Protective effect of antioxidants against sarcoplasmic reticulum (SR) oxidation by Fenton reaction, however without prevention of Ca-pump activity

In many nonexcitable cells, hormones and neurotransmitters activate Na+ influx and mobilize Ca2+ from intracellular stores. The stores are replenished by Ca2+influx via “store-operated” Ca2+ channels (SOC). The main routes of Na+ entry in these cells are unresolved, and no role for Na+ in signaling has been recognized. We demonstrate that the SOC are a major Na+ entry route in arterial myocytes. Unloading of the Ca2+stores with cyclopiazonic acid (a sarcoplasmic reticulum Ca2+ pump inhibitor) and caffeine induces a large external Na+-dependent rise in the cytosolic Na+ concentration. One component of this rise in cytosolic Na+ concentration is likely due to Na+/Ca2+exchange; it depends on elevation of cytosolic Ca2+ and is insensitive to 10 mM Mg2+ and 10 μM La3+. Another component is inhibited by Mg2+ and La3+, blockers of SOC; this component persists in cells preloaded with 1,2-bis(2-aminophenoxy)ethane- N, N, N′, N′-tetraacetic acid to buffer Ca2+ transients and prevent Na+/Ca2+exchange-mediated Na+ entry. This Na+ entry apparently is mediated by SOC. The Na+ entry influences Na+ pump activity and Na+/Ca2+exchange and has unexpectedly large effects on cell-wide Ca2+ signaling. The SOC pathway may be a general mechanism by which Na+ participates in signaling in many types of cells.

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Negative relationships between erythrocyte Ca-pump activity and lead levels in mothers and newborns

Life Sciences ◽

10.1016/s0024-3205(00)00928-0 ◽

2000 ◽

Vol 68 (2) ◽

pp. 203-215 ◽

Cited By ~ 23

Author(s):

Dave Campagna ◽

Guy Huel ◽

Georgette Hellier ◽

Francoise Girard ◽

Josiane Sahuquillo ◽

...

Keyword(s):

Ca Pump ◽

Pump Activity ◽

Lead Levels ◽

Negative Relationships

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Oxidative injury induced by hypochlorous acid to Ca-ATPase from sarcoplasmic reticulum of skeletal muscle and protective effect of trolox

General Physiology and Biophysics ◽

10.4149/gpb_2009_02_195 ◽

2009 ◽

Vol 28 (2) ◽

pp. 195-209 ◽

Cited By ~ 10

Author(s):

M. Strosova ◽

J. Karlovska ◽

C. Spickett ◽

T. Grune ◽

Z. Orszagova ◽

...

Keyword(s):

Skeletal Muscle ◽

Sarcoplasmic Reticulum ◽

Protective Effect ◽

Hypochlorous Acid ◽

Oxidative Injury

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Short-chain alkanols and the functional efficiency of the Ca pump in the sarcoplasmic reticulum of rabbit skeletal muscles

FEBS Letters ◽

10.1016/0014-5793(88)80888-3 ◽

1988 ◽

Vol 227 (2) ◽

pp. 157-160 ◽

Cited By ~ 5

Author(s):

Vladimir I. Melgunov ◽

Satish Jindal ◽

Marina P. Belikova

Keyword(s):

Sarcoplasmic Reticulum ◽

Skeletal Muscles ◽

Short Chain ◽

Ca Pump ◽

Functional Efficiency ◽

Rabbit Skeletal Muscles

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Effect of Astragalosides on Intracellular Calcium Overload in Cultured Cardiac Myocytes of Neonatal Rats

The American Journal of Chinese Medicine ◽

10.1142/s0192415x05002618 ◽

2005 ◽

Vol 33 (01) ◽

pp. 11-20 ◽

Cited By ~ 26

Author(s):

Dan Meng ◽

Xiang-Jian Chen ◽

Yun-Yun Bian ◽

Ping Li ◽

Di Yang ◽

...

Keyword(s):

Sarcoplasmic Reticulum ◽

Protective Effect ◽

Intracellular Calcium ◽

Cardiac Myocytes ◽

Myocardial Injury ◽

Chinese Herb ◽

Calcium Overload ◽

Neonatal Rats ◽

Active Components ◽

Sod Activity

Astragalosides were the main active components from a native Chinese herb Astragalus membranaceus. Recent studies have shown that Astragalosides have a protective effect on myocardial injury in rats. The present study was designed to investigate the effect of Astragalosides on intracellular calcium overload and sarcoplasmic reticulum calcium load (SR Ca 2+ load) in cultured cardiac myocytes from neonatal rats. Astragalosides (100 μg/ml) were incubated in the presence of isoproterenol (ISO) (10-5 M) for 72 hours in cardiomyocytes. Metoprorol (10-6 M), a β1-selective antagonist, was cultured in the same condition as Astragalosides. The result showed that intracellular calcium concentration ([ Ca 2+] i ) and SR Ca 2+ load increased in ISO-treated cardiac myocytes as compared to control (P<0.01). Astragalosides prevented ISO-induced increase in [ Ca 2+] i and SR Ca 2+ load. Metoprolol also inhibited those increase. The mRNA expression and activity of sarcoplasmic reticulum Ca 2+ ATPase (SERCA) were enhanced following ISO treatment in cardiac myocytes, and these increases were inhibited by Astragalosides or metoprolol (P<0.05). The decrease of superoxide dismutase (SOD) activity and the elevation of intracellular maleic dialdehyde (MDA) were observed after ISO treatment in cardiac myocytes. Both Astragalosides and metoprolol restored the SOD activity and reduced the level of MDA. We conclude that Astragalosides have the effects on reducing [ Ca 2+] i and SR Ca 2+ load, enhancing free radical removal and decreasing lipid peroxidation in ISO-treated cardiomyocytes, which might account for their protective effect on myocardial injury.

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Myocardial calcium cycling defect in furazolidone cardiomyopathy

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y91-271 ◽

1991 ◽

Vol 69 (12) ◽

pp. 1833-1840 ◽

Cited By ~ 6

Author(s):

Peter James O'Brien ◽

Hua Shen ◽

Janice E. Weiler ◽

S. Mehdi Mirsalimi ◽

Richard J. Julian

Keyword(s):

Heart Failure ◽

Congestive Heart Failure ◽

Sarcoplasmic Reticulum ◽

Ruthenium Red ◽

Channel Activity ◽

Release Channel ◽

Calcium Sequestration ◽

Pump Activity ◽

Highly Correlated ◽

Sarcoplasmic Reticulum Calcium

We have previously demonstrated that in furazolidone-induced congestive heart failure in turkeys the specific Ca2+-ATPase activity of myocardial sarcoplasmic reticulum (SR) is 60% increased in compensation for a 50% depression in net Ca2+-sequestration activity. This study tested the hypothesis that SR Ca2+-uptake and Ca2+-ATPase activities were uncoupled in this cardiomyopathy because of increased Ca2+-release channel activity. A novel microassay was used to monitor Ca2+ transport by myocardial homogenates using the fluorescent Ca2+ dye indo 1 to indicate extravesicular ionized Ca2+. The method is applied to cyropreserved biopsy specimens of myocardium and requires only 50 mg tissue. Both SR Ca2+-pump and SR Ca2+-channel activity were estimated using the channel-inhibitor ruthenium red (RR) and the mitochondrial inhibitor sodium azide. The specificity of the RR inhibition was confirmed using ryanodine. Cardiomyopathy was induced in 2-week-old turkey pouits by the addition of 0.07% furazolidone to their feed for 4 weeks. Compared with controls, myocardial maximal Ca2+-channel activity relative to maximal Ca2+-pump activity was 22% greater and duration of Ca2+-channel activity was 100% increased. However, the heart failure birds had 43 and 53% decreases in absolute maximal Ca2+-pumping and Ca2+-channel activities, respectively. The abnormal Ca2+-channel activity resulted in 200% greater time before initiation of net Ca2+ sequestration and 700% greater final myocardial Ca2+ concentrations. For all birds, the Ca2+-accumulating activity was highly correlated with Ca2+-release activity (all p < 0.05). These data indicate that in this animal model of congestive heart failure there is defective SR Ca2+-channel function resulting in abnormal Ca2+ homeostasis. However, this defect can only partially explain our previous finding of furazolidone-induced uncoupling of Ca2+ uptake from Ca2+-ATPase activities. The consequent myocardial Ca2+ overload predisposes the heart to fatigue and irreversible failure.Key words: sarcoplasmic reticulum, calcium sequestration, furazolidone cardiomyopathy, indo 1 spectrofluorometry.

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