Acute effects of reactive oxygen and nitrogen species on the contractile function of skeletal muscle

Lamb, Graham D.; Westerblad, Håkan

doi:10.1113/jphysiol.2010.199059

Cited by 139 publications

(157 citation statements)

References 48 publications

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“…2, A and C), it is likely that Ca 2ϩ uptake rate could not be reduced (39). Thus, the reduced tension of Tg ϩ EDL was associated with a decreased cross bridge dissociation rate, which could be affected by either NO or ROS as shown in the literature (14,24,38,39). These results suggested that chronic production of TNF-␣ likely affected the cross bridge dissociation rate of Tg ϩ EDL under both PO 2 conditions, consistent with the hypothesis by Reid et al (31) that TNF-␣ negatively affected either myosin ATPase activity or the thin-filament Ca 2ϩ kinetics.…”

Section: Discussionmentioning

confidence: 95%

Effect of pulmonary TNF-α overexpression on mouse isolated skeletal muscle function

Zuo

Nogueira

Hogan

2011

American Journal of Physiology-Regulatory, Integrative and Comp

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Zuo L, Nogueira L, Hogan MC. Effect of pulmonary TNF-␣ overexpression on mouse isolated skeletal muscle function. Am J Physiol Regul Integr Comp Physiol 301: R1025-R1031, 2011. First published June 22, 2011 doi:10.1152/ajpregu.00126.2011.-TNF-␣ is a proinflammatory cytokine that is involved in numerous pathological processes including chronic obstructive pulmonary disease (COPD). In the present study, we used a transgenic mouse model that overexpresses TNF-␣ in the lung (Tg ϩ ) to test the hypothesis that chronic exposure to TNF-␣ (as seen in COPD) reduces skeletal muscle force production and fatigue resistance, particularly under low PO 2 conditions. At 7-12 mo, body and muscle weight of both extensor digitorum longus (EDL) and soleus were significantly smaller in Tg ϩ compared with littermate wild-type (WT) mice; however, the bodyto-muscle weight ratio was not different between groups. EDL and soleus muscles were subjected to in vitro fatiguing contractile periods under high (ϳ550 Torr) and low PO 2 (ϳ40 Torr). Although all muscles were less fatigue-resistant during low PO 2 compared with high PO 2, only the soleus fatigued more rapidly in Tg ϩ mice (ϳ12%) compared with WT at high PO 2. The maximal tension of EDL was equally reduced in Tg ϩ mice (28 -34% decrease from WT under both PO 2 conditions); but for soleus this parameter was smaller only under low PO 2 in Tg ϩ mice (ϳ31% decrease from WT). The peak rate of relaxation and the peak rate of contraction were both significantly reduced in Tg ϩ EDL muscles compared with WT EDL under low PO 2 conditions, but not in soleus. These results demonstrate that TNF-␣ upregulation in the lung impairs peripheral skeletal muscle function but affects fast-and slow-twitch muscles differentially at high and low PO 2.

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Section: Discussionmentioning

confidence: 95%

Effect of pulmonary TNF-α overexpression on mouse isolated skeletal muscle function

Zuo

Nogueira

Hogan

2011

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Although troponin I harbours several cysteine residues, some of these cysteines are insensitive to Ca 2+ -induced conformational changes in native troponin I (Chong and Hodges 1981). Therefore, the impaired contractility could, in part, be unrelated to reduced Ca 2+ concentrations but might instead be due to the oxidation of amino acids in myofilament proteins (Gao et al 1995;Gao et al 1996;Andrade et al 1998Andrade et al , 2001Lamb and Westerblad 2011). In spite of suggestions that SH oxidation of tropomyosin and/or actin in combination with myosin light chain1 (MLC1) (Hertelendi et al 2008) are potential mediators of oxidative myocardial contractile depression, it is currently difficult to clearly state that oxidation of myofilament proteins causes cardiac dysfunction, since studies have reported equivocal effects in different muscle types and even within a single muscle type.…”

Section: Impact Of Oxidative Stress On Cardiomyocyte Stiffness Sarcommentioning

confidence: 99%

A change of heart: oxidative stress in governing muscle function?

Breitkreuz

Hamdani

2015

Biophys Rev

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Redox/cysteine modification of proteins that regulate calcium cycling can affect contraction in striated muscles. Understanding the nature of these modifications would present the possibility of enhancing cardiac function through reversible cysteine modification of proteins, with potential therapeutic value in heart failure with diastolic dysfunction. Both heart failure and muscular dystrophy are characterized by abnormal redox balance and nitrosative stress. Recent evidence supports the synergistic role of oxidative stress and inflammation in the progression of heart failure with preserved ejection fraction, in concert with endothelial dysfunction and impaired nitric oxide-cyclic guanosine monophosphate-protein kinase G signalling via modification of the giant protein titin. Although antioxidant therapeutics in heart failure with diastolic dysfunction have no marked beneficial effects on the outcome of patients, it, however, remains critical to the understanding of the complex interactions of oxidative/nitrosative stress with pro-inflammatory mechanisms, metabolic dysfunction, and the redox modification of proteins characteristic of heart failure. These may highlight novel approaches to therapeutic strategies for heart failure with diastolic dysfunction. In this review, we provide an overview of oxidative stress and its effects on pathophysiological pathways. We describe the molecular mechanisms driving oxidative modification of proteins and subsequent effects on contractile function, and, finally, we discuss potential therapeutic opportunities for heart failure with diastolic dysfunction.

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“…For a detailed description of the potential sources of exercise-induced reactive species production, the reader is referred to specific reviews (Sjodin et al, 1990;Jackson et al, 2007;Sachdev and Davies, 2008;Lamb and Westerblad, 2011;Powers et al, 2011c).…”

Section: Multiple Sources and Tissues Generate Reactive Species Durinmentioning

confidence: 99%

Redox biology of exercise: an integrative and comparative consideration of some overlooked issues

Nikolaidis

Kyparos

Spanou

et al. 2012

Journal of Experimental Biology

124

152

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SummaryThe central aim of this review is to address the highly multidisciplinary topic of redox biology as related to exercise using an integrative and comparative approach rather than focusing on blood, skeletal muscle or humans. An attempt is also made to redefine ʻoxidative stressʼ as well as to introduce the term ʻalterations in redox homeostasisʼ to describe changes in redox homeostasis indicating oxidative stress, reductive stress or both. The literature analysis shows that the effects of non-muscledamaging exercise and muscle-damaging exercise on redox homeostasis are completely different. Non-muscle-damaging exercise induces alterations in redox homeostasis that last a few hours post exercise, whereas muscle-damaging exercise causes alterations in redox homeostasis that may persist for and/or appear several days post exercise. Both exhaustive maximal exercise lasting only 30s and isometric exercise lasting 1-3min (the latter activating in addition a small muscle mass) induce systemic oxidative stress. With the necessary modifications, exercise is capable of inducing redox homeostasis alterations in all fluids, cells, tissues and organs studied so far, irrespective of strains and species. More importantly, ʻexercise-induced oxidative stressʼ is not an ʻoddityʼ associated with a particular type of exercise, tissue or species. Rather, oxidative stress constitutes a ubiquitous fundamental biological response to the alteration of redox homeostasis imposed by exercise. The hormesis concept could provide an interpretative framework to reconcile differences that emerge among studies in the field of exercise redox biology. Integrative and comparative approaches can help determine the interactions of key redox responses at multiple levels of biological organization.Key words: antioxidant, biomarker, eccentric, free radical, training. THE JOURNAL OF EXPERIMENTAL BIOLOGY 1616The ʻgoodʼ (antioxidants), the ʻbadʼ (reactive species) and the ʻuglyʼ (oxidative stress) 1 The distinction drawn in the section heading is schematically used to parody the popular manichaeistic view that antioxidants are considered 'useful' entities, reactive species are considered 'harmful' entities and oxidative stress is considered a 'negative' state. Certainly, the reality is much more complicated and antioxidants, reactive species and oxidative stress can serve both useful and detrimental roles, which are dependent on the biological context (within an organism), which in turn are greatly dependent on the environmental context (outside an organism). AntioxidantsAdmittedly, to define the term 'antioxidant' is a difficult task. In this paper, antioxidant is defined as any mechanism, structure and/or substance that delays, prevents or removes oxidative modifications to a target molecule (Halliwell and Gutteridge, 2007;Pamplona and Costantini, 2011). Antioxidants can be complex molecules such as the superoxide dismutases and peroxiredoxins, or simpler ones such as uric acid and glutathione (Gutteridge and Halliwell, 2010). They can be broa...

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Acute effects of reactive oxygen and nitrogen species on the contractile function of skeletal muscle

Cited by 139 publications

References 48 publications

Effect of pulmonary TNF-α overexpression on mouse isolated skeletal muscle function

Effect of pulmonary TNF-α overexpression on mouse isolated skeletal muscle function

A change of heart: oxidative stress in governing muscle function?

Redox biology of exercise: an integrative and comparative consideration of some overlooked issues

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