Browse
You are looking at 11 - 20 of 50 items
Search for other papers by Tania Medali in
Google Scholar
PubMed
Search for other papers by Dominique Couchie in
Google Scholar
PubMed
Search for other papers by Nathalie Mougenot in
Google Scholar
PubMed
Search for other papers by Maria Mihoc in
Google Scholar
PubMed
Search for other papers by Olaf Bergmann in
Google Scholar
PubMed
Search for other papers by Wouter Derks in
Google Scholar
PubMed
Search for other papers by Celio X Santos in
Google Scholar
PubMed
Search for other papers by Bertrand Friguet in
Google Scholar
PubMed
Search for other papers by Mustapha Rouis in
Google Scholar
PubMed
Graphical abstract
Experimental Myocardial infarction (MI) using ligation procedure induces cardiac dysfunction, high level of ROS, inflammation, apoptosis, fibrosis and cardiomyocyte (CM) loss. AAV overexpressing human Trx-2, specifically in CM mitochondria improves mouse cardiac function, reduces the size of cardiac infarct, increases the expression of cardiac anti-inflammatory markers, reduces apoptosis and oxidative stress. However, it does not increase CM proliferation.
Abstract
Introduction and objective
Myocardial infarction (MI), which in general results from complications of atherosclerosis, is characterized by high inflammation and cardiomyocytes (CMs) apoptosis and by major loss of CMs. Regeneration of these lost CMs represents a major challenge for MI therapy. The increase of mitochondrial reactive oxygen species (ROS) is involved in cell cycle arrest which can be restarted by hypoxia or in the presence of ROS scavengers. Among ROS scavengers, mitochondrial thioredoxin 2 (Trx-2), an important antioxidant protein, could play a role in the CMs renewal.
Method
In this study, we investigated the effect of Trx-2 on mouse heart after an experimental MI.
Results
Trx-2 improves mouse cardiac function, reduces cardiac infarction size and increases the expression of cardiac anti-inflammatory markers. In addition, it reduces apoptosis and oxidative stress in heart tissue of mice after MI but it does not increase CM proliferation in cell culture or in heart tissue.
Conclusion
Mitochondrial Trx-2 effectively protects against heart infarction, likely via the reduction of oxidative stress, inflammation and apoptosis but not through CM renewal.
Significance statement
The current study unveils the complexities of MI and highlights mitochondrial Trx-2 role. Post-MI, marked by inflammation, CM apoptosis and significant CM loss. Trx-2 emerges as a vital protector. Its intervention improves mouse cardiac function, reduces infarction size and fosters an anti-inflammatory environment. By uncovering these mechanisms, the study suggests potential therapeutic strategies for oxidative stress, inflammation and apoptosis in MI, positioning Trx-2 as a promising candidate for future cardiac interventions.
Search for other papers by Cristina Russo in
Google Scholar
PubMed
Search for other papers by Maria Stella Valle in
Google Scholar
PubMed
Search for other papers by Lucia Malaguarnera in
Google Scholar
PubMed
Graphical abstract
Abstract
Pathological conditions characterized by systemic inflammation and oxidative stress can often impair the muscle cells efficiency. The gradual decline of muscle mass and tone drastically reduces the motor skills of the patient affecting the simplest daily activities. Muscle dysfunction, resulting in the deterioration of muscle tissue, can lead to a serious situation of muscle wasting that can evolve into sarcopenia. In addition, muscle dysfunction causing metabolic disorders impairs the quality of life. The function of skeletal muscle is deeply conditioned by environmental, nutritional, physical, and genetic factors. Proper nutrition with balanced protein and vitamins intake and an active lifestyle helps to strengthen tissues and counteract pathological conditions and generalized weakness. Vitamin D performs antioxidant actions, indispensable in skeletal muscle. Epidemiological data indicate that vitamin D deficiency is a widespread status in the world. Vitamin D deficiency induces mitochondrial failure, reduced production of adenosine triphosphate, oxidative injury, and compromised muscle function. Among the different types of antioxidants, vitamin D has been identified as the main compound that can improve the effectiveness of the treatment for muscle weakness and improve conditions related to sarcopenia. The purpose of this review is to analyze molecular processes used by vitamin D against oxidative stress and how it can affect muscle function in order to assess whether its use as a supplement in inflammatory pathologies and oxidative stress can be useful to prevent deterioration and improve/maintain muscle function.
Food4Future (F4F), c/o Leibniz Institute of Vegetable and Ornamental Crops (IGZ), Grossbeeren, Germany
NutriAct Competence Cluster Nutrition Research Berlin-Potsdam, Nuthetal, Germany
Search for other papers by Daniela Weber in
Google Scholar
PubMed
Food4Future (F4F), c/o Leibniz Institute of Vegetable and Ornamental Crops (IGZ), Grossbeeren, Germany
NutriAct Competence Cluster Nutrition Research Berlin-Potsdam, Nuthetal, Germany
Institute of Nutritional Science, University of Potsdam, Potsdam, Germany
Department of Physiological Chemistry, Faculty of Chemistry, University of Vienna, Vienna, Austria
Search for other papers by Tilman Grune in
Google Scholar
PubMed
The aim of this review is to provide a comprehensive and simple graphical overview on carotenoids. The review describes in four detailed figures the course of carotenoids from food to skin. Differences in chemical structures of the six most prominent carotenoids, namely, α-carotene, β-carotene, lutein, zeaxanthin, lycopene and β-cryptoxanthin, and their seasonal variations in plasma concentrations resulting from different availability of fruits and vegetables are highlighted. Furthermore, factors affecting carotenoid status, sites of storage and how and where they can be assessed (dietary intake and in vivo) are discussed. The route of carotenoid transport after ingestion, transport across the enterocyte and receptors involved in carotenoid uptake in peripheral cells are shown followed by the routes of carotenoid delivery to the skin and reasons for variations in skin carotenoid status are visualized.
Search for other papers by Maret G Traber in
Google Scholar
PubMed
This is a narrative review of the evidence of α-tocopherol importance in human health, especially with regards to its vitamin role. α-Tocopherol is a potent peroxyl radical scavenger, and this role is prominent in its efficacy in maintaining the metabolic health of tissues. Vitamin E deficiency is discussed as a tool to understand the impact of α-tocopherol’s absence promoting increased lipid peroxidation and polyunsaturated fatty acid depletion. Downstream deficiency consequences include impacts on choline and one-carbon metabolism, glucose and energy metabolism, and their interactions with critical thiols, such as glutathione. Importantly, human vitamin E deficiency, caused by genetic defects in the α-tocopherol transfer protein (α-TTP), provides important clues for the necessity of α-tocopherol for the peripheral nervous system. Moreover, α-TTP expression in the liver, brain, eyes, and placenta illustrates that these tissues are especially vulnerable and require this specific α-tocopherol delivery mechanism for their protection. Although clinical trial evidence is limited and equivocal about the health benefits of vitamin E supplements, there is epidemiologic evidence of the long-term benefits of increased α-tocopherol intakes in ’healthy’ diets (high in vegetables and fruits, fish, nuts, and seeds, as well as fiber).
Significance statement
The elaborate regulation of α-tocopherol concentrations by the human body suggests that the consistent consumption of the recommended amounts of dietary α-tocopherol (15 mg) over a lifetime are protective of the at-risk tissues, as well as providing protection from chronic diseases.
Search for other papers by Noemi Iaia in
Google Scholar
PubMed
Search for other papers by Federico Canzoneri in
Google Scholar
PubMed
Search for other papers by Ginevra Rosso in
Google Scholar
PubMed
Search for other papers by Roberto Menta in
Google Scholar
PubMed
Search for other papers by Fiorella Biasi in
Google Scholar
PubMed
Background
In both Western and Westernized diets, together with a relatively high amount of cholesterol, variable amountsof its oxidized metabolites, oxysterols, are consistently consumed. These oxysterols, mostly of non-enzymatic origin, are produced during sterol autoxidation in foodstuff manufacturing and storage.
Objective
This study aimed to analyze the potential enterotoxic effects of all main oxysterols of non-enzymatic origin so far identified in a variety of foods.
Experimental plan
Differentiated human intestinal cell monolayers (CaCo-2) were incubated up to 48 h in the presence or absence of 0.5, 1 or 5 µM with one out of seven non-enzymatic oxysterols, prior to the verification of minimal irreversible cell damage within the chosen concentration range.
Results
All tested oxysterols were proven to exert damaging effects on cell monolayers in vitro. The inflammatory interleukin-8 and monocyte chemotactic protein-1 were mostly upregulated by 7-ketocholesterol and 7β-hydroxycholesterol, respectively, then to a lower extent by 5α,6α-epoxycholesterol, 7α-hydroxycholesterol and 5β,6β-epoxycholesterol. 7-Ketocholesterol and 7β-hydroxycholesterol also appeared to be most effective in impairing claudin-1, occludin and E-cadherin proteins, followed by 25-hydroxycholesterol and triol.
Conclusions
The oxysterols consistently derived by food autoxidation were tested; they potentially impaired the integrity of the intestinal epithelial barrier and triggered an inflammatory response within 0.5–5 µM concentrations, easily reachable in a single Western meal.
Significance Statement
This comprehensive analysis focused on the potential impairment of the intestinal barrier by the main dietary non-enzymatic oxysterols, should guide further nutrition research aiming at defining a threshold amount of these cholesterol derivatives in order not to derange the physiological gut–brain axis.
Search for other papers by Giulia Elda Valenti in
Google Scholar
PubMed
Search for other papers by Bruno Tasso in
Google Scholar
PubMed
Search for other papers by Nicola Traverso in
Google Scholar
PubMed
Search for other papers by Cinzia Domenicotti in
Google Scholar
PubMed
Search for other papers by Barbara Marengo in
Google Scholar
PubMed
Glutathione (GSH) is one of the most important components of the cellular antioxidant system, and it is able to exert several pleiotropic functions influencing cell growth, proliferation, adaptation and death. It has been demonstrated that changes in GSH levels underlie the pathogenesis of many human diseases, including cancer. In detail, although on one hand GSH homeostasis plays a protective role from the onset of cancer, on the other, it is involved in cancer progression and in therapy resistance. In this review, after a brief report on the physiological role of GSH, we have focused the attention on its role in cancer and refractoriness to anticancer therapy giving an update on the preclinical and clinical studies relied on the compounds targeting GSH system. Based on these considerations, a deeper knowledge of GSH-dependent network can be crucial to identify new strategies for preventing and/or curing cancer.
Anatomy unit, Nursing Science Department, Elizade University, Ilara-Mokin, Ondo State, Nigeria
Search for other papers by O A Adedotun in
Google Scholar
PubMed
Search for other papers by C C Chukwunenye in
Google Scholar
PubMed
Search for other papers by A F Balogun in
Google Scholar
PubMed
Search for other papers by M A Olawale in
Google Scholar
PubMed
Search for other papers by J O Babatunde in
Google Scholar
PubMed
Search for other papers by B Ogunlade in
Google Scholar
PubMed
Graphical Abstract
Abstract
Background
This study aims to study the histomorphological response of d-ribose-l-cysteine (DRLC) to ketamine-induced testicular damage in adult male Wistar rats.
Methods
A total of 20 adult male Wistar rats were used for this experiment. The animals were randomly divided into four groups (A–D) (n = 5). Group A served as the control, receiving distilled water as placebo; animals in group B were administered with 50 mg/kg body weight (bw) of ketamine only; animals in group C were administered with 50 mg/kg bw of ketamine and 30 mg/kg bw of DRLC; animals in group D were administered with 30 mg/kg bw of DRLC only. At the end of the experiment, blood was taken from the heart via cardiac puncture and stored, semen was collected from the caudal epididymis for immediate sperm analysis, while the testes were excised and preserved for histological examination and biochemical analysis.
Results
The results showed abnormalities marked by a significant decrease in the weights, sperm parameters, as well as antioxidants, serum hormonal levels and abnormal testicular microarchitecture in the rats as a result of ketamine treatment. However, DRLC exhibits significant quenching effects and attenuating activities on the ketamine-induced abnormalities by increasing the rats' weights, restoring the sperm parameters, as well as increasing the antioxidants and serum hormonal levels with restored testicular histoarchitecture.
Conclusion
DRLC in the current study attenuated the toxic effects of ketamine on the testes; therefore, it could be used as adjuvant therapy for reproductive toxicant-induced testicular toxicity due to its potent antioxidant property.
Significance statement
The testis is a vital secreting organ that produces and stores spermatozoa and is crucial for producing male sexual hormones and is thus the main target of infertility when overdoses of chemicals and toxins are introduced to it. In view of the facts above, studies of the potential of chemicals like ketamine to induce testicular toxicity are important as well as the methods aimed at mitigating this effect. Various studies have been conducted on the effectiveness of DRLC in subsiding different chronic health conditions, but there is no published literature on the effects of DRLC in ketamine-induced testicular toxicity in adult male Wistar rats. Hence we present this study.
Search for other papers by Elisabetta Murru in
Google Scholar
PubMed
Search for other papers by Gianfranca Carta in
Google Scholar
PubMed
Search for other papers by Claudia Manca in
Google Scholar
PubMed
Search for other papers by Alessia Leone in
Google Scholar
PubMed
Search for other papers by Chiara Murru in
Google Scholar
PubMed
Search for other papers by Michele Ruggiu in
Google Scholar
PubMed
Search for other papers by Roberto Solinas in
Google Scholar
PubMed
Search for other papers by Roberta Montisci in
Google Scholar
PubMed
Search for other papers by Filippo Tocco in
Google Scholar
PubMed
Search for other papers by Sebastiano Banni in
Google Scholar
PubMed
Objective
This study aimed to assess the relationship between dietary palmitic acid (PA) intake and its association with body fat deposition and metabolic flexibility (MF) in middle-aged healthy individuals.
Methods
Fifteen healthy participants (n = 15; 6 males, 9 females) with a mean age of 54 were enlisted. They were subjected to graded exercise tests using a cycle ergometer coupled with a calorimeter. Respiratory gas exchange was evaluated to determine two MF parameters. First, the MF index was derived by multiplying peak fatty acid oxidation (PFO) per kg of fat-free mass (FFM) with the percentage of VO2max at PFO. The second parameter, peak energy substrates’ oxidation (aka PESO), was computed by aggregating the kilocalories from PFO and peak carbohydrate oxidation, normalized per kg FFM. Dietary intake was gauged using a 7-day dietary record. Spearman’s regression was employed to analyze the association between dietary intake of specific fat classes, PA, MF parameters, and body fat percentage.
Results
Preliminary results demonstrate that dietary saturated fatty acids (SFA) within physiological limits correlate with enhanced substrate oxidation capacity. This suggests augmented MF in middle-aged subjects. Among dietary SFA, PA was identified as the primary factor in this favorable correlation.
Conclusions
Our initial observations, even though preliminary, strongly suggest a beneficial association between PA intake, MF, and body fat percentage. This underscores the potential nutritional importance of PA in promoting MF.
Significance Statement
Disparities in data regarding the health effects of dietary fats may arise from the distinct roles various dietary fatty acids play in MF.
Search for other papers by Teresa Vezza in
Google Scholar
PubMed
Department of Physiology, University of Valencia, INCLIVA, Valencia, Spain
Search for other papers by Clara Luna-Marco in
Google Scholar
PubMed
Department of Physiology, University of Valencia, INCLIVA, Valencia, Spain
Search for other papers by Susana Rovira-Llopis in
Google Scholar
PubMed
Department of Physiology, University of Valencia, INCLIVA, Valencia, Spain
CIBERehd, University of Valencia, Valencia, Spain
Search for other papers by Víctor M Víctor in
Google Scholar
PubMed
Type 2 diabetes (T2D) is a long-term metabolic disease characterized by progressive β-cell functional decline and insulin resistance, which increases the risk of cardiovascular complications as well as associated-morbidity and mortality. Evidence suggests a strong relationship between hyperglycaemia, oxidative stress and the development and progression of T2D. Indeed, a hyperglycaemic state can reduce the activity of antioxidant enzymes and increase lipid peroxidation and protein oxidation products, as well as DNA damage. At present, metformin is the recommended first-line glucose-lowering agent in patients with T2D. Despite the vast clinical experience gained over several decades of use, several mechanisms of action of metformin have yet to be fully elucidated. This review provides an overview of the existing literature concerning the complicated interplay between oxidative stress and T2D and the molecular mechanisms underlying the redox-related mechanisms of action of metformin, which include (but are not limited to) interaction with AMP-activated protein kinase (AMPK)-dependent and AMPK-independent mechanisms, inhibition of gluconeogenesis and action on leukocyte–endothelium interactions.
