Cellular responses to H2O2 and bleomycin-induced oxidative stress in L6C5 rat myoblasts

Caporossi, Daniela; Ciafrè, Silvia Anna; Pittaluga, Monica; Savini, Isabella; Farace, Maria Giulia

doi:10.1016/j.freeradbiomed.2003.08.008

Cited by 62 publications

(24 citation statements)

References 48 publications

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“…3f, h). In accordance with recent in vitro observations (Caporossi et al 2003), in this setting ROS was interpreted as a physiological modulator of skeletal muscle functions independent of bleomycin toxicity.…”

Section: Ros Demonstrationsupporting

confidence: 89%

In situ assessment of oxidant and nitrogenic stress in bleomycin pulmonary fibrosis

Inghilleri

Morbini

Oggionni

et al. 2005

Histochem Cell Biol

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Reactive oxygen species (ROS) and nitric oxide (NO) have a role in the development of pulmonary fibrosis after bleomycin administration. The ROS production induces an antioxidant response, involving superoxide dismutases (SODs), catalase, and glutathione peroxidases. We compared in situ oxidative burden and antioxidant enzyme activity in bleomycin-injured rat lungs and normal controls. ROS expression and catalase, glucose-6-phosphate-dehydrogenase (G6PHD), and NOS/NADPH-diaphorase activity were investigated by using histochemical reactions. Nitric oxide synthase (e-NOS and i-NOS) and SOD (MnSOD, Cu/ZnSOD, ECSOD) expression was investigated immunohistochemically. After treatment ROS production was enhanced in both phagocytes and in type II alveolar epithelial cells. Mn, Cu/Zn, and ECSOD were overexpressed in parenchymal cells, whereas interstitium expressed ECSOD. Catalase and G6PHD activity was moderately increased in parenchymal and inflammatory cells. NOS/NADPH-d activity and i-NOS expression increased in alveolar and bronchiolar epithelia and in inflammatory cells. It can be suggested that the concomitant activation of antioxidant enzymes is not adequate to scavenge the oxidant burden induced by bleomycin lung damage. Inflammatory cells and also epithelial cells are responsible of ROS and NO production. This oxidative and nitrosative stress may be a substantial trigger in TGF-beta1 overexpression by activated type II pneumocytes, leading to fibrotic lesions.

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Section: Ros Demonstrationsupporting

confidence: 89%

In situ assessment of oxidant and nitrogenic stress in bleomycin pulmonary fibrosis

Inghilleri

Morbini

Oggionni

et al. 2005

Histochem Cell Biol

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“…Excessive oxidative stress is able to induce a delay in myoblast proliferation [45] and extensive inflammatory response alters differentiation. Because oxidative stress and low grade of systemic inflammation have been reported in COPD [46-48], this ambient milieu could promote dysfunctional proliferation pattern of satellite cells in COPD.…”

Section: Discussionmentioning

confidence: 99%

Regenerative defect in vastus lateralis muscle of patients with chronic obstructive pulmonary disease

et al. 2014

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BackgroundImpaired skeletal muscle regeneration could contribute to the progression of muscle atrophy in patients with chronic obstructive pulmonary disease (COPD).MethodsSatellite cells and myogenesis-related proteins were compared between healthy subjects and patients with COPD, with or without muscle atrophy. Satellite cells were isolated and cultured to assess their proliferative and differentiation aptitudes.ResultsAlthough satellite cell numbers in muscle samples were similar between groups, the proportion of muscle fibers with central nuclei was increased in COPD. In muscle homogenates, increased expression of MyoD and decreased expression of myogenin and MRF4 were observed in COPD. In cultured satellite cells of patients with COPD, increased protein content was observed for Pax7, Myf5 (proliferation phase) and myogenin (differentiation phase) while myosin heavy chain protein content was significantly lower during differentiation.ConclusionIn COPD, the number of central nuclei was increased in muscle fibers suggesting a greater number of attempts to regenerate muscle tissue than in healthy subjects. Myogenesis signaling was also altered in muscle homogenates in patients with COPD and there was a profound reduction in the differentiation potential in this population as indicated by a reduced ability to incorporate myosin heavy chain into newly formed myotubes. Collectively, these results indicate that skeletal muscle regenerative capacity termination is impaired in COPD and could contribute to the progression of muscle atrophy progression in this population.

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“…However, the concentration of H 2 O 2 used in experiments differs widely in different cell types. In experiments conducted using myoblasts, a low concentration (1–10 μM) of H 2 O 2 was found to enhance growth, while moderate and high concentrations (50–300 μM) were detrimental to the cells (Caporossi et al 2003; Orzechowski et al 2002; Shao et al 2012). …”

Section: Methodsmentioning

confidence: 99%

A comparison of melatonin and α-lipoic acid in the induction of antioxidant defences in L6 rat skeletal muscle cells

Favero

Rodella

Nardo

et al. 2015

AGE

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Aging is characterized by a progressive deterioration in physiological functions and metabolic processes. The loss of cells during aging in vital tissues and organs is related to several factors including oxidative stress and inflammation. Skeletal muscle degeneration is common in elderly people; in fact, this tissue is particularly vulnerable to oxidative stress since it requires large amounts of oxygen, and thus, oxidative damage is abundant and accumulates with increasing age. Melatonin (N-acetyl-5-methoxytryptamine) is a highly efficient scavenger of reactive oxygen species and it also exhibits beneficial anti-inflammatory and anti-aging effects. This study investigated the susceptibility of rat L6 skeletal muscle cells to an induced oxidative stress following their exposure to hydrogen peroxide (50 μM) and evaluating the potential protective effects of pre-treatment with melatonin (10 nM) compared to the known beneficial effect of alpha-lipoic acid (300 μM). Hydrogen peroxide-induced obvious oxidative stress; it increased the expression of tumour necrosis factor-alpha and in turn promoted nuclear factor kappa-B and overrode the endogenous defence mechanisms. Conversely, pre-treatment of the hydrogen peroxide-exposed cells to melatonin or alpha-lipoic acid increased endogenous antioxidant enzymes, including superoxide dismutase-2 and heme oxygenase-1; moreover, they ameliorated significantly oxidative stress damage and partially reduced alterations in the muscle cells, which are typical of aging. In conclusion, melatonin was equally effective as alpha-lipoic acid; it exhibited marked antioxidant and anti-aging effects at the level of skeletal muscle in vitro even when it was given in a much lower dose than alpha-lipoic acid.

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Cellular responses to H2O2 and bleomycin-induced oxidative stress in L6C5 rat myoblasts

Cited by 62 publications

References 48 publications

In situ assessment of oxidant and nitrogenic stress in bleomycin pulmonary fibrosis

In situ assessment of oxidant and nitrogenic stress in bleomycin pulmonary fibrosis

Regenerative defect in vastus lateralis muscle of patients with chronic obstructive pulmonary disease

A comparison of melatonin and α-lipoic acid in the induction of antioxidant defences in L6 rat skeletal muscle cells

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