ABSTRACT
Abstract Hibernation is a natural condition of animals that lives in the temperate zone, although some tropical lizards also experience hibernation annually, such as the lizard native from South America, Salvator merianae, or "tegu" lizard. Even though physiological and metabolic characteristic associated with hibernation have been extensively studied, possible alterations in the red blood cells (RBC) integrity during this period remains unclear. Dehydration and fasting are natural consequences of hibernating for several months and it could be related to some cellular modifications. In this study, we investigated if the osmotic tolerance of RBCs of tegu lizard under hibernation is different from the cells obtained from animals while normal activity. Additionally, we indirectly investigated if the RBCs membrane of hibernating tegus could be associated with oxidation by quantifying oxidized biomolecules and the activity of antioxidant enzymes. Our findings suggest that RBCs are more fragile during the hibernation period, although we did not find evidence of an oxidative stress scenario associated with the accentuated fragility. Even though we did not exclude the possibility of oxidative damage during hibernation, we suggested that an increased RBCs volume as a consequence of hypoosmotic blood during hibernation could also affect RBCs integrity as noted.
Resumo A hibernação é uma condição natural dos animais que vivem na zona temperada, embora alguns lagartos tropicais também experenciem hibernação anualmente, como é o caso do lagarto nativo da América do Sul, Salvator merianae ou "teiú". Embora as características fisiológicas e metabólicas associadas à hibernação tenham sido amplamente estudadas, possíveis alterações na integridade das hemácias durante esse período ainda permanecem obscuras. A desidratação e o jejum são consequências naturais da hibernação por vários meses e podem estar relacionadas a algumas modificações celulares. Neste estudo, investigamos se a tolerância osmótica de hemácias do lagarto teiú sob hibernação são diferentes das células obtidas de animais em atividade normal. Além disso, investigamos indiretamente por meio da quantificação de biomoléculas oxidadas e da atividade de enzimas antioxidantes se a membrana das hemácias dos teiús em hibernação poderia estar associada à oxidação. Nossos resultados sugerem que as hemácias possuem maior fragilidade durante o período de hibernação, embora não tenhamos encontrado evidências de um cenário de estresse oxidativo associado à essa fragilidade acentuada. Embora não tenhamos excluído a possibilidade de dano oxidativo durante a hibernação, sugerimos que um aumento no volume das hemácias como consequência de sangue hipoosmótico durante a hibernação também poderia afetar a integridade de hemácias, tal como foi observado.
Subject(s)
Animals , Hibernation , Lizards , Oxidation-Reduction , Oxidative Stress , ErythrocytesABSTRACT
This study expounded the great impacts of excess energy intake and oxidative inflammation on national health in China and put forward the pathological mirror-image hypothesis of the relationship between obesity and oxidative inflammation. On this basis, an ideological framework was constructed to deal with oxidative stress and oxidative inflammation centered on the development of natural antioxidant products. The study contained the following four parts: the ways to improve national health in China; the promotion of cognition to oxidative inflammation to improve national health in China; prospects for the prevention and treatment of oxidative inflammation in China; the reason why Northwest Yunnan is a good place to develop high-quality natural antioxidants.
Subject(s)
China , Energy Intake , Humans , Inflammation , Oxidation-Reduction , Oxidative StressABSTRACT
Numerosos reportes demuestran la presencia de biomarcadores de estreÌs oxidativo en la saliva de fumadores y hay un creciente intereÌs en correlacionar estos procesos moleculares con la etiología de algunas enfermedades orales, como la periodontitis, una enfermedad inmunoinflamatoria croÌnica relacionada con un desequilibrio de la homeostasis redox celular. Objetivo: realizar una revisioÌn narrativa sobre la relacioÌn entre la disminucioÌn de la capacidad antioxidante salival inducida por humo de tabaco, la periodontitis y el potencial uso de farmacología redox para el tratamiento de esta patología. Métodos: se realizoÌ una buÌsqueda bibliograÌfica en bases de datos como PUBMED (NLM, NIH, NCBI) y SciELO. Resultados: existe evidencia que relaciona la baja capacidad antioxidante salival con un retraso en el restablecimiento de las condiciones normales en la cavidad oral ante el desarrollo de periodontitis. A su vez, el estado inflamatorio asociado colabora sineÌrgicamente, provocando un mayor danÌo tisular con peÌrdida de tejidos de soporte dentario, fenoÌmeno que podría ser modulado por la accioÌn de farmacología redox. Conclusiones: la intervencioÌn con farmacología redox, podría atenuar los biomarcadores de progresioÌn de la enfermedad periodontal, constituyendo una herramienta prometedora para utilizar en conjunto con las estrategias de tratamiento tradicionales.
Numerous reports demonstrate the presence of oxidative stress biomarkers in the saliva of smokers and there is a growing interest in correlating these molecular processes with the etiology of some oral diseases, such as periodontitis, a chronic immunoinlammatory disease related to an imbalance of cellular redox homeostasis. Aims: achieve a narrative review on the relationship between the decrease in salivary antioxidant capacity induced by tobacco smoke, periodontitis, and the potential use of redox pharmacology for the treatment of this pathology. Methods: a bibliographic search was carried out in databases such as PUBMED (NLM, NIH, NCBI) and SciELO. Results: there is evidence that relates the low salivary antioxidant capacity with a delay in the reestablishment of normal conditions in the oral cavity before the development of periodontitis. In turn, the associated inflammatory state collaborates synergistically, causing greater tissue damage with loss of dental support tissues, a phenomenon that could be modulated by the action of redox pharmacology. Conclusions: intervention with redox pharmacology could attenuate the biomarkers of periodontal disease progression, constituting a promising tool to be used in conjunction with traditional treatment strategies.
Muitos artigos demonstram a presença de biomarcadores de estresse oxidativo na saliva de fumantes e haÌ um interesse crescente em correlacionar esses processos moleculares com a etiologia de algumas doenças bucais, como a periodontite, uma doença imunoinlamatoÌria croÌnica relacionada a um desequiliÌbrio da redox celular homeostase. Objetivo: realizar uma revisaÌo narrativa sobre a relaçaÌ o entre a diminuiçaÌ o da capacidade antioxidante salivar induzida pela fumaça do tabaco, periodontite e o uso potencial da farmacologia redox para o tratamento desta patologia. Métodos: uma pesquisa bibliográica foi realizada usando bases de dados como PUBMED (NLM, NIH, NCBI) e SciELO. Resultados: haÌ evideÌncias que relacionam a baixa capacidade antioxidante salivar com o retardo no restabelecimento das condiçoÌes normais da cavidade oral antes do desenvolvimento da periodontite. Por sua vez, o estado inflamatório associado colabora sinergicamente, causando maior dano tecidual com perda de tecidos de suporte dentário, fenoÌmeno que poderia ser modulado pela açaÌ o da farmacologia redox. Conclusões: a intervençaÌ o com a farmacologia redox poderia atenuar os biomarcadores de progressaÌ o da doença periodontal, constituindo-se em uma ferramenta promissora para ser utilizada em conjunto com estrateÌgias tradicionais de tratamento.
Subject(s)
Humans , Periodontitis/etiology , Periodontitis/drug therapy , Saliva/metabolism , Oxidative Stress , Tobacco Smoking/adverse effects , Antioxidants/therapeutic use , Oxidation-Reduction , Biomarkers , Oxidative Stress/drug effects , HomeostasisABSTRACT
Most bacterial cell surface glycans are structurally unique, and have been considered as ideal target molecules for the developments of detection and diagnosis techniques, as well as vaccines. Chemical synthesis has been a promising approach to prepare well-defined oligosaccharides, facilitating the structure-activity relationship exploration and biomedical applications of bacterial glycans. L-Galactosaminuronic acid is a rare sugar that has been only found in cell surface glycans of gram-negative bacteria. Here, an orthogonally protected L-galactosaminuronic acid building block was designed and chemically synthesized. A synthetic strategy based on glycal addition and TEMPO/BAIB-mediated C6 oxidation served well for the transformation of commercial L-galactose to the corresponding L-galactosaminuronic acid. Notably, the C6 oxidation of the allyl glycoside was more efficient than that of the selenoglycoside. In addition, a balance between the formation of allyl glycoside and the recovery of selenoglycoside was essential to improve efficiency of the NIS/TfOH-catalyzed allylation. This synthetically useful L-galactosaminuronic acid building block will provide a basis for the syntheses of complex bacterial glycans.
Subject(s)
Carbohydrates , Glycosides , Oligosaccharides , Oxidation-Reduction , Polysaccharides/chemistryABSTRACT
OBJECTIVE@#To explore the expression of microRNA-132 (miR-132) and its potential role in the development of atherosclerosis (AS).@*METHODS@#Thirty AS samples and 30 samples of normal peripheral vessels were collected from atherosclerotic patients undergoing peripheral angiostomy in our hospital for detecting the expression level of miR-132 using RT-qPCR. The expression of miR-132 in human umbilical vein endothelial cells (HUVEC) was up-regulated by liposome transfection, and intracellular reactive oxygen species (ROS), localization relationship between ROS and mitochondria, functional changes of mitochondrial reactive oxygen superoxide species (mtROS), mitochondrial membrane potential (MMP) and opening of mitochondrial permeability transition pore (mPTP) were analyzed by flow cytometry and laser confocal microscopy. The activity of mitochondrial redox respiratory chain complex (type I, II, III, IV and V) in HUVECs was detected using ELISA, and the expression levels of key iron death proteins were detected with Western blotting.@*RESULTS@#RT-qPCR results showed that miR-132 was significantly up-regulated in atherosclerotic plaques compared with normal vascular samples (P < 0.001). Compared with control HUVECs, HUVECs overexpressing miR-132 showed a significantly increased level of intracellular ROS (P < 0.001), and most of ROS was colocalized with mitochondria. HUVECs overexpressing miR-132 also showed significantly decreased MMP (P < 0.001) and obviously increased mtROS (P < 0.001) and opening of mPTP (P < 0.001), which led to mitochondrial REDOX respiratory chain stress disorder. The key iron death protein GPX4 was significantly down-regulated and the oxidized protein NOX4 was significantly increased in miR-132-overexpressing HUVECs (P < 0.001).@*CONCLUSION@#MiR-132 promotes atherosclerosis by inducing mitochondrial oxidative stress-mediated ferroptosis, which may serve as a promising therapeutic target for AS.
Subject(s)
Apoptosis , Atherosclerosis/genetics , Ferroptosis , Human Umbilical Vein Endothelial Cells/metabolism , Humans , Membrane Potential, Mitochondrial , MicroRNAs/metabolism , Mitochondria/metabolism , Oxidation-Reduction , Oxidative Stress , Reactive Oxygen Species/metabolismABSTRACT
Anaerobic ammonia oxidation (ANAMMOX) process is an efficient and low-cost biological nitrogen removal process. However, it still faces some challenges in mainstream applications due to the limitation of substrate types and nitrate accumulation. In recent years, the combined process of anammox has been widely studied to solve the above problems. In this paper, the combined processes of anammox developed in recent years are reviewed, and discussed from the process principle, advantages and disadvantages, influencing factors, process extensibility and the key bottlenecks existing in the promotion and application, as well as the relevant work of the subject group. Finally, we take an outlook on the development of the combined anaerobic ammonia oxidation process in municipal domestic wastewater treatment.
Subject(s)
Ammonium Compounds , Anaerobiosis , Bioreactors , Denitrification , Nitrogen , Oxidation-Reduction , Sewage , WastewaterABSTRACT
Aerobic methane oxidizing bacteria (methanotrophs) can use methane as carbon source and energy source, eliminating 10%-20% of global methane. Methanotrophs can also effectively synthesize valuable methane-derived products. This article introduced the methane oxidizing mechanism of methanotrophs, and summarized the practical application and research hotspots of methanotrophs in the field of methane emission reduction in the landfill, ventilation air methane mitigation in coal mines, valuable chemicals biosynthesis, as well as oil and gas reservoir exploration. Main factors influencing the pollutant removal and the biosynthesis efficiency in various applications were also discussed. Based on the study of large-scale cultivation of methanotrophs, some measures to benefit the application and promotion of aerobic methane oxidizing biotechnology were proposed. This includes investigating the effect of intermediate metabolites on methanotrophs activity and population structure, and exploiting economical and efficient alternative culture media and culture techniques.
Subject(s)
Biotechnology , Carbon , Culture Media/chemistry , Methane/metabolism , Methylococcaceae/metabolism , Oxidation-ReductionABSTRACT
Manganese is an element essential for living organisms. Development of industrial technologies and exploitation of mineral resources have led to the release of large amount of Mn(Ⅱ) into the environment, posing a serious threat to human health. Bioremediation can remove the Mn(Ⅱ) from the environment rapidly and effectively without generating secondary pollution, thus received increasing attention. This review summarized the diversity and distribution of Mn(Ⅱ) removal microorganisms and the associated mechanisms, followed by discussing the effect of environmental factors on microbial Mn(Ⅱ) removal. Finally, the challenges and prospects for bioremediation of Mn(Ⅱ) polluted wastewater were proposed.
Subject(s)
Biodegradation, Environmental , Humans , Manganese , Oxidation-Reduction , WastewaterABSTRACT
Objective@#To develop effective alternatives to natural enzymes, it is crucial to develop nanozymes that are economical, resource efficient, and environmentally conscious. Carbon nanomaterials that have enzyme-like activities have been extensively developed as substitutes for traditional enzymes.@*Methods@#Carbide-derived carbons (CDCs) were directly synthesized via a one-step electrochemical method from a MAX precursor using an ammonium bifluoride electrolyte at ambient conditions. The CDCs were characterized by systematic techniques.@*Results@#CDCs showed bienzyme-like activities similar to that of peroxidase and superoxide dismutase. We systematically studied the dependence of CDC enzyme-like activity on different electrolytes and electrolysis times to confirm activity dependence on CDC content. Additionally, the synthesis mechanism and CDC applicability were elaborated and demonstrated, respectively.@*Conclusion@#The demonstrated synthesis strategy eliminates tedious intercalation and delamination centrifugation steps and avoids using high concentrations of HF, high temperatures, and halogen gases. This study paves the way for designing two-dimensional material-based nanocatalysts for nanoenzyme and other applications.
Subject(s)
Ammonium Compounds/chemical synthesis , Carbon/chemistry , Electrochemical Techniques , Enzymes , Fluorides/chemical synthesis , Humans , Nanostructures , Oxidation-ReductionABSTRACT
ABSTRACT Background: In Philadelphia chromosome-negative myeloproliferative neoplasm (MPN) models, reactive oxygen species (ROS) are elevated and have been implicated in genomic instability, JAK2/STAT signaling amplification, and disease progression. Although the potential effects of ROS on the MPN phenotype, the effects of ruxolitinib treatment on ROS regulation have been poorly explored. Herein, we have reported the impact of ruxolitinib on redox signaling transcriptional network, and the effects of diphenyleneiodonium (DPI), a pan NOX inhibitor, in JAK2V617F-driven cellular models. Method: Redox signaling-related genes were investigated in SET2 cells upon ruxolitinib treatment by RNA-seq (GEO accession GSE69827). SET2 and HEL cells, which represent JAK2V617F-positive MPN cellular models with distinct sensitivity to apoptosis induced by ruxolitinib, were used. Cell viability was evaluated by MTT, apoptosis by annexin V/PI and flow cytometry, and cell signaling by quantitative PCR and Western blot. Main results: Ruxolitinib impacted on a network composed of redox signaling-related genes, and DUOX1 and DUOX2 were identified as potential modulators of ruxolitinib response. In SET2 and HEL cells, DPI reduced cell viability and, at low doses, it significantly potentiated ruxolitinib-induced apoptosis. In the molecular scenario, DPI inhibited STAT3, STAT5 and S6 ribosomal protein phosphorylation and induced PARP1 cleavage in JAK2V617F-positive cells. DPI combined with ruxolitinib increased PARP1 cleavage in SET2 cells and potentiated ruxolitinib-reduced STAT3, STAT5 and S6 ribosomal protein in HEL cells. Conclusion: Our study reveals a potential adaptation mechanism for resistance against ruxolitinib by transcriptionally reprogramming redox signaling in JAK2V617F cells and exposes redox vulnerabilities with therapeutic value in MPN cellular models.
Subject(s)
Janus Kinase 2 , Myelodysplastic-Myeloproliferative Diseases/drug therapy , Oxidation-Reduction , NADPH Oxidases , Dual Oxidases , Myeloproliferative DisordersABSTRACT
La catarata comprende la opacidad del cristalino, la cual puede afectar la corteza y el núcleo subcapsular anterior y posterior de manera progresiva, secundario a la acumulación de proteínas dañadas a este nivel, con pérdida del equilibrio entre la producción y la eliminación de las especies reactivas libres de oxígeno. La importancia de retrasar o identificar marcadores específicos, además de promover un nuevo blanco terapéutico, también es motivo de análisis y de estudio en diferentes líneas de investigación. Se realizó una revisión de la literatura del 01 de enero al 20 de julio del año 2020. Se utilizaron metabuscadores en inglés y español de PUBMED, INFOMED, CLINICALKEY, LILACS, EBSCO, SCIELO, PRISMA y UPTODATE, con el objetivo de identificar la nueva evidencia científica relacionada con el estrés oxidativo y su participación en la formación de la catarata. La barrera del cristalino funciona como un medio de intercambio entre diferentes moléculas, lo que impide el paso de antioxidantes al núcleo y provoca su opacificación. Las mitocondrias a nivel de la corteza del cristalino permiten la remoción de oxígeno. Posteriormente la fosforilación oxidativa forma radicales libres de superóxido que, de manera natural, con el paso del tiempo se acumulan a este nivel. Con la edad, la homeostasis adaptativa pierde la capacidad de responder ante los cambios de estrés oxidativo, por lo que el uso de antioxidantes -de manera profiláctica e intencionada- puede cambiar el destino último para esta patología. La falta de equilibrio en los procesos de óxido-reducción es responsable de la formación de la catarata(AU)
Cataract comprises opacification of the crystalline lens, which may progressively affect the cortex and the anterior subcapsular nucleus, secondary to accumulation of damaged proteins on this level, with loss of balance between production and elimination of free reactive oxygen species. The importance of delaying or identifying specific markers, as well as promoting a new therapeutic target, is the object of study and analysis of a variety of research lines. A review was conducted of the literature published from 1 January to 20 July 2020. Use was made of PubMed, Infomed, Clinical Key, Lilacs, EBSCO, SciELO, Prisma and UpToDate metasearch engines in English and Spanish to identify new scientific evidence about oxidative stress and its involvement in cataract formation. The crystalline lens barrier serves as a medium for exchange between various molecules, preventing entrance of antioxidants into the nucleus, which results in opacification. Mitochondria on the crystalline lens cortex allow oxygen removal. Oxidative phosphorylation then forms free superoxide radicals which naturally accumulate on this level with the passing of time. With aging, adaptive homeostasis loses its ability to respond to oxidative stress changes, but the prophylactic, targeted use of antioxidants may change the ultimate fate of this condition. Lack of balance in oxidation-reduction processes is the cause of cataract formation(AU)
Subject(s)
Humans , Oxidation-Reduction , Cataract/etiology , Reactive Oxygen Species , Homeostasis , Lens Cortex, Crystalline , Review Literature as TopicABSTRACT
ABSTRACT Purpose: Understanding the effects of high oxidation reduction potential (ORP) levels on sperm parameters will help to identify patients with unexplained and male factor infertility who may have seminal oxidative stress and determine if ORP testing is needed. This study aimed to evaluate the association between seminal ORP and conventional sperm parameters. Materials and Methods: A total of 58 patients who provided a semen sample for simultaneous evaluation of sperm parameters and ORP between January and September 2019 were enrolled in this retrospective study. To identify normal and high ORP levels, a static ORP (sORP) cut-off value of 1.36mV/106sperm/mL was used. Sperm parameters were compared between infertile men with normal sORP (control group, n=23) and high sORP values (study group, n=35). Results: Men with sORP values >1.36mV/106sperm/mL had significantly lower total sperm count (TSC) (p <0.001), sperm concentration (p <0.001) and total motile sperm count (TMSC) (p <0.001). In addition, progressive motility (p=0.04) and fast forward progressive motility (p <0.001) were significantly lower in the study group. A negative correlation was found between sORP and TSC (r=-0.820, p <0.001), sperm concentration (r=-0.822, p <0.001), TMSC (r=-0.808, p <0.001) and progressive motility (r=-0.378, p=0.004). Non-progressive motility positively correlated with sORP (r=0.344, p=0.010). Conclusions: This study has shown that TSC, sperm concentration, progressive motility and TMSC are associated with seminal oxidative stress, indicated by a sORP cut-off of 1.36mV/106sperm/mL. Presence of oligozoospermia, reduced progressive motilty or low TMSC in sperm analysis should raise the suspicion of oxidative stress and warrants seminal ROS testing.
Subject(s)
Humans , Male , Sperm Motility , Infertility, Male , Oxidation-Reduction , Semen , Sperm Count , Spermatozoa , Retrospective StudiesABSTRACT
Objective: In this work, rats isolated hearts were infused EPA before the ischemia period and during reperfusion for available get well in parameter relatives to redox reactions. Methods: The effect of EPA was tested on isolated hearts induced to ischemia and reperfusion, treatment occurred at different times (ischemia or reperfusion). Antioxidant capacity against peroxyl radicals, glutathione cysteine ligase activity, glutathione concentration, lactate dehydrogenase, and creatine kinase concentration was analyzed. Results: Hearts treated with eicosapentaenoic acid had the minor generation of species reactive oxygen and lipid damage after reperfusion. The GSH concentration was higher when the hearts were treated with eicosapentaenoic acid in the period of reperfusion. Conclusion: In conclusion, this study demonstrates that the dose of EPA (20µM) used before ischemia can act as a cardioprotective antioxidant molecule, prevented damage heart from ischemic and reperfusion injury
Objetivo: Neste trabalho, corações isolados de ratos foram infundidos com EPA antes do período de isquemia e durante a reperfusão para obtenção de melhora em parâmetros relativos às reações redox. Métodos: O efeito do EPA foi testado em corações isolados induzidos a isquemia e reperfusão, o tratamento ocorreu em diferentes momentos (isquemia ou reperfusão). A capacidade antioxidante contra os radicais peroxil, atividade da glutationa cisteína ligase, concentração de glutationa, lactato desidrogenase e concentração de creatina quinase foi analisada. Resultados: Corações tratados com ácido eicosapentaenóico tiveram a menor geração de espécies reativas de oxigênio e danos lipídicos após a reperfusão. A concentração de GSH foi maior quando os corações foram tratados com ácido eicosapentaenóico no período de reperfusão. Conclusão: Em conclusão, este estudo demonstra que a dose de EPA (20µM) utilizada antes da isquemia pode atuar como uma molécula antioxidante cardioprotetora, prevenindo danos ao coração por isquemia e lesão de reperfusão.
Subject(s)
Heart , Infarction , Ischemia , Oxidation-Reduction , Oxidoreductases , Reperfusion , Eicosapentaenoic Acid , Lactic Acid , Reference Standards , GlutathioneABSTRACT
ABSTRACT Objective: To evaluate the effects of photobiomodulation therapy in redox status, angiogenesis marker - vascular endothelial growth factor - and in the functional recovery in denervated muscle. Methods: A total of 32 female Wistar rats underwent a crush injury and were randomly divided into four groups: Light Emitting Diode Group 2 and Control Group 2 (muscle collected 2 days after injury), and Light Emitting Diode Group 21 and Control Group 21 (muscle collected 21 days afterinjury). Light Emitting Diode Group 2 and Light Emitting Diode Group 21 received two and ten light emitting diode applications (630±20nm, 9J/cm2, 300mW), respectively, and the Control Group 2 and Control Group 21 did not receive any treatment. The function was evaluated by grasping test at four moments (pre-injury, 2, 10 and 21 post-injury days). The flexor digitorum muscle was collected for analysis of immunolocalization of vascular endothelial growth factor and redox parameters. Results: Functional improvement was observed at the second and tenth post-injury day in treated groups compared to control (p<0.005). The muscle tissue of treated groups presented higher immunohistochemical expression of vascular endothelial growth factor. Photobiomodulation therapy decreased the oxidative damage to lipid in Light Emitting Diode Group 2 compared to Control Group 2 (p=0.023) in the denervated muscle. Conclusion: Photobiomodulation therapy accelerated the functional recovery, increased angiogenesis and reduced lipid peroxidation in the denervated muscle at 2 days after injury.
RESUMO Objetivo: Avaliar os efeitos da terapia de fotobiomodulação no estado redox, no marcador de angiogênese - fator de crescimento endotelial vascular - e na recuperação funcional do músculo desnervado. Métodos: Um total de 32 ratas Wistar foi submetido a uma lesão por esmagamento e dividido aleatoriamente em quatro grupos: Grupo Diodo Emissor de Luz 2 e Grupo Controle 2 (músculo coletado 2 dias após a lesão), além do Grupo Diodo Emissor de Luz 21 e do Grupo Controle 21 (músculo coletado 21 dias após a lesão). Grupo Diodo Emissor de Luz 2 e Grupo Diodo Emissor de Luz 21 receberam duas e dez aplicações de diodo emissor de luz (630±20nm, 9J/cm2e 300mW), respectivamente, e Grupo Controle 2 e Grupo Controle 21 não receberam tratamento. A função foi avaliada pelo teste de preensão em quatro momentos (pré-lesão, 2, 10 e 21 dias após a lesão). O músculo flexor dos dedos foi coletado para análise dos parâmetros redox e da imunolocalização do fator de crescimento endotelial vascular. Resultados: Houve melhora funcional no segundo e décimo dia pós-lesão nos grupos tratados em comparação aos controles (p<0,005). O tecido muscular dos grupos tratados apresentou maior expressão imuno-histoquímica do fator de crescimento endotelial vascular. A terapia de fotobiomodulação diminuiu o dano oxidativo aos lipídeos no Grupo Diodo Emissor de Luz 2 comparado ao Grupo Controle 2 (p=0,023) no músculo desnervado. Conclusão: A terapia de fotobiomodulação acelerou a recuperação funcional, aumentou a angiogênese e reduziu a peroxidação lipídica no músculo desnervado 2 dias após a lesão.
Subject(s)
Animals , Female , Rats , Low-Level Light Therapy , Oxidation-Reduction , Rats, Wistar , Muscle, Skeletal , Vascular Endothelial Growth Factor AABSTRACT
Methanogens are unique microorganisms for methane production and the main contributor of the biogenic methane in atmosphere. Methyl-coenzyme M reductase (Mcr) catalyzes the last step of methane production in methanogenesis and the first step of methane activation in anaerobic oxidation of methane. The genes encoding this enzyme are highly conserved and are widely used as a marker in the identification and phylogenetic study of archaea. There has been a longstanding interest in its unique cofactor F430 and the underpinning mechanisms of enzymatic cleavage of alkane C-H bond. The recent breakthroughs of high-resolution protein and catalytic-transition-state structures further advanced the structure-function study of Mcr. In particular, the recent discovery of methyl-coenzyme M reductase-like (Mcr-like) enzymes that activates the anaerobic degradation of non-methane alkanes has attracted much interest in the molecular mechanisms of C-H activation without oxygen. This review summarized the advances on function-structure-mechanism study of Mcr/Mcr-like enzymes. Additionally, future directions in anaerobic oxidation of alkanes and greenhouse-gas control using Mcr/Mcr-like enzymes were proposed.
Subject(s)
Archaea/metabolism , Methane , Oxidation-Reduction , Oxidoreductases/metabolism , PhylogenyABSTRACT
Nrf2 is the key transcription factor mainly for regulating oxidative homeostasis and cytoprotective responses against oxidative stress. Nrf2/Keap1 pathway is one of the most important cellular defense mechanisms against endogenous or exogenous oxidative stress. With its activation, a wide range of stress-related genes is transactivated to restore the cellular homeostasis. Recent studies revealed that the aberrant activation of Nrf2 is related to the malignant progression, chemotherapeutic drug resistance and poor prognosis. Nrf2 plays a crucial role in cancer malignancy and chemotherapeutic resistance by controlling the intracellular redox homeostasis through the activation of cytoprotective antioxidant genes. Nrf2 inhibitor containing many natural products has been deemed as a novel therapeutic strategy for human malignancies. This article reviews the progress of studies of the Nrf2/Keap1 pathway, and its biological impact in solid malignancies and molecular mechanisms for causing Nrf2 hyperactivation in cancer cells. In conclusion, we summarized the deve-lopment of Nrf2 inhibitors in recent years, in the expectation of providing reference for further drug development and clinical studies.
Subject(s)
Humans , Kelch-Like ECH-Associated Protein 1/metabolism , NF-E2-Related Factor 2/metabolism , Neoplasms/genetics , Oxidation-Reduction , Oxidative StressABSTRACT
Due to abundant availability of shale gas and biogas, methane has been considered as one of the most potential carbon sources for industrial biotechnology. Methanotrophs carrying the native methane monooxygenase are capable of using methane as a sole energy and carbon source, which provides a novel strategy for reducing greenhouse gas emission and substituting edible substrates used in bioconversion processes. With the rapid development of genetic engineering tools and biosynthesis techniques, various strategies for improving the efficiency of methane bioconversion have been achieved to produce a variety of commodity bio-based products. Herein, we summarize several important aspects related with methane utilization and metabolic engineering of methanotrophs, including the modification of methane oxidation pathways, the construction of efficient cell factories, and biosynthesis of chemicals and fuels. Finally, the prospects and challenges of the future development of methane bioconversion are also discussed.
Subject(s)
Biofuels , Biotechnology , Metabolic Engineering , Methane , Oxidation-ReductionABSTRACT
Phospholipids are important components of biomembrane and lipoproteins. Phospholipids can be oxidized by free radicals/nonradicals and enzymes to form oxidized phospholipids (OxPLs), which can lead to further generation of oxidation products with different biological activities. Clinical evidence shows that OxPLs are constantly generated and transformed during the pathogenesis of atherosclerosis and accumulated at the lesion sites. OxPLs are highly heterogeneous mixtures that can influence the progress of atherosclerosis through a variety of related receptors or signaling pathways. This review summarizes the process of phospholipid oxidation, the related products, the interaction of OxPLs with endothelial cells, monocytes/macrophages, smooth muscle cells, platelets and lipoproteins involved in the pathological process of atherosclerosis, and the progress of the researches using OxPLs as a target to inhibit atherosclerosis in recent years.
Subject(s)
Atherosclerosis , Endothelial Cells , Humans , Myocytes, Smooth Muscle , Oxidation-Reduction , PhospholipidsABSTRACT
BACKGROUND: There Is an emerging field to put Into practice new strategies for developing molecules with antimicrobial properties. In this line, several metals and metalloids are currently being used for these purposes, although their cellular effect(s) or target(s) in a particular organism are still unknown. Here we aimed to investigate and analyze Au3+ toxicity through a combination of biochemical and molecular approaches. RESULTS: We found that Au3+ triggers a major oxidative unbalance in Escherichia coli, characterized by decreased intracellular thiol levels, increased superoxide concentration, as well as by an augmented production of the antioxidant enzymes superoxide dismutase and catalase. Because ROS production is, in some cases, associated with metal reduction and the concomitant generation of gold-containing nanostructures (AuNS), this possibility was evaluated in vivo and in vitro. CONCLUSIONS: Au3+ is toxic for E. coli because it triggers an unbalance of the bacterium's oxidative status. This was demonstrated by using oxidative stress dyes and antioxidant chemicals as well as gene reporters, RSH concentrations and AuNS generation.
Subject(s)
Oxidation-Reduction/drug effects , Oxidative Stress/drug effects , Escherichia coli/drug effects , Metal Nanoparticles/toxicity , Gold/toxicityABSTRACT
Abstract In live organisms, there is a balance between the production of reactive oxygen species (ROS) and their neutralization. The increased level of these species leads to a condition called redox imbalance. The aim of this study was to evaluate the protective action of isobenzofuranones in primary cultures of hippocampal neurons subjected to redox imbalance. To accomplish this, MTT and LIVE/DEAD assays were initially performed. In the cultures pretreated with isobenzofuranones 1 and 2, there was a higher number of live cells when compared to that in the untreated ones. Regarding redox imbalance, there was a significant increase in the intracellular levels of ROS. The cultures pretreated with isobenzofuranones showed a reduction in ROS levels. Lipid peroxidation caused by oxidative damage was significantly reduced in the cultures pretreated with isobenzofuranones 1 and 2. Taken together, these data show the ability of isobenzofuranones 1 and 2 to significantly minimize cytotoxicity, cell death, intracellular levels of ROS and lipid peroxidation induced by redox imbalance. These results suggest that isobenzofuranones 1 and 2 represent a possible alternative therapy for the neurodegenerative disturbances that are triggered by ROS production increases.