Prolonged oxidative stress inverts the cardiac force–frequency relation: role of altered calcium handling and myofilament calcium responsiveness

Luo, Jianzhu; Xuan, Yu-Ting; Gu, Yu; Prabhu, Sumanth D.

doi:10.1016/j.yjmcc.2005.09.013

Cited by 40 publications

(31 citation statements)

References 40 publications

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“…O 2 -production in cardiac fibroblasts DETC also reduces the intracellular ROS production in control and ANG II-treated cardiac fibroblasts [97]. Colston et al [177] also reported a decreased ROS production by DETC in adult rat cardiac fibroblasts, while in adult rat cardiac myocytes an increased ROS generation is found [178]. These data indicate that in adult rat cardiac fibroblasts oxidative stress is increased by ANG II, partially through down-regulation of antioxidant enzymes as SOD, and that DETC enhances…”

Section: An Enhancedmentioning

confidence: 87%

Modulation of Reactive Oxygen Species and Collagen Synthesis by Angiotensin II in Cardiac Fibroblasts

Lijnen¹

2011

TOHYPERJ

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Angiotensin II increases the NAD(P)H-dependent superoxide anion production and the intracellular generation of reactive oxygen species in cardiac fibroblasts and apocynin, a NAD(P)H oxidase inhibitor, abrogates this rise. The membrane associated NAD(P)H oxidase complex is the predominant source of superoxide anion and reactive oxygen species generation in angiotensin II-stimulated adult cardiac fibroblasts. Inhibition of this NAD(P)H oxidase complex with apocynin completely blocks the angiotensin II-stimulated collagen production, collagen I and III protein and mRNA expression.Superoxide anion production is also increased by the Cu,Zn-superoxide dismutase (SOD) inhibitor diethyldithiocarbamic acid (DETC) and decreased by the superoxide scavenger tempol in control and ANG II-treated fibroblasts. ANG II and DETC stimulate the collagen production and the collagen I and fibronectin content in fibroblasts. The SOD mimetics tempol and EUK-8 as well as polyethyleneglycol-SOD reduce the collagen production.ANG II also decreases the activity and mRNA and protein expression of the mitochondrial antioxidants Mn-SOD and peroxiredoxin-3. Upon phosphorylation of Akt by ANG II, P-Akt is translocated from the cytoplasm to the nucleus and nuclear phosphorylation of FOXO3a by P-Akt leads to relocalisation of FOXO3a from the nucleus to the cytosol, resulting in a decrease in its transcriptional activity and in Mn-SOD expression. These data indicate that ANG II inactivates FOXO3a by activating Akt and this leads to a reduction in the expression of the antioxidant Mn-SOD. A role of SOD and the formed reactive oxygen species in the regulation and organization of collagen in cardiac fibroblasts is suggested.

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Section: An Enhancedmentioning

confidence: 87%

Modulation of Reactive Oxygen Species and Collagen Synthesis by Angiotensin II in Cardiac Fibroblasts

Lijnen¹

2011

TOHYPERJ

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“…Nevertheless, the oxidative stress and redox status loss plays a critical role in some cellular processes that are important in heart failure, including hypertrophy, impairment of excitation-contraction coupling and contractile dysfunction, reduced myofilament Ca 2? responsiveness and programmed cell death (Choudhary and Dudley 2002;Luo et al 2006;Hidaldo and Donoso 2008).…”

Section: Discussionmentioning

confidence: 99%

Inorganic mercury exposure: toxicological effects, oxidative stress biomarkers and bioaccumulation in the tropical freshwater fish matrinxã, Brycon amazonicus (Spix and Agassiz, 1829)

2009

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Alterations in the antioxidant cellular system have often been proposed as biomarkers of pollutant-mediated toxicity. This study evaluated the effects of mercury on oxidative stress biomarkers and bioaccumulation in the liver, gills, white muscle and heart of the freshwater fish matrinxã, Brycon amazonicus, exposed to a nominal and sub-lethal concentration (~20% of 96 h-LC(50)) of 0.15 mg L(-1) of mercury chloride (HgCl(2)) for 96 h in a static system. Increases in superoxide dismutase, catalase, glutathione peroxidase (GPx), glutathione S-transferase (GST) and glutathione reductase (GR) were observed in all tissues after HgCl(2) exposure, except for white muscle GR activity and hepatic GPx. In the liver and gills, the exposure to HgCl(2) also induced significant increases in reduced glutathione (GSH). Conversely, exposure to HgCl(2) caused a significant decrease in the GSH levels and an increase in the oxidized glutathione (GSSG) content in the white muscle, while both GSH and GSSG levels increased significantly in the heart muscle. Metallothionein concentrations were significantly high after HgCl(2) exposure in the liver, gills and heart, but remained at control values in the white muscle. HgCl(2) exposure induced oxidative damage, increasing the lipid peroxidation and protein carbonyl content in all tissues. Mercury accumulated significantly in all the fish tissue. The pattern of accumulation follows the order gills > liver >> heart > white muscle. In conclusion, these data suggest that oxidative stress in response to inorganic mercury exposure could be the main pathway of toxicity induced by this metal in fish.

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“…The prolonged superoxide anion exposure resulted in inversion and reductions of force-and Ca 2+ -frequency responses, respectively. The prolonged exposure to superoxide anion reduced the dihydropyridine receptor number, but increased Na + -Ca 2+ exchange and the sarcoplasmic reticular (SR) Ca 2+ pump [34] . It was concluded that the reduced Ca 2+ influx via L-type Ca 2+ channels is more determinant of the oxidative stress-mediated Ca 2+ dysregulation than the reduced SR Ca 2+ uptake.…”

Section: Discussionmentioning

confidence: 99%

Superoxide Anion Stress Attenuates the Contractile Response of the Guinea Pig Vas Deferens to ATP and Diadenosine Tetraphosphate

Al-Rawi

Aleisa²,

Khattab³

2008

Pharmacology

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Induction of endogenous superoxide anion stress by the use of the superoxide dismutase inhibitor diethylthiocarbamate (DETCA; 10 mmol/l) produced a potent inhibition of the ATP (0.3–10 mmol/l) and diadenosine tetraphosphate (AP₄A) contractile activity in the isolated vas deferens by 29–92 and 24–90%, respectively. Pyrogallol (0.1 mmol/l), the exogenous superoxide anion generator, produced a significant inhibition on the contractile activity of the vas deferens induced by ATP and AP₄A by 33–89 and 25–82%, respectively. DETCA (10 mmol/l) and pyrogallol (0.1 mmol/l) attenuated the contractile response of isolated guinea pig vas deferens strips to the selective P2X agonist α,β-methyleneATP (α,β-meATP; 50 µmol/l) by 25 and 47%, respectively. In Ca²⁺-free high-K⁺ (80 mmol/l) Krebs solution, pyrogallol and DETCA produced inhibition of the contractile response to α,β-meATP (50 µmol/l) in similar way to that in normal Krebs solution. The further addition of CaCl₂ (1 mmol/l) abolished the inhibitory effects exerted by pyrogallol and DETCA. The control contractile response to α,β-meATP (50 µmol/l) was not affected in Ca²⁺-free high-K⁺ (80 mmol/l) Krebs solution. It may be concluded that superoxide anion stress produces a significant inhibitory effect on both mono- and di-nucleotide purinergic contraction of the vas deferens. Superoxide anion appears to interrupt the P2X₁-mediated transduction cascade at some step(s) of intracellular calcium handling.

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Prolonged oxidative stress inverts the cardiac force–frequency relation: role of altered calcium handling and myofilament calcium responsiveness

Cited by 40 publications

References 40 publications

Modulation of Reactive Oxygen Species and Collagen Synthesis by Angiotensin II in Cardiac Fibroblasts

Modulation of Reactive Oxygen Species and Collagen Synthesis by Angiotensin II in Cardiac Fibroblasts

Inorganic mercury exposure: toxicological effects, oxidative stress biomarkers and bioaccumulation in the tropical freshwater fish matrinxã, Brycon amazonicus (Spix and Agassiz, 1829)

Superoxide Anion Stress Attenuates the Contractile Response of the Guinea Pig Vas Deferens to ATP and Diadenosine Tetraphosphate

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