Gene expression profile of oxidative stress in the lung of inbred mice after intestinal ischemia/reperfusion injury

Ikejiri, Adauto Tsutomu; Neto, Frederico Somaio; Chaves, José Carlos; Bertoletto, Paulo Roberto; Teruya, Roberto; Bertoletto, Eduardo Rodrigues; Taha, Murched Omar; Fagundes, Djalma José

doi:10.1590/s0102-86502014000300007

Cited by 10 publications

(6 citation statements)

References 35 publications

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“…This approach, which has been applied to heart [100] , [101] , kidney [102] , skin [103] , retina [104] , lung [105] , intestine [106] , liver [107] , and monolayers of cultured cells [108] , [109] , has revealed that the enhanced ROS production elicited by I/R is detected immediately (within 20 s) following reperfusion and that superoxide (

) is the parent radical that serves as a precursor for the hydroxyl radical, carbon-centered radicals and other secondary species [2] , [110] . The more recent application of proteomic and genomic mapping to tissues (or cells) exposed to I/R (or H/R) is providing novel insights into the responses of specific proteins and genes to the oxidative stress that accompanies this condition [111] , [112] , [113] , [114] .…”

Section: Reactive Oxygen Species Contribute To Reperfusion Injurymentioning

confidence: 99%

Reperfusion injury and reactive oxygen species: The evolution of a concept

2015

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Reperfusion injury, the paradoxical tissue response that is manifested by blood flow-deprived and oxygen-starved organs following the restoration of blood flow and tissue oxygenation, has been a focus of basic and clinical research for over 4-decades. While a variety of molecular mechanisms have been proposed to explain this phenomenon, excess production of reactive oxygen species (ROS) continues to receive much attention as a critical factor in the genesis of reperfusion injury. As a consequence, considerable effort has been devoted to identifying the dominant cellular and enzymatic sources of excess ROS production following ischemia-reperfusion (I/R). Of the potential ROS sources described to date, xanthine oxidase, NADPH oxidase (Nox), mitochondria, and uncoupled nitric oxide synthase have gained a status as the most likely contributors to reperfusion-induced oxidative stress and represent priority targets for therapeutic intervention against reperfusion-induced organ dysfunction and tissue damage. Although all four enzymatic sources are present in most tissues and are likely to play some role in reperfusion injury, priority and emphasis has been given to specific ROS sources that are enriched in certain tissues, such as xanthine oxidase in the gastrointestinal tract and mitochondria in the metabolically active heart and brain. The possibility that multiple ROS sources contribute to reperfusion injury in most tissues is supported by evidence demonstrating that redox-signaling enables ROS produced by one enzymatic source (e.g., Nox) to activate and enhance ROS production by a second source (e.g., mitochondria). This review provides a synopsis of the evidence implicating ROS in reperfusion injury, the clinical implications of this phenomenon, and summarizes current understanding of the four most frequently invoked enzymatic sources of ROS production in post-ischemic tissue.

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Section: Reactive Oxygen Species Contribute To Reperfusion Injurymentioning

confidence: 99%

Reperfusion injury and reactive oxygen species: The evolution of a concept

2015

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“…In general, less expressed or oxidized proteins localized in the mitochondria were detected NADH dehydrogenase, succinate dehydrogenase, voltage-dependent anion channel [ 53 , 54 ]. In a lung IRI male model, Ikejiri showed that 79.7% of genes related with the oxidative stress were upregulate and 20.2% of them were downregulated [ 55 ]. These genes are related with the production of ROS or of antioxidant enzyme, with no other precision about their identity [ 55 ].…”

Section: Proteasome and The Oxidative Stressmentioning

confidence: 99%

Proteasome and Organs Ischemia-Reperfusion Injury

Oliva

2017

IJMS

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The treatment of organ failure on patients requires the transplantation of functional organs, from donors. Over time, the methodology of transplantation was improved by the development of organ preservation solutions. The storage of organs in preservation solutions is followed by the ischemia of the organ, resulting in a shortage of oxygen and nutrients, which damage the tissues. When the organ is ready for the transplantation, the reperfusion of the organ induces an increase of the oxidative stress, endoplasmic reticulum stress, and inflammation which causes tissue damage, resulting in a decrease of the transplantation success. However, the addition of proteasome inhibitor in the preservation solution alleviated the injuries due to the ischemia-reperfusion process. The proteasome is a protein structure involved in the regulation the inflammation and the clearance of damaged proteins. The goal of this review is to summarize the role of the proteasome and pharmacological compounds that regulate the proteasome in protecting the organs from the ischemia-reperfusion injury.

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“…In conclusion, the detection of BPDE in human cells [10,11], the fact that buccal cells are one of the common biological sources of DNA for adduct analysis [12,13] and the stability of BPDE-DNA damage in human cells [14][15][16] in previous studies including our results suggest that MAWI collection tubes cannot preserve BPDE-DNA damage and may not be able to allow the detection of oxidative stress.Other oxidative stress markers should be used to evaluate the previous statement.…”

Section: Discussionmentioning

confidence: 64%

Oxidative Stress Levels in Buccal Cells Using MAWI Collection Tubes

Tabbouny¹,

Chamoun²,

Павлюченко³

et al. 2017

J Pharmacovigilance

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Background: Oxidative Stress (OS) is defined as an imbalance between oxidants and antioxidants, in favor of oxidants, potentially leading to DNA damage. Benzo[a] pyrene (B(a)P), a representative DNA-damaging mutagenic/ carcinogenic Polycyclic Aromatic Hydrocarbons (PAH), can lead to the final mutagen Benzo(a)Pyrene Diol Epoxide (BPDE). Methods: The extent of oxidative DNA damage is investigated in population studies using easily obtained cells. Buccal cell usage has been shown by many to be a cost effective, non-invasive and safe method to isolate DNA for various biological experiments. In this experimental research of 40 participants, equally divided between industry and academia, we compared the DNA concentration, purity, and associated levels of BPDE-DNA damage. Buccal cells were collected using ISWAB-DNA tubes, and DNA was then extracted to study the extent of DNA damage via ELISA Kit. Results: Results showed pure samples with no DNA degradation. DNA yields were as high as 35.657 μg/mL. In addition, none of the samples showed a presence of BPDE-DNA damage. Conclusions: MAWI collection tubes may not be able to detect BPDE-DNA damage. Other OS markers should be used to eradicate the previous statement.

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Gene expression profile of oxidative stress in the lung of inbred mice after intestinal ischemia/reperfusion injury

Cited by 10 publications

References 35 publications

Reperfusion injury and reactive oxygen species: The evolution of a concept

Reperfusion injury and reactive oxygen species: The evolution of a concept

Proteasome and Organs Ischemia-Reperfusion Injury

Oxidative Stress Levels in Buccal Cells Using MAWI Collection Tubes

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