The mitochondria-targeted antioxidant MitoQ protects against organ damage in a lipopolysaccharide–peptidoglycan model of sepsis

Lowes, Damon A.; Thottakam, Bensita Mary Viju Jose; Webster, Nigel R.; Murphy, Michael P.; Galley, Helen F.

doi:10.1016/j.freeradbiomed.2008.09.003

Cited by 228 publications

(197 citation statements)

References 41 publications

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“…Lots of studies have shown that excessive production of ROS and other free radicals in sepsis, such as H 2 O 2 , superoxides and NO, which are associated with inflammation, lead to a condition of oxidative stress and contribute to high mortality rates [6,25]. However, direct detection of ROS and other free radicals is quite difficult since they are all short-lived and highly reactive in a nonspecific manner [37].…”

Section: Discussionmentioning

confidence: 99%

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Chitosan oligosaccharides protect mice from LPS challenge by attenuation of inflammation and oxidative stress

Qiao

2011

International Immunopharmacology

154

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Section: Discussionmentioning

confidence: 99%

“…Besides, sepsis is associated with a significant redox imbalance. Recent studies pointed out that some anti-oxidant agents have beneficial effects in treating sepsis [5], such as N-acetylcysteine (NAC), MitoQ and deferoxamine (DFX) [6][7][8].…”

Section: Introductionmentioning

confidence: 99%

Chitosan oligosaccharides protect mice from LPS challenge by attenuation of inflammation and oxidative stress

Qiao

2011

International Immunopharmacology

154

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“…17,27 Moreover, MitoQ 10 has been shown to be effective against mitochondrial oxidative damage in vivo and in rodent models of sepsis and reperfusion injury. 18,28 The stroke-prone spontaneously hypertensive rat (SHRSP) is a well-characterized experimental model for human essential hypertension that develops a number of cardiovascular complications, including cardiac hypertrophy, stroke, and endothelial dysfunction. We have demonstrated previously that endothelial dysfunction in the SHRSP is attributed to a marked but reversible imbalance between NO and O 2 Ϫ at the level of the vascular endothelium.…”

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confidence: 99%

Mitochondria-Targeted Antioxidant MitoQ ₁₀ Improves Endothelial Function and Attenuates Cardiac Hypertrophy

et al. 2009

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Abstract-Mitochondria are a major site of reactive oxygen species production, which may contribute to the development of cardiovascular disease. Protecting mitochondria from oxidative damage should be an effective therapeutic strategy; however, conventional antioxidants are ineffective, because they cannot penetrate the mitochondria. This study investigated the role of mitochondrial oxidative stress during development of hypertension in the stroke-prone spontaneously hypertensive rat, using the mitochondria-targeted antioxidant, MitoQ 10 . Eight-week-old male strokeprone spontaneously hypertensive rats were treated with MitoQ 10 (500 mol/L; nϭ16), control compound decyltriphenylphosphonium (decylTPP; 500 mol/L; nϭ8), or vehicle (nϭ9) in drinking water for 8 weeks. Ϫ goes on to produce a range of damaging ROS that lead to nonspecific modification of mitochondrial proteins, lipids, and nucleic acids, thereby altering mitochondrial function. 3-5 Mitochondrial DNA is particularly susceptible to modification by ROS, and this damage can rapidly lead to functional changes in the cell, because it encodes 13 essential polypeptide components of the mitochondrial respiratory chain. 4 Extensive evidence suggests that mitochondrial DNA damage occurs in cardiovascular disease in humans, animal models, and cellular models. 3,[7][8][9] Mitochondria are normally protected from oxidative damage by a multilayer network of mitochondrial antioxidant systems. 10,11 These include the mitochondrial matrix enzyme manganese superoxide dismutase, which converts the O 2 Ϫ anion to hydrogen peroxide, glutathione peroxidase, and peroxiredoxins 3 and 5, which readily convert hydrogen peroxide to water 7,10 and ultimately prevent forms of mitochondrial oxidative damage, eg, lipid peroxidation. Modification of these antioxidant enzymes resulting from the knockout of manganese superoxide dismutase or glutathione peroxidase genes can significantly affect mitochondrial activity and ROS production and has been linked to hypertension and salt sensitivity in mice. [12][13][14][15] The precise contribution of mitochondria to the total ROS production in the vessel wall or other cardiovascular tissues

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“…MitoQ, MitoE and melatonin are known antioxidants and their administration in animal models with sepsis like states [endothelial damage with LPS induction, and PgG in mice] can diminish the cytokine response [47,48], they even showed an improvement in the mitochondrial respiration, improvement in oxidative stress and diminish of the levels of interlekin 6 compared with mice in the control group [49].…”

Section: Treating the Hypoperfusionmentioning

confidence: 99%

Perfusion Measurement of the Septic Patient in the Emergency Department

Devia-Jaramillo¹

2014

Emergency Medicine

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Sepsis is a deadly disease, more complex and frequent every day, that requires management from different specialists. The emergency physician is the first and one of the most important physicians that has to deal with the septic critically ill patients, because an appropriate initial management is key to a favorable outcome.In the emergency department it can be hard to predict which patients will become sicker just with information from the vital signs, and it's even harder to predict which patients will require a more intensive medical treatment. That is the reason why there must be more resources to measure tissue perfusion in an early and simple way in the emergency room, so that the emergency physician can manage to establish which patients requires earlier intervention to improve their perfusion state, despite not showing any clinically evident signs that help in the diagnosis of their current state.The goal of this paper is to propose a diagnostic and therapeutic algorithm for the hypoperfused patient with septic shock in the emergency department.venous oxygen saturation, arterial and venous lactate, microcirculatory study in different anatomical sites and oxygenation indexes.The emergency department, a place of rapid transit, with time constraints, progressive overcrowding and limited physical space, requires efficient indicators of early appearance and simple implementation in the system. That is why this article aims to show a proposal of early detection of hypoperfusion in the septic patient in the emergency room.

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The mitochondria-targeted antioxidant MitoQ protects against organ damage in a lipopolysaccharide–peptidoglycan model of sepsis

Cited by 228 publications

References 41 publications

Chitosan oligosaccharides protect mice from LPS challenge by attenuation of inflammation and oxidative stress

Chitosan oligosaccharides protect mice from LPS challenge by attenuation of inflammation and oxidative stress

Mitochondria-Targeted Antioxidant MitoQ ₁₀ Improves Endothelial Function and Attenuates Cardiac Hypertrophy

Perfusion Measurement of the Septic Patient in the Emergency Department

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The mitochondria-targeted antioxidant MitoQ protects against organ damage in a lipopolysaccharide–peptidoglycan model of sepsis

Cited by 228 publications

References 41 publications

Chitosan oligosaccharides protect mice from LPS challenge by attenuation of inflammation and oxidative stress

Chitosan oligosaccharides protect mice from LPS challenge by attenuation of inflammation and oxidative stress

Mitochondria-Targeted Antioxidant MitoQ 10 Improves Endothelial Function and Attenuates Cardiac Hypertrophy

Perfusion Measurement of the Septic Patient in the Emergency Department

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Product

Resources

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Mitochondria-Targeted Antioxidant MitoQ ₁₀ Improves Endothelial Function and Attenuates Cardiac Hypertrophy