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Schizophrenia Research May 2018Current diagnosis of schizophrenia relies exclusively on the potentially subjective interpretation of clinical symptoms and social functioning as more objective... (Review)
Review
Current diagnosis of schizophrenia relies exclusively on the potentially subjective interpretation of clinical symptoms and social functioning as more objective biological measurement and medical diagnostic tests are not presently available. The use of metabolomics in the discovery of disease biomarkers has grown in recent years. Metabolomic methods could aid in the discovery of diagnostic biomarkers of schizophrenia. This systematic review focuses on biofluid metabolites associated with schizophrenia. A systematic search of Web of Science and Ovid Medline databases was conducted and 63 studies investigating metabolite biomarkers of schizophrenia were included. A review of these studies revealed several potential metabolite signatures of schizophrenia including reduced levels of essential polyunsaturated fatty acids (EPUFAs), vitamin E and creatinine; and elevated levels of lipid peroxidation metabolites and glutamate. Further research is needed to validate these biomarkers and would benefit from large cohort studies and more homogeneous and well-defined subject groups.
Topics: Biomarkers; Databases, Bibliographic; Fatty Acids, Unsaturated; Humans; Lipid Peroxidation; Metabolomics; Schizophrenia; Vitamin E
PubMed: 28947341
DOI: 10.1016/j.schres.2017.09.021 -
Biomedicine & Pharmacotherapy =... Jan 2022Ferroptosis is a programmed iron-dependent cell death characterized by accumulation of lipid peroxides (LOOH) and redox disequilibrium. Ferroptosis shows unique...
Ferroptosis is a programmed iron-dependent cell death characterized by accumulation of lipid peroxides (LOOH) and redox disequilibrium. Ferroptosis shows unique characteristics in biology, chemistry, and gene levels, compared to other cell death forms. The metabolic disorder of intracellular LOOH catalyzed by iron causes the inactivity of GPX4, disrupts the redox balance, and triggers cell death. Metabolism of amino acid, iron, and lipid, including associated pathways, is considered as a specific hallmark of ferroptosis. Epidemiological studies and animal experiments have shown that ferroptosis plays an important character in the pathophysiology of cardiovascular disease such as atherosclerosis, myocardial infarction (MI), ischemia/reperfusion (I/R), heart failure (HF), cardiac hypertrophy, cardiomyopathy, and abdominal aortic aneurysm (AAA). This review systematically summarized the latest research progress on the mechanisms of ferroptosis. Then we report the contribution of ferroptosis in cardiovascular diseases. Finally, we discuss and analyze the therapeutic approaches targeting for ferroptosis associated with cardiovascular diseases.
Topics: Animals; Cardiovascular Diseases; Cell Death; Ferroptosis; Humans; Lipid Peroxides; Metabolic Diseases; Oxidation-Reduction
PubMed: 34800783
DOI: 10.1016/j.biopha.2021.112423 -
Oxidative Medicine and Cellular... 2015Because the function and mechanisms of sleep are partially clear, here we applied a meta-analysis to address the issue whether sleep function includes antioxidative... (Meta-Analysis)
Meta-Analysis Review
Because the function and mechanisms of sleep are partially clear, here we applied a meta-analysis to address the issue whether sleep function includes antioxidative properties in mice and rats. Given the expansion of the knowledge in the sleep field, it is indeed ambitious to describe all mammals, or other animals, in which sleep shows an antioxidant function. However, in this paper we reviewed the current understanding from basic studies in two species to drive the hypothesis that sleep is a dynamic-resting state with antioxidative properties. We performed a systematic review of articles cited in Medline, Scopus, and Web of Science until March 2015 using the following search terms: Sleep or sleep deprivation and oxidative stress, lipid peroxidation, glutathione, nitric oxide, catalase or superoxide dismutase. We found a total of 266 studies. After inclusion and exclusion criteria, 44 articles were included, which are presented and discussed in this study. The complex relationship between sleep duration and oxidative stress is discussed. Further studies should consider molecular and genetic approaches to determine whether disrupted sleep promotes oxidative stress.
Topics: Animals; Databases, Factual; Glutathione; Lipid Peroxidation; Models, Animal; Nitric Oxide; Oxidative Stress; Oxidoreductases; Reactive Oxygen Species; Sleep Deprivation
PubMed: 25945148
DOI: 10.1155/2015/234952 -
International Journal of Environmental... Feb 2022The purpose of this systematic review was to determine the effect of antioxidant consumption on markers of oxidative stress and muscle damage after performing a muscle... (Review)
Review
BACKGROUND
The purpose of this systematic review was to determine the effect of antioxidant consumption on markers of oxidative stress and muscle damage after performing a muscle strength exercise.
METHODS
The Preferred Reporting Items for Systematic Review and Meta-Analyses (PRISMA) statements were followed. Four databases were used: Scopus, PubMed, WOS and SportDiscus. Methodological quality was assessed using the PEDro scale.
RESULTS
A total of 1709 articles were retrieved and following duplicate removal and application of exclusion criteria seven articles were reviewed. Supplementation with pomegranate juice alleviates oxidative stress, taurine reduces muscle damage, melatonin protects the skeletal muscles, blueberries decrease oxidation and oats mitigate muscle damage.
CONCLUSIONS
Acute administration of antioxidants immediately before or during an exercise session can have beneficial effects, such as delay of fatigue and a reduction in the recovery period. Administration of antioxidant susbtances may reduce muscle damage and oxidative stress markers.
Topics: Antioxidants; Dietary Supplements; Exercise; Muscle Strength; Muscle, Skeletal; Oxidative Stress
PubMed: 35162826
DOI: 10.3390/ijerph19031803 -
Nutrients Nov 2020A number of previous investigations have been designed to determine the effect of acute caffeine intake on the rate of fat oxidation during exercise. However, these... (Meta-Analysis)
Meta-Analysis
A number of previous investigations have been designed to determine the effect of acute caffeine intake on the rate of fat oxidation during exercise. However, these investigations have shown contradictory results due to the differences in the exercise protocols used or the co-ingestion of caffeine with other substances. Hence, to date, there is no consensus about the effect of caffeine on fat oxidation during exercise. The purpose of this study was to conduct a systematic review followed by a meta-analysis to establish the effect of acute intake of caffeine (ranging from 2 to 7 mg/kg of body mass) on the rate of fat oxidation during exercise. A total of 19 studies published between 1978 and 2020 were included, all of which employed crossover experimental designs in which the ingestion of caffeine was compared to a placebo. Studies were selected if the exercise intensity was consistent in the caffeine and placebo trials and if these were preceded by a fasting protocol. A subsequent meta-analysis was performed using the random effects model to calculate the standardized mean difference (SMD). The meta-analysis revealed that caffeine significantly ( = 0.008) increased the fat oxidation rate (SMD = 0.73; 95% CI = 0.19 to 1.27). This increment was consistent with a significant ( = 0.04) reduction of the respiratory exchange ratio (SMD = -0.33; 95% CI = -0.65 to -0.01) and a significant ( = 0.049) increase in the oxygen uptake (SMD = 0.23; 95% CI = 0.01 to 0.44). The results also showed that there was a dose-response effect of caffeine on the fat oxidation rate, indicating that more than 3.0 mg/kg is necessary to obtain a statistically significant effect of this stimulant on fat oxidation during exercise. Additionally, the ability of caffeine to enhance fat oxidation during exercise was higher in sedentary or untrained individuals than in trained and recreational athletes. In conclusion, pre-exercise intake of a moderate dose of caffeine may effectively increase fat utilization during aerobic exercise of submaximal intensity performed after a fasting period. However, the fitness level of the participant may modulate the magnitude of the effect of caffeine on fat oxidation during exercise.
Topics: Adipose Tissue; Caffeine; Central Nervous System Stimulants; Exercise; Humans; Lipid Metabolism
PubMed: 33255240
DOI: 10.3390/nu12123603 -
Journal of the International Society of... Sep 2020L-carnitine (LC) is used as a supplement by recreationally-active, competitive and highly trained athletes. This systematic review aims to evaluate the effect of...
BACKGROUND
L-carnitine (LC) is used as a supplement by recreationally-active, competitive and highly trained athletes. This systematic review aims to evaluate the effect of prolonged LC supplementation on metabolism and metabolic modifications.
METHODS
A literature search was conducted in the MEDLINE (via PubMed) and Web of Science databases from the inception up February 2020. Eligibility criteria included studies on healthy human subjects, treated for at least 12 weeks with LC administered orally, with no drugs or any other multi-ingredient supplements co-ingestion.
RESULTS
The initial search retrieved 1024 articles, and a total of 11 studies were finally included after applying inclusion and exclusion criteria. All the selected studies were conducted with healthy human subjects, with supplemented dose ranging from 1 g to 4 g per day for either 12 or 24 weeks. LC supplementation, in combination with carbohydrates (CHO) effectively elevated total carnitine content in skeletal muscle. Twenty-four-weeks of LC supplementation did not affect muscle strength in healthy aged women, but significantly increased muscle mass, improved physical effort tolerance and cognitive function in centenarians. LC supplementation was also noted to induce an increase of fasting plasma trimethylamine-N-oxide (TMAO) levels, which was not associated with modification of determined inflammatory nor oxidative stress markers.
CONCLUSION
Prolonged LC supplementation in specific conditions may affect physical performance. On the other hand, LC supplementation elevates fasting plasma TMAO, compound supposed to be pro-atherogenic. Therefore, additional studies focusing on long-term supplementation and its longitudinal effect on the cardiovascular system are needed.
Topics: Age Factors; Body Composition; Carnitine; Cognition; Dietary Carbohydrates; Dietary Supplements; Energy Metabolism; Exercise; Exercise Tolerance; Humans; Lipid Metabolism; Methylamines; Muscle Proteins; Muscle Strength; Muscle, Skeletal; Obesity; Oxidation-Reduction; Physical Conditioning, Human; Sarcopenia
PubMed: 32958033
DOI: 10.1186/s12970-020-00377-2 -
Oncotarget Aug 2017Oxidative stress results from an imbalance of the reactive oxygen species/reactive nitrogen species (ROS/RNS) production and the oxidants defense system. Extensive... (Review)
Review
Oxidative stress results from an imbalance of the reactive oxygen species/reactive nitrogen species (ROS/RNS) production and the oxidants defense system. Extensive research during the last decades has revealed that oxidative stress can mediate cancer initiation and development by leading not only to molecular damage but also to a disruption of reduction-oxidation (redox) signaling. In order to provide a global overview of the redox signaling pathways, which play a role in cancer formation, we conducted a systematic literature search in PubMed and ISI Web of Science and identified 185 relevant reviews published in the last 10 years. The 20 most frequently described pathways were selected to be presented in this systematic review and could be categorized into 3 groups: Intracellular ROS/RNS generating organelles and enzymes, signal transduction cascades kinases/phosphatases and transcription factors. Intracellular ROS/RNS generation organelles are mitochondria, endoplasmic reticulum and peroxisomes. Enzymes, including NOX, COX, LOX and NOS, are the most prominent enzymes generating ROS/RNS. ROS/RNS act as redox messengers of transmembrane receptors and trigger the activation or inhibition of signal transduction kinases/phosphatases, such as the family members of protein tyrosine kinases and protein tyrosine phosphatases. Furthermore, these reactions activate downstream signaling pathways including protein kinase of the MAPK cascade, PI3K and PKC. The kinases and phosphatases regulate the phosphorylation status of transcription factors including APE1/Ref-1, HIF-1α, AP-1, Nrf2, NF-κB, p53, FOXO, STAT, and β-catenin. Finally, we briefly discuss cancer prevention and treatment opportunities, which address redox pathways and further research needs.
PubMed: 28881698
DOI: 10.18632/oncotarget.17128 -
Arab Journal of Urology 2019: To review and present the most distinct concepts on the association of reactive oxygen species (ROS) with male reproduction. : The Preferred Reporting Items for... (Review)
Review
: To review and present the most distinct concepts on the association of reactive oxygen species (ROS) with male reproduction. : The Preferred Reporting Items for Systematic Reviews and Meta Analyses (PRISMA) guidelines were used to search PubMed, Medline, EMBASE, and the Cochrane electronic databases for studies investigating the role of oxidative stress (OS) on sperm function. : The literature search yielded 1857 studies, of which 1791 articles were excluded because of irrelevance of data, non-English language, non-human nature or because they were case reports or commentaries. All included studies were reviews (46), meta-analyses (one), original research studies (18) and guideline articles (one). The studies were published between 1984 and 2018. Under normal physiological conditions, ROS are vital for sperm maturation, hyperactivation, capacitation, acrosome reaction, as well as fertilisation. However, a number of endogenous and exogenous causes may induce supra-physiological levels of ROS resulting in lipid peroxidation, sperm DNA fragmentation and apoptosis, and consequently infertility. Several laboratory testing methods can be used in infertile men to diagnose OS. Treatment usually involves antioxidant supplementation and, when possible, elimination of the causative factor. : OS is an important cause of male factor infertility. Its assessment provides essential information that can guide treatment strategies aimed at improving the male's reproductive potential. bp: base-pair; CAT: catalase; LPO: lipid peroxidation; MDA: malondialdehyde; MiOXSYS: Male Infertility Oxidative System; mtDNA: mitochondrial DNA; NAD(PH): nicotinamide adenine dinucleotide (phosphate); NO: nitric oxide; 8-OHdG: 8-hydroxy-2'-deoxyguanosine; ORP: oxidation-reduction potential; OS: oxidative stress; PKA: protein kinase A; PLA2: phospholipase A2; PRISMA: Preferred Reporting Items for Systematic Reviews and Meta-Analyses; PUFA: poly-unsaturated fatty acid; ROS: reactive oxygen species; SOD: superoxide dismutase; TAC: total antioxidant capacity; TBA: thiobarbituric acid.
PubMed: 31285919
DOI: 10.1080/2090598X.2019.1599624 -
International Journal of Environmental... May 2022Over the past two decades, scientists have attempted to evaluate whether the point of maximal fat oxidation (FAT) and the aerobic threshold (AerT) are connected. The... (Meta-Analysis)
Meta-Analysis Review
Over the past two decades, scientists have attempted to evaluate whether the point of maximal fat oxidation (FAT) and the aerobic threshold (AerT) are connected. The existence of such a relationship would allow a more tailored training approach for athletes while improving the efficacy of individualized exercise prescriptions when treating numerous health-related issues. However, studies have reported conflicting results, and this issue remains unresolved. This systematic review and meta-analysis aimed: (i) to examine the strength of the association between FAT and AerT by using the effect size (ES) of correlation coefficient (r) and standardized mean difference (SMD); (ii) to identify potential moderators and their influence on ES variability. This study was registered with PROSPERO (CRD42021239351) and ClinicalTrials (NCT03789045). PubMed and Google Scholar were searched and fourteen articles, consisting of overall 35 ES for and 26 ES for SMD were included. Obtained ESs were analyzed using a multilevel random-effects meta-analysis. Our results support the presence of a significant association between FAT and AerT exercise intensities. In conclusion, due to the large ES variance caused by clinical and methodological differences among the studies, we recommend that future studies follow strict standardization of data collection and analysis of FAT and AerT-related outcomes.
Topics: Athletes; Exercise; Exercise Test; Humans; Oxidation-Reduction
PubMed: 35682065
DOI: 10.3390/ijerph19116479 -
Cells Apr 2023Betel quid and areca nut are complex mixture carcinogens, but little is known about whether their derived single-agent arecoline or arecoline -oxide (ANO) is...
Betel quid and areca nut are complex mixture carcinogens, but little is known about whether their derived single-agent arecoline or arecoline -oxide (ANO) is carcinogenic, and the underlying mechanisms remain unclear. In this systematic review, we analyzed recent studies on the roles of arecoline and ANO in cancer and strategies to block carcinogenesis. In the oral cavity, flavin-containing monooxygenase 3 oxidizes arecoline to ANO, and both alkaloids conjugate with -acetylcysteine to form mercapturic acid compounds, which are excreted in urine, reducing arecoline and ANO toxicity. However, detoxification may not be complete. Arecoline and ANO upregulated protein expression in oral cancer tissue from areca nut users compared to expression levels in adjacent normal tissue, suggesting a causal relationship between these compounds and oral cancer. Sublingual fibrosis, hyperplasia, and oral leukoplakia were diagnosed in mice subjected to oral mucosal smearing of ANO. ANO is more cytotoxic and genotoxic than arecoline. During carcinogenesis and metastasis, these compounds increase the expression of epithelial-mesenchymal transition (EMT) inducers such as reactive oxygen species, transforming growth factor-β1, Notch receptor-1, and inflammatory cytokines, and they activate EMT-related proteins. Arecoline-induced epigenetic markers such as sirtuin-1 hypermethylation, low protein expression of miR-22, and miR-886-3-p accelerate oral cancer progression. Antioxidants and targeted inhibitors of the EMT inducers used reduce the risk of oral cancer development and progression. Our review findings substantiate the association of arecoline and ANO with oral cancer. Both of these single compounds are likely carcinogenic to humans, and their mechanisms and pathways of carcinogenesis are useful indicators for cancer therapy and prognosis.
Topics: Arecoline; Cyclic N-Oxides; Mouth Neoplasms; Carcinogenesis; Humans; Animals; Mice; Areca; Oxygenases; Oxidation-Reduction; Acetylcysteine; Epigenesis, Genetic; Carcinogens
PubMed: 37190117
DOI: 10.3390/cells12081208