NADPH Oxidase Plays a Role on Ethanol-Induced Hypertension and Reactive Oxygen Species Generation in the Vasculature

Marchi, Kátia Colombo; Ceron, Carla S.; Muniz, Jaqueline Jóice; Martinis, Bruno Spinosa De; Tanus‐Santos, Jose E.; Tirapelli, Carlos Renato

doi:10.1093/alcalc/agw043

Cited by 37 publications

(38 citation statements)

References 36 publications

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“…In this model, stimulated peritoneal macrophages had a lower free radical release when pretreated with butyrate, which was related to a reduction in NADPH oxidase and inducible nitric oxide synthase. Marchi et al recently showed that ethanol-induced hypertension is mediated by NADPH oxidase and that NOX1 expression is related to the generation of reactive oxygen species by ethanol [2]. In our chronic-binge ethanol exposure model, mice only receiving ethanol had induced mRNA levels of NOX1 and reduced mRNA levels of antioxidant genes.…”

Section: Discussionmentioning

confidence: 57%

“…Reactive oxygen species derived from NADPH oxidase are involved with the development of tissue dysfunction induced by ethanol [39, 40]. Activity of NADPH oxidase is involved with ethanol-induced hypertension and ROS generation in the vasculature [2]. Ideally in order to facilitate recovery, angiogenesis follows tissue ischemia and hypoxia.…”

Section: Resultsmentioning

confidence: 99%

“…It is generally recognized that lipid peroxidation, immune damage, and antioxidant defenses may play an important role in the pathogenesis of ethanol-induced cellular injury [1]. Ethanol promotes the generation of superoxide anion and hydrogen peroxide, and these byproducts contribute to endothelial dysfunction, vasoconstriction, and hypertension [2]. …”

Section: Introductionmentioning

confidence: 99%

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Tributyrin Supplementation Protects Immune Responses and Vasculature and Reduces Oxidative Stress in the Proximal Colon of Mice Exposed to Chronic-Binge Ethanol Feeding

Glueck

Han

Cresci

2018

Journal of Immunology Research

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Excessive ethanol consumption causes adverse effects and contributes to organ dysfunction. Ethanol metabolism triggers oxidative stress, altered immune function, and gut dysbiosis. The gut microbiome is known to contribute to the maintenance of intestinal homeostasis, and disturbances are associated with pathology. A consequence of gut dysbiosis is also alterations in its metabolic and fermentation byproducts. The gut microbiota ferments undigested dietary polysaccharides to yield short-chain fatty acids, predominantly acetate, propionate, and butyrate. Butyrate has many biological mechanisms of action including anti-inflammatory and immunoprotective effects, and its depletion is associated with intestinal injury. We previously showed that butyrate protects gut-liver injury during ethanol exposure. While the intestine is the largest immune organ in the body, little is known regarding the effects of ethanol on intestinal immune function. This work is aimed at investigating the effects of butyrate supplementation, in the form of the structured triglyceride tributyrin, on intestinal innate immune responses and oxidative stress following chronic-binge ethanol exposure in mice. Our work suggests that tributyrin supplementation preserved immune responses and reduced oxidative stress in the proximal colon during chronic-binge ethanol exposure. Our results also indicate a possible involvement of tributyrin in maintaining the integrity of intestinal villi vasculature disrupted by chronic-binge ethanol exposure.

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Section: Discussionmentioning

confidence: 57%

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Tributyrin Supplementation Protects Immune Responses and Vasculature and Reduces Oxidative Stress in the Proximal Colon of Mice Exposed to Chronic-Binge Ethanol Feeding

Glueck

Han

Cresci

2018

Journal of Immunology Research

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“…Применение другого ингибитора НАДФН-оксидазы -апоцинина -при анализе эффектов алкоголя устраняло повышение активности NOX2 и увеличение генерации супероксида в крови крыс линии Wistar [24]. Аналогичным образом апоцинин воздействует на экспрессию NOX2 в ткани аорты алкоголизированных крыс указанной линии [25].…”

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He Role of Nadph Oxidases in the Formation of Alcohol-Induced Oxidative Stress

Efremenko¹

2020

НО МН (SR MS)

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Высокая заболеваемость алкоголизмом является важной медико-социальной проблемой в Российской Федерации. Значимость усиленной генерации свободных радикалов при алкогольной интоксикации и алкогольной зависимости подчеркивается широким использованием термина «алкоголь-индуцированный окислительный стресс». Существует большое количество молекулярных механизмов, обеспечивающих формирование дисбаланса между продукцией и устранением свободнорадикальных веществ. Наиболее важной группой свободных радикалов считаются активные формы кислорода. Данные субстанции отвечают за формирование состояния окислительного стресса, при котором продукция свободных радикалов превалирует над возможностью компонентов антиоксидантной системы по их нейтрализации. Окислительный стресс рассматривается не только как простой дисбаланс в соотношении генерации и устранения АФК, но и как проявление нарушения функционирования ферментов, вовлеченных в образование свободных радикалов. Одним из важнейших ферментативных направлений может считаться работа супероксидпродуцирующих энзимов, главными из которых является семейство НАДФН-оксидаз. НАДФН-оксидазы представляют собой сложные ферментные комплексы, основная функция которых связана с генерацией активных форм кислорода. Общая функция НАДФН-оксидаз, расположенных на плазматической мембране, заключается в переносе электронов от цитозольного НАДФН 2 через кофермент ФАД и гем к кислороду с формированием супероксидного анион-радикала и пероксида водорода. Предложенная информация содержит данные об участии НАДФН-оксидаз в нарушении обмена веществ при алкоголизме.ключевые слова: алкоголь, алкоголизм, окислительный стресс, свободные радикалы, антиоксиданты, ферменты, клетки, патогенезThe high incidence of alcoholism is an important medical and social problem in the Russian Federation. The importance of enhanced free radical generation in alcohol intoxication and alcohol dependence is emphasized by the widespread use of the term «alcohol-induced oxidative stress». There are a large number of molecular mechanisms that ensure the formation of an imbalance between the production and elimination of free radical substances. The most important group of free radicals is considered reactive oxygen species. These substances are responsible for the formation of a state of oxidative stress, in which the production of free radicals prevails over the ability of the components of the antioxidant system to neutralize them. Oxidative stress is considered not only as a simple imbalance in the ratio of generation and elimination of ROS, but also as a manifestation of a violation of the functioning of enzymes involved in the formation of free radicals. One of the most important enzymatic directions can be considered the work of superoxide-producing enzymes, the main of which is the family of NADPH oxidases. NADPH oxidases are enzyme complexes whose main function is related to the generation of reactive oxygen species. The general function of NADPH oxidases located on the plasma membrane is to transfer electrons from cytosolic NADP...

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“…Essas alterações foram acompanhadas por um menor ganho de peso corpóreo dos animais. Essa redução de peso corrobora estudos de Chan et al (1985), Wilsnack & Wilsnack et al (1997), Aguiar et al (2004), Tirapelli et al(2008), Marchi et al (2016) (Lieber, 1991;Aguiar et al, 2004). O menor ganho de peso observado pode ser justificado pela redução da ingestão de ração e líquido durante o tratamento crônico com etanol.…”

Section: Discussionunclassified

Participação do TNF-a nas disfunções vasculares induzidas pelo consumo crônico de etanol: envolvimento do tecido adiposo perivascular

Simplicio¹

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À Deus por tudo! Não tenho palavras que descrevam meus sinceros agradecimentos ao Ser mais grandioso deste Universo, que com sua força onipresente soube guiar meus passos dando-me força para cultivar as sementes e regozijar desta colheita. Sem Ele eu jamais teria chegado até aqui! Obrigada meu amado Deus por nuca desistir de mim! Aos meus amados pais, Lucy e Moacyr, pela educação proporcionada, pelo carinho oferecido, pela confiança em mim depositada, pelos gestos solidários ao longo destes anos. Mãe, obrigada por me confortar nos momentos que eu mais precisei, obrigada pelo colo e pelas palavras de sabedoria que me ajudaram a seguir em frente. Pai, obrigada por me guiar aos caminhos do conhecimento, por me achar tão capaz e sempre apoiar minhas escolhas. O amor de vocês é essencial para a minha vida e minhas conquistas. Amo vocês incondicionalmente! Ao meu grande companheiro Zeino, por sempre acreditar em mim, apoiar minhas escolhas, me confortar e me proporcionar tanto carinho. Obrigada por toda sua dedicação, por sua capacidade de compreensão e pelo aguardo paciente nos momentos de ausência. Amo-te sempre e para sempre! Ao meu orientador, Prof. Dr. Carlos Renato Tirapelli, pela amizade, pela oportunidade de aprendizado, pelo profissionalismo e pela orientação ao longo desses anos que foram essenciais para o desenvolvimento desta tese e para meu crescimento acadêmico. Meus sinceros agradecimentos. Aos membros da banca examinadora, professores Fernando Silva Carneiro, Michele M. de Castro, Eliana Hiromi Akamine e Cristina Antoniali, pela disponibilidade, contribuições e sugestões para a melhoria deste projeto. Às minhas eternas amigas Carla Brigagão, Letícia Nogueira e ao meu grande amigo Gabriel, um presente que a USP me deu para a eternidade. Obrigada por me ouvirem, me ajudarem e me apoiarem sempre! Obrigada por cada palavra e por toda ajuda concedida ao longo desses anos! Mesmo com a distância, sinto-me abraçada diariamente por vocês! Vocês fazem parte do meu dia e da minha vida! Amo vocês! Aos meus amados "pupilos" Marcelo Nakashima e Paola Salamanca por me ensinarem a ensinar e aprender. Obrigada por todo apoio e amparo oferecido para o desenvolvimento deste trabalho e para o meu crescimento. Vocês moram eternamente em meu coração.

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NADPH Oxidase Plays a Role on Ethanol-Induced Hypertension and Reactive Oxygen Species Generation in the Vasculature

Cited by 37 publications

References 36 publications

Tributyrin Supplementation Protects Immune Responses and Vasculature and Reduces Oxidative Stress in the Proximal Colon of Mice Exposed to Chronic-Binge Ethanol Feeding

Tributyrin Supplementation Protects Immune Responses and Vasculature and Reduces Oxidative Stress in the Proximal Colon of Mice Exposed to Chronic-Binge Ethanol Feeding

He Role of Nadph Oxidases in the Formation of Alcohol-Induced Oxidative Stress

Participação do TNF-a nas disfunções vasculares induzidas pelo consumo crônico de etanol: envolvimento do tecido adiposo perivascular

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