and neuronal loss of Parkinson’s disease. With the growing discovery of genes associated with Parkinson’s disease and mitochondrial function, there is emerging evidence of the convergent role of mitochondrial dysfunction, subsequent reactive oxygen species generation and ensuing iron accumulation working in concert to facilitate neuronal loss and injury in Parkinson’s disease. This subsequently leads to a vicious cycle where mitochondrial dysfunction may stimulate iron accumulation and inflammation as part of a synergistic feed-forward cycle resulting in neuronal death after the antioxidant cellular defense systems are overwhelmed. We reviewed the existing literature on mitochondrial and iron homeostasis and described the potential intersections of the disease mechanisms leading to iron accumulation, ferroptosis and dopaminergic cell death, ultimately culminating in the onset and progression of Parkinson’s disease.
Search for other papers by Yumi Abiko in
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Search for other papers by Yoshito Kumagai in
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Graphical abstract
Abstract
Intake of a variety of vegetables and fruit is found to be effective in promoting health; one of the reasons for this is activation of nuclear factor erythroid 2-related factor 2 (Nrf2), a basic leucine zipper protein. Nrf2 is activated by chemical modification of Kelch-like ECH-associated protein 1 (Keap1), a negative regulator for this transcription factor, and specific phosphorylation of Nrf2, resulting in upregulation of its downstream gene products for antioxidant proteins, phase-II xenobiotic-metabolizing enzymes, and phase-III transporters. This type of activation plays a role in adaptive response and protection against oxidative and electrophilic stress. Multiple phytochemicals, such as curcumin, sulforaphane, and (E)-2-alkenals, have been identified as Nrf2 activators and may reduce the adverse health effects of oxidants and electrophiles. In this review, we introduce plant components that are known as Nrf2 activators and associated phytochemical-mediated reduction of risk from chemicals which cause oxidative and electrophilic stress. We also discuss the capture and inactivation of methylmercury, an electrophile, by sulfane sulfur atoms contained in garlic.
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Search for other papers by Emmanuelle Prost-Camus in
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Abstract
Sarcopenia is a very disabling age-related disease which affects the mass and strength of skeletal muscles. This syndrome has no efficient treatment and is associated with important oxidative stress which could play important role in skeletal muscle degeneration. In this context, the cytoprotective activity and the antioxidant properties of a polyphenol-rich plant extract (PRPE) were evaluated in undifferentiated C2C12 murine skeletal muscle cells (myoblasts). PRPE is a potent antioxidant mixture as shown by its reactive oxygen species (ROS) scavenging properties by using the Kit Radicaux Libres method and the dihydroethidium (DHE) scavenging assay. In addition, PRPE has significant protecting properties in C2C12 cells toward oxidative stress triggered by 2, 2′-azobis (2-amidinopropane) dihydrochloride (AAPH) which is an ROS generator, as measured by different complementary approaches. PRPE counteracts several AAPH-induced cytotoxic effects. PRPE prevents morphological changes evaluated by phase contrast microscopy and decreases the number of dying cells determined by counting in the presence of trypan blue and the intracellular ROS overproduction evaluated by flow cytometry after staining with DHE. In addition, PRPE tends to normalize the expression of genes (peroxiredoxin 1 (Pdrx1), nuclear factor erythroid 2-related factor 2 (Nrf2), and peroxisome proliferator-activator receptor gamma coactivator 1-alpha (Pgc1α)) involved in the oxidant stress defense under ROS exposure. Altogether; our data show that PRPE has potent antioxidant properties and protects C2C12 skeletal muscle cells toward AAPH-induced oxidative stress. These cytoprotective properties of PRPE in skeletal muscle cells submitted to a pro-oxidant environment deserve further investigation in the context of sarcopenia.
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During aging loss of skeletal muscle mass and function has a significant effect of an individual’s quality of life and ability to maintain independence. Both loss of muscle fibres and atrophy of the remaining fibres play a role in the muscle decline and this is associated with loss of motor units and a reduction in the number of motor neurons. Increased oxidative damage has long been claimed to be associated with aging and many studies have reported increased amounts of oxidative damage markers are found in tissues from old organisms. Reactive oxygen species (ROS) are recognised to play a major role in cell signalling and in muscle ROS generated during contractile play an important role in signalling adaptations to contractile activity. These ’redox-regulated’ pathways are beneficial adaptations which are attenuated during aging. This review will briefly cover what is currently known about the mechanisms underlying these muscle adaptations to exercise, how they are affected by aging and assess the importance of these pathways in age-related loss of skeletal muscle mass and function.
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The inducible enzyme heme oxygenase 1 (HO-1) plays a pivotal role in cell defense against different kind of stressors, from oxidative stress to hypoxia. For this reason, HO-1 overexpression has been correlated to cancer aggressiveness in different tumors, being one of the molecular mechanisms used by tumor cells to become resistant to therapies. In addition, HO-1 has a well-recognized role in restraining immune response and in maintaining tolerance. In this context, the possibility that HO-1 induction in immune cells can reduce immune response to cancer and impair cancer immune therapy becomes a hot topic in cancer research. In this review, the most recent evidence pointing out the role of HO-1 in generating a permissive tumor microenvironment has been discussed as well as the most promising therapeutic approaches to increase effectiveness of immune therapies.
Homi Bhabha National Institute, Training School Complex, Anushaktinagar, Mumbai, India
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Homi Bhabha National Institute, Training School Complex, Anushaktinagar, Mumbai, India
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Homi Bhabha National Institute, Training School Complex, Anushaktinagar, Mumbai, India
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Homi Bhabha National Institute, Training School Complex, Anushaktinagar, Mumbai, India
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Nonalcoholic fatty liver disease or NAFLD is a complex and multifactorial liver disease that is affecting a majority of the world’s population now more than ever. The review focuses on two major contributing factors in the etiology of the disease – oxidative stress and the gut microbiota. There is a complex interplay between oxidative stress and the gut microbiota in the pathogenesis of NAFLD. Oxidative stress in NAFLD can result from both the accumulation of lipids in the liver and the interactions between gut-derived metabolites and the liver. Dysbiosis in the gut microbiota can contribute to oxidative stress by promoting the production of reactive oxygen species and altering the balance of antioxidant systems. This interplay between oxidative stress and the gut microbiota can create a vicious cycle, where dysbiosis contributes to oxidative stress, and oxidative stress further promotes dysbiosis, exacerbating liver damage in NAFLD. Understanding the intricate relationship between oxidative stress, the gut microbiota, and NAFLD is essential for developing targeted therapeutic strategies. In this context, more scientific research is required to unravel the complex and interconnecting pathways underlying NAFLD pathogenesis and progression. Modulating the gut microbiota through dietary interventions, prebiotics, probiotics, and change in lifestyle may help restore microbial balance and reduce oxidative stress in NAFLD.
PULSALYS SATT Lyon-Saint Etienne, Villeurbanne, France
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Graphical abstract
Abstract
Reactive oxygen species (ROS) are important signaling molecules that play key roles in the progression of inflammatory disorders. Owing to a mismatch of the antioxidant level to balance the overproduction of ROS, the induced chronic inflammation can lead to several type of diseases such as cancer, inflammatory bowel disease, atherosclerosis, diabetes or neurodegenerative disorders. Over the last years, nanomedicine has shown tremendous promise in ROS-regulating approaches. The development of advanced redox-active nanomaterials opened the range of possibilities to anti-inflammatory therapies, with the production of ROS-responsive nanosystems enabling targeted drug delivery or with the manufacture of ROS-scavenging nanomaterials reducing ROS excess levels. This review summarizes the latest developments and novel designs of ROS-based nanomedicines and discusses their therapeutical strategies and applications.
Search for other papers by Carlo Cervellati in
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Department of Animal Science, Plants for Human Health Institute, North Carolina State University, Kannapolis, North Carolina, USA
Department of Food and Nutrition, Kyung Hee University, Seoul, Korea
Search for other papers by Giuseppe Valacchi in
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Objective
Chronic obstructive pulmonary disease (COPD) is one of the main causes of morbidity and mortality in the United States. Oxidative stress due to cigarette smoking seems to be one of the major driving mechanisms in COPD pathogenesis. Since the scavenger receptor B1 (SR-B1) appears to play a key role in mediating the uptake for ɑ-tocopherol and other antioxidants in lung tissue, we aimed to investigate its role in COPD pathogenesis.
Methods
Lung tissue biopsies were obtained from 12 subjects; 6 of these had a diagnosis of COPD in a stable clinical state, the others 6 were current (n = 1) or ex-smokers (n = 5) with normal lung function (controls). 4-Hydroxynonenal (4-HNE)–SR-B1 adducts were detected by immunoprecipitation. ɑ-tocopherol concentration was determined by HPLC.
Results
SR-B1 levels were lower in COPD patients and these results parallel with lower levels of vitamin E in lung tissue found in COPD patients. This effect can be the consequence of oxidative posttranslational modifications, confirmed by the binding of the peroxidation product 4-HNE to SR-B1 possibly leading to its degradation.
Conclusions
The loss of SR-B1 may be involved in lung ɑ-tocopherol content decrease with the consequence of making lung tissue more susceptible to oxidative damage as suggested by the SR-B1–4-HNE adduct formation, and more prone to COPD development. Thus, our findings suggest a novel role of SR-B1 in pathomechanisms underlying COPD.
Significance statement
Chronic obstructive pulmonary disease (COPD) is one of the main causes of morbidity and mortality in the United States. Oxidative stress has been suggested to be the major driving mechanism in COPD pathogenesis. Loss of scavenger receptor BI (SR-B1) significantly decreases tocopherol lung content making lung tissue more susceptible to oxidative damage. The results of our study show that SR-B1 levels were lower in COPD patients and these results parallel with lower levels of vitamin E in lung tissue. Our findings suggest a novel role of SR- B1 in pathomechanisms underlying COPD.
Search for other papers by Ludovica Spagnuolo in
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Search for other papers by Greta Lattanzi in
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NBFC, National Biodiversity Future Center, Palermo, Italy
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Unità di Ricerca di Geriatria, Facoltà Dipartimentale di Medicina e Chirurgia. Università Campus Bio-Medico di Roma
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NBFC, National Biodiversity Future Center, Palermo, Italy
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Graphical abstract
Abstract
The use of phenolic compounds, derived by plants, has recently emerged as a promising approach to prolong the lifespan by modulating metabolic pathways involved in aging. Phenolic compounds possess a broad spectrum of biochemical and pharmacological effects beneficial to human health such as modulating cellular senescence processes by interacting with molecular targets that regulate aging-related pathways. Phenolic compounds represent the major phytochemicals in our diet and possess several biological activities such as antioxidant and anti-inflammatory effects; protection against aging-related diseases (cancer, diabetes and cardiovascular diseases) with potential therapeutic applications and this could suggest that these compounds could be used as anti-aging nutraceutical support. In this review, we have considered the possible effects of some phenolic compounds in different aging pathways, to provide an overview of recent knowledge on their anti-aging mechanism of action.
Search for other papers by Kota Saito in
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Search for other papers by Kazushi Morimoto in
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Search for other papers by Ken-ichi Yamada in
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Abstract
Objective
Nonalcoholic steatohepatitis is a chronic liver disease caused by the progression of hepatocellular death and inflammation from simple steatosis. However, the pathogenesis of this disease remains unclear. Lipid peroxidation is one of the most critical factors in the development of nonalcoholic steatohepatitis; however, oxidised lipids – the products of lipid peroxidation – are insufficiently analysed. Here, we comprehensively analysed oxidised lipids in the liver during nonalcoholic steatohepatitis development in a choline-deficient, l-amino acid-defined, high-fat diet-fed mouse model.
Methods
Liver from C57BL/6J mice, fed a standard diet or a choline-deficient l-amino acid-defined high-fat diet for 1, 3, or 6 weeks, were collected to evaluate fibrosis, steatosis, inflammation, liver injury, and oxidised lipid production and to observe the suppression of these parameters upon vitamin E administration. In addition, organellar localisation of lipid peroxidation was assessed using fluorescence imaging. Finally, a mitochondria-targeted antioxidant was administered to model mice to investigate the mechanism underlying lipid peroxidation.
Results
We found an accumulation of oxidised triglycerides in the early stages of nonalcoholic steatohepatitis. Furthermore, our data indicate that oxidised triglycerides are generated by lipid peroxidation in lipid droplets due to mitochondria-derived reactive oxygen species.
Conclusion
These results suggest the importance of lipid droplet peroxidation in the progression of nonalcoholic steatohepatitis and may contribute to the development of therapeutic methods for nonalcoholic steatohepatitis in the future.
Significance statement
We demonstrate the specific and early occurrence of lipid peroxidation in nonalcoholic steatohepatitis pathogenesis and propose a previously unknown mechanism of disease progression.
