Lipid peroxidation in the skeletal muscle of hamsters with emphysema

Mattson, John P.; Sun, Jie; Murray, Dennis; Poole, David C.

doi:10.1016/s0928-4680(02)00011-1

Cited by 16 publications

(31 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…and Lewis 2000, Mattson et al 2002, Degens et al 2007, Lüthje et al 2009). Lüthje and colleagues (2009) have observed that repeated instillations of elastase induce a more severe emphysematous state than single dose.…”

Section: Comparison Of Elastase Modelsmentioning

confidence: 96%

“…Animal models also develop increased protein synthesis by lipid peroxidation products, such as 4-hydroxynonenal, and depletion of antioxidant substances, such as superoxide dismutase, catalase, ascorbic acid and glutathione (McCusker and Hoidal 1990, Churg and Cherukupalli 1993, Cavarra et al 2001, Aoshiba et al 2003a). Few studies have investigated the association of protease-induced emphysema with oxidative stress (Mattson et al 2002, Petrache et al 2008, Borzone et al 2009). It has been evidenced that oxidant attack diminishes α1-antitrypsin (α1-AT) affinity for elastase by the oxidation of a methionine residue at its active site.…”

Section: Elastase Vs Smoke-induced Emphysemamentioning

confidence: 99%

See 1 more Smart Citation

Elastase-induced pulmonary emphysema: insights from experimental models

Antunes

Rocco

2011

An. Acad. Bras. Ciênc.

View full text Add to dashboard Cite

Several distinct stimuli can be used to reproduce histological and functional features of human emphysema, a leading cause of disability and death. Since cigarette smoke is the main cause of emphysema in humans, experimental researches have attempted to reproduce this situation. However, this is an expensive and cumbersome method of emphysema induction, and simpler, more efficacious alternatives have been sought. Among these approaches, elastolytic enzymes have been widely used to reproduce some characteristics of human cigarette smoke-induced disease, such as: augmentation of airspaces, inflammatory cell influx into the lungs, and systemic inflammation. Nevertheless, the use of elastase-induced emphysema models is still controversial, since the disease pathways involved in elastase induction may differ from those occurring in smoke-induced emphysema. This indicates that the choice of an emphysema model may impact the results of new therapies or drugs being tested. The aim of this review is to compare the mechanisms of disease induction in smoke and elastase emphysema models, to describe the differences among various elastase models, and to establish the advantages and disadvantages of elastase-induced emphysema models. More studies are required to shed light on the mechanisms of elastase-induced emphysema.

show abstract

Section: Comparison Of Elastase Modelsmentioning

confidence: 96%

Section: Elastase Vs Smoke-induced Emphysemamentioning

confidence: 99%

Elastase-induced pulmonary emphysema: insights from experimental models

Antunes

Rocco

2011

An. Acad. Bras. Ciênc.

View full text Add to dashboard Cite

show abstract

“…There is also some evidence that links the wasting that occurs in COPD patients to both oxidative stress and oxidative stress-mediated processes, such as apoptosis, inflammation, disruption of the excitation-contraction coupling and atrophy [97,[102][103][104]. This effect of oxidative stress on skeletal muscle wasting in COPD is shown in figure 2.…”

Section: Body Composition and Chronic Obstructive Pulmonary Diseasementioning

confidence: 98%

“…Increased lipid peroxidation, a result of ROS, in chronicallyloaded diaphragms is related positively with reduction in strength and with fatigability [139]. Noteworthy is the fact that in most studies the effect of oxidative stress could successfully be reversed by various types of antioxidants [141,142], suggesting a possible mechanistic role for oxidative stress in the pathophysiology of muscle dysfunction [104].…”

Section: Protein Oxidationmentioning

confidence: 99%

See 1 more Smart Citation

Oxidant metabolism in chronic obstructive pulmonary disease

Boots

Haenen

Bast

2003

European Respiratory Journal

105

View full text Add to dashboard Cite

The development and progression of chronic obstructive pulmonary disease (COPD) have been associated with increased oxidative stress or reduced antioxidant resources. Several indicators of oxidative stress, such as hydrogen peroxide exhalation, lipid peroxidation products and degraded proteins, are indeed elevated in COPD patients. As a result, the antioxidant capacity decreases in COPD patients.The fall in antioxidant capacity of blood from COPD patients should not only be regarded as a reflection of the occurrence of oxidative stress but also as evidence that oxidative stress spreads out to the circulation and can therefore generate a systemic effect.COPD is linked to weight loss and in particular to loss in fat-free mass by skeletal muscle wasting. This systemic effect can be mediated by both oxidative stress and oxidative stress-mediated processes like apoptosis and inflammation. Furthermore, COPD is a predisposition for lung cancer through several mechanisms including oxidative stress and oxidative stress-mediated processes such as inflammation and disruption of genomic integrity.Current therapeutic interventions against the far-reaching consequences of the systemic oxidative stress in chronic obstructive pulmonary disease are not yet optimised. A diet designed to reduce chronic metabolic stress might form an effective therapeutic strategy in chronic obstructive pulmonary disease.

show abstract

Oxygen Uptake Kinetics

Poole

Jones

2012

Comprehensive Physiology

416

493

View full text Add to dashboard Cite

Muscular exercise requires transitions to and from metabolic rates often exceeding an order of magnitude above resting and places prodigious demands on the oxidative machinery and O2-transport pathway. The science of kinetics seeks to characterize the dynamic profiles of the respiratory, cardiovascular, and muscular systems and their integration to resolve the essential control mechanisms of muscle energetics and oxidative function: a goal not feasible using the steady-state response. Essential features of the O2 uptake (VO2) kinetics response are highly conserved across the animal kingdom. For a given metabolic demand, fast VO2 kinetics mandates a smaller O2 deficit, less substrate-level phosphorylation and high exercise tolerance. By the same token, slow VO2 kinetics incurs a high O2 deficit, presents a greater challenge to homeostasis and presages poor exercise tolerance. Compelling evidence supports that, in healthy individuals walking, running, or cycling upright, VO2 kinetics control resides within the exercising muscle(s) and is therefore not dependent upon, or limited by, upstream O2-transport systems. However, disease, aging, and other imposed constraints may redistribute VO2 kinetics control more proximally within the O2-transport system. Greater understanding of VO2 kinetics control and, in particular, its relation to the plasticity of the O2-transport/utilization system is considered important for improving the human condition, not just in athletic populations, but crucially for patients suffering from pathologically slowed VO2 kinetics as well as the burgeoning elderly population.

show abstract

Lipid peroxidation in the skeletal muscle of hamsters with emphysema

Cited by 16 publications

References 27 publications

Elastase-induced pulmonary emphysema: insights from experimental models

Elastase-induced pulmonary emphysema: insights from experimental models

Oxidant metabolism in chronic obstructive pulmonary disease

Oxygen Uptake Kinetics

Contact Info

Product

Resources

About