Effects of active oxygen generated by DTTFe2+ on cardiac Na+Ca2+ exchange and membrane permeability to Ca2+

Shi, Zhong; Davison, Allan J.; Tibbits, Glen F.

doi:10.1016/0022-2828(89)90799-2

Cited by 34 publications

(14 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Based on these data, they considered that the redox agents may activate exchange activity by promoting thiol-disulfide interchange in the carrier protein [106]. Shi et al [ 107] reported that exposure of bovine heart sarcolemmal vesicles to 50 gM FeSo 4 plus 1 mM DTT for 1 to 40 min stimulated Na+-Ca 2 § exchange and decreased the apparent Km for Ca 2 § of Na*~-dependent Ca 2 § uptake. Conversley, others [102,[108][109][110] reported that Na+-Ca 2+ exchange activity was reduced by oxygen free radicals.…”

Section: Na+-ca 2+ Exchangementioning

confidence: 99%

Oxygen free radicals and calcium homeostasis in the heart

et al. 1994

View full text Add to dashboard Cite

Many experiments have been done to clarify the effects of oxygen free radicals on Ca 2+ homeostasis in the hearts. A burst of oxygen free radicals occurs immediately after reperfusion, but we have to be reminded that the exact levels of oxygen free radicals in the hearts are yet unknown in both physiological and pathophysiological conditions. Therefore, we should give careful consideration to this point when we perform the experiments and analyze the results.It is, however, evident that Ca 2+ overload occurs when the hearts are exposed to an excess amount of oxygen free radicals. Though ATP-independent Ca 2+ binding is increased, Ca 2+ influx through Ca 2 § channel does not increase in the presence of oxygen free radicals. Another possible pathway through which Ca 2. can enter the myocytes is Na+-Ca 2+ exchanger. Although, the activities ofNa § + ATPase and Na+-H + exchange are inhibited by oxygen free radicals, it is not known whether intracellular Na § level increases under oxidative stress or not. The question has to be solved for the understanding of the importance of Na § Ca z+ exchange in Ca 2+ influx process from extracellular space. Another question is 'which way does Na+-Ca 2+ exchange work under oxidative stress? Net influx or efflux of Ca 2 § ?' Membrane permeability for Ca 2+ may be maintained in a relatively early phase of free radical injury. Since sarcolemmal Ca2+-pumpATPase activity is depressed by oxygen free radicals, Ca 2 § extrusion from cytosol to extracellular space is considered to be reduced. It has also been shown that oxygen free radicals promote Ca 2 § release from sarcoplasmic reticulum and inhibit Ca 2+ sequestration to sarcoplasmic reticulum. Thus, these changes in Ca 2+ handling systems could cause the Ca 2+ overload due to oxygen free radicals. (Mol Cell Biochem 139: 91-100, 1994)

show abstract

Section: Na+-ca 2+ Exchangementioning

confidence: 99%

Oxygen free radicals and calcium homeostasis in the heart

et al. 1994

View full text Add to dashboard Cite

show abstract

“…Kaminishi, Matsuoka, Yanagishita & Kako, 1989;Goldhaber & Liu, 1994) or other free radical generating systems (e.g. Reeves, Bailey & Hale, 1986;Shi et at. 1989).…”

mentioning

confidence: 99%

H2O2‐induced chloride currents are indicative of an endogenous Na(+)‐Ca2+ exchange mechanism in Xenopus oocytes.

Schlief

Heinemann

1995

The Journal of Physiology

View full text Add to dashboard Cite

1. Defolliculated Xenopus oocytes were voltage clamped in bathing solutions containing 115 mM KCl and 1.8 mM CaCl2. External application of H2O2 transiently elicited voltage‐dependent outward rectifying currents within several seconds. Upon depolarization to +50 mV these currents had an activation time constant of 370 ms and reached amplitudes of up to 70 microA. This current was also observed in oocytes without the vitelline membrane. 2. The current was abolished by 500 microM niflumic acid, by the replacement of external Cl‐ by methanesulphonate, or when extracellular Ca2+ was removed indicating the involvement of Ca2+‐activated Cl‐ channels, which are very abundant in Xenopus oocytes. 3. While the current could be recorded in bathing solutions containing Li+, K+, Rb+, Cs+ and NH4+, extracellular Na+ abolished the current completely (IC50 = 6 mM Na+). 4. The H2O2‐induced Cl‐ current was half‐maximally blocked by approximately 25 microM 2'4'‐dichlorobenzamil, 250 microM MgCl2, 100 microM CdCl2 and 100 microM NiCl2. These substances have been shown to block Na+‐Ca2+ exchangers in various tissues. 5. The data are consistent with the existence of an endogenous Na+‐Ca2+ exchanger in the plasma membrane of Xenopus oocytes, which runs in reverse mode in the absence of high external Na+ and the presence of external Ca2+. This endogenous component has to be considered when Xenopus oocytes are used for heterologous expression studies.

show abstract

“…from the extracellular space via the agonist-sensitive Ca 2? -influx pathway, and the non-selective cation channel in cells (Shi et al 1989, Robert et al 1991 (Lu et al 1994;Li and Zhang 1992;Wang et al 1996).…”

Section: Discussionmentioning

confidence: 95%

Guattegaumerine Protects Primary Cultured Cortical Neurons Against Oxidative Stress Injury Induced by Hydrogen Peroxide Concomitant with Serum Deprivation

Lü

et al. 2008

Cell Mol Neurobiol

View full text Add to dashboard Cite

Guattegaumerine is a natural product with characteristics of being lipophilic and reaching high concentration in the brain, but its function in the central nervous system has not yet been observed. This study was designed to evaluate the neuroprotective effects of guattegaumerine on rat primary cultured cortical neurons. Following a 24-h exposure of the cells to combined serum-starvation and hydrogen peroxide, a significant augment in neuron damage as determined by 3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenyl-tetrazolium bromide (MTT) assay and lactate dehydrogenase (LDH) release were observed. Preincubation of guattegaumerine dramatically improved the cell viability and inhibited LDH release. Preincubation of guattegaumerine also dramatically inhibited malondialhehyde (MDA) production and elevated the decreased total antioxidative capacity in cells caused by the combined injury. Results of flow cytometry and immunohistochemistry showed that pre-addition of guattegaumerine interrupted the apoptosis of the neurons, reversed the up regulation of the pro-apoptotic gene (Bax) and the down regulation of the anti-apoptotic gene (Bcl-2). Furthermore, guattegaumerine suppressed the increase of intracellular calcium ([Ca(2+)](i)) stimulated by either H(2)O(2) or KCl in Ca(2+)-containing extracellular solutions, and high concentration of 2.5 microM guattegaumerine also suppressed the increase of [Ca(2+)](i) induced by H(2)O(2) in Ca(2+)-free solution. These observations suggested that guattegaumerine may possess potential protection against oxidative stress injury, which might be beneficial for neurons.

show abstract

Effects of active oxygen generated by DTTFe2+ on cardiac Na+Ca2+ exchange and membrane permeability to Ca2+

Cited by 34 publications

References 24 publications

Oxygen free radicals and calcium homeostasis in the heart

Oxygen free radicals and calcium homeostasis in the heart

H2O2‐induced chloride currents are indicative of an endogenous Na(+)‐Ca2+ exchange mechanism in Xenopus oocytes.

Guattegaumerine Protects Primary Cultured Cortical Neurons Against Oxidative Stress Injury Induced by Hydrogen Peroxide Concomitant with Serum Deprivation

Contact Info

Product

Resources

About