نتایج جستجو برای: oxidative stress injury

تعداد نتایج: 777419  

Journal: :Cell 2012
Angelina V. Vaseva Natalie D. Marchenko Kyungmin Ji Stella E. Tsirka Sonja Holzmann Ute M. Moll

Ischemia-associated oxidative damage leading to necrosis is a major cause of catastrophic tissue loss, and elucidating its signaling mechanism is therefore of paramount importance. p53 is a central stress sensor responding to multiple insults, including oxidative stress to orchestrate apoptotic and autophagic cell death. Whether p53 can also activate oxidative stress-induced necrosis is, howeve...

Journal: :Annals of the New York Academy of Sciences 2008
Gary Fiskum Camelia A Danilov Zara Mehrabian Linda L Bambrick Tibor Kristian Mary C McKenna Irene Hopkins E M Richards Robert E Rosenthal

Oxidative stress and mitochondrial dysfunction have been closely associated in many subcellular, cellular, animal, and human studies of both acute brain injury and neurodegenerative diseases. Our animal models of brain injury caused by cardiac arrest illustrate this relationship and demonstrate that both oxidative molecular modifications and mitochondrial metabolic impairment are exacerbated by...

Journal: :American journal of physiology. Renal physiology 2013
Partab Rai Andrei Plagov Xiqian Lan Nirupama Chandel Tejinder Singh Rivka Lederman Kamesh R Ayasolla Peter W Mathieson Moin A Saleem Mohammad Husain Ashwani Malhotra Praveen N Chander Pravin C Singhal

Oxidative stress has been implicated to contribute to HIV-induced kidney cell injury; however, the role of p53, a modulator of oxidative stress, has not been evaluated in the development of HIV-associated nephropathy (HIVAN). We hypothesized that mammalian target of rapamycin (mTOR) may be critical for the induction of p53-mediated oxidative kidney cell injury in HIVAN. To test our hypothesis, ...

2013
Charis R. Szymanski Wissam Chiha Natalie Morellini Nadia Cummins Carole A. Bartlett Ryan L. O'Hare Doig Donna L. Savigni Sophie C. Payne Alan R. Harvey Sarah A. Dunlop Melinda Fitzgerald

Secondary degeneration of nerve tissue adjacent to a traumatic injury results in further loss of neurons, glia and function, via mechanisms that may involve oxidative stress. However, changes in indicators of oxidative stress have not yet been demonstrated in oligodendrocytes vulnerable to secondary degeneration in vivo. We show increases in the oxidative stress indicator carboxymethyl lysine a...

2017
Ahreum Baek Sung-Rae Cho Sung Hoon Kim

Spinal cord injury (SCI) is a devastating neurological disease. The pathophysiological mechanisms of SCI have been reported to be relevant to central nervous system injury such as brain injury. In this study, gene expression of the brain after SCI was elucidated using transcriptome analysis to characterize the temporal changes in global gene expression patterns in a SCI mouse model. Subjects we...

2017
Quanchao Sun You Wu Feng Zhao Jianjun Wang

Lung ischemia/reperfusion (I/R) injury occurs in various clinical conditions and heavily damaged lung function. Oxidative stress reaction and antioxidant enzymes play a pivotal role in the etiopathogenesis of lung I/R injury. In the current study, we investigated the impact of Maresin 1 on lung I/R injury and explored the possible mechanism involved in this process. MaR 1 ameliorated I/R-induce...

2016
Kimberly B Bjugstad Leonard T Rael Stewart Levy Matthew Carrick Charles W Mains Denetta S Slone David Bar-Or

There are few reliable markers for assessing traumatic brain injury (TBI). Elevated levels of oxidative stress have been observed in TBI patients. We hypothesized that oxidation-reduction potential (ORP) could be a potent biomarker in TBI. Two types of ORP were measured in patient plasma samples: the static state of oxidative stress (sORP) and capacity for induced oxidative stress (icORP). Diff...

Journal: :Journal of biochemistry and molecular biology 2002
Seok Joon Won Doo Yeon Kim Byoung Joo Gwag

Three routes have been identified triggering neuronal death under physiological and pathological conditions. Excess activation of ionotropic glutamate receptors cause influx and accumulation of Ca2+ and Na+ that result in rapid swelling and subsequent neuronal death within a few hours. The second route is caused by oxidative stress due to accumulation of reactive oxygen and nitrogen species. Ap...

2009
Robert G Fassett Vincent D'Intini Helen Healy John Gowardman Jay-Sen Gan James E Sharman Jeff S Coombes

BACKGROUND It is well know that arterial stiffness, oxidative stress and inflammation are features of chronic kidney disease. The arterial changes have a multitude of potential interconnected causes including endothelial dysfunction, oxidative stress, inflammation, atherosclerosis and vascular calcification. There is evidence that arterial stiffness becomes progressively worse as CKD progresses...

Journal: :The Journal of clinical investigation 1998
P A Dennery D R Spitz G Yang A Tatarov C S Lee M L Shegog K D Poss

Heme oxygenase (HO) activity leads to accumulation of the antioxidant bilirubin, and degradation of the prooxidant heme. Moderate overexpression of the inducible form, HO-1, is associated with protection against oxidative injury. However, the role of HO-2 in oxidative stress has not been explored. We evaluated survival, indices of oxidative injury, and lung and HO expression in HO-2 null mutant...

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