Oxygen radical-mediated lipid peroxidation and inhibition of Ca2+-ATPase activity of cardiac sarcoplasmic reticulum

Kukreja, Rakesh C.; Okabe, Eiichiro; Schrier, Gayle M.; Heß, Michael

doi:10.1016/0003-9861(88)90361-x

Cited by 143 publications

(43 citation statements)

References 34 publications

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“…IA and 2A). Previously, we have shown that the signal produced by DHF/Fe3+-ADP was replaced by the ethanol-radical adduct, characteristic of ethanol scavenged 'OH radical, verifying that the DMPO-OH signal was, in fact, spin trapped 'OH radical (12). The data of Figs.…”

Section: Spin-trapping Of Hydroxyl Radicalsupporting

confidence: 65%

Mechanisms of the Hypolipidemic Effect of NIP-200 in Rats

Sakashita

Toyoda

Kitahara

et al. 1993

Japanese Journal of Pharmacology

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ABSTRACT-To understand the direct involvement of hydroxyl radical ('OH) in the modification of func tional reactivity in isolated rabbit lingual artery ring preparations, this study was undertaken to examine the effect of 'OH generated from dihydroxy fumarate (DHF) plus Fe31-ADP or from H202 plus FeSO4. When vasodilators (acetylcholine and nitroglycerin) were given after the 'OH-generating system was removed from the organ chamber, the earlier 'OH exposure produced an attenuation of the ring relaxation induced by acetylcholine but not that by nitroglycerin. Moreover, the earlier 'OH exposure attenuated caffeine induced contraction and depressed the phasic response, but potently enhanced the tonic response of norepinephrine-induced contraction. Both the enhanced tonic response of KC1-induced contraction pro duced by earlier 'OH exposure and norepinephrine-induced contraction was inhibited by nisoldipine. These results are consistent with the view that 'OH radicals can potentiate the voltage-dependent influx of Ca. It is also postulated that 'OH may damage sarcoplasmic reticulum (SR) function in the smooth muscle cells, thus reducing Ca release from the SR (this may be reflected by the attenuation of the phasic response), and may selectively attenuate endothelium-dependent relaxation as opposed to endothelium-independent relaxation.

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Section: Spin-trapping Of Hydroxyl Radicalsupporting

confidence: 65%

Mechanisms of the Hypolipidemic Effect of NIP-200 in Rats

Sakashita

Toyoda

Kitahara

et al. 1993

Japanese Journal of Pharmacology

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“…Unsaturated fatty acids are particularly susceptible to oxygen radical attack, owing to the presence of double bonds which can undergo peroxidation through a chain of oxidative reactions (12). Studies performed in vitro suggest that exposure to oxygen radicals results in peroxidation of membrane lipids, which is accompanied by damage to cellular organelles and to membrane-bound enzymes (13)(14)(15)(16). If a similar mechanism were also operative in vivo, increased levels oflipid peroxidation products should be found in reperfused hearts as a consequence of oxygen radical formation at reflow.…”

Section: Introductionmentioning

confidence: 99%

Oxygen radicals generated at reflow induce peroxidation of membrane lipids in reperfused hearts.

Ambrosio

Flaherty²,

Duilio³

et al. 1991

J. Clin. Invest.

245

120

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To test whether generation of oxygen radicals during postischemic reperfusion might promote peroxidation of cardiac membrane lipids, four groups of Langendorff-perfused rabbit hearts were processed at the end of (a) control perfusion, (b) 30 min of total global ischemia at 370C without reperfusion, (c) 30 min of ischemia followed by reperfusion with standard perfusate, (d) 30 min of ischemia followed by reperfusion with the oxygen radical scavenger human recombinant superoxide dismutase (h-SOD). The left ventricle was homogenized and tissue content of malonyldialdehyde (MDA), an end product of lipid peroxidation, was measured on the whole homogenate as well as on various subcellular fractions. Reperfusion was accompanied by a significant increase in MDA content of the whole homogenate and of the fraction enriched in mitochondria and lysosomes. This phenomenon was not observed in hearts subjected to ischemia but not reperfused, and was similarly absent in those hearts which received h-SOD at reflow. Reperfused hearts also had significantly greater levels of conjugated dienes (another marker of lipid peroxidation) in the mitochondrial-lysosomal fraction. Again, this phenomenon did not occur in ischemic hearts or in reperfused hearts treated with h-SOD. Unlike the effect on tissue MDA and conjugated dienes, reperfusion did not significantly stimulate release of MDA in the cardiac effluent. Treatment with h-SOD was also associated with significant improvement in the recovery ofcardiac function. In conclusion, these data directly demonstrate that postischemic reperfusion results in enhanced lipid peroxidation of cardiac membranes, which can be blocked by h-SOD, and therefore is most likely secondary to oxygen radical generation at reflow. (J. Clin.

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“…13 Their study demonstrated a direct correlation between the production of reactive oxygen species and an early increase in intracellular calcium in neonatal cardiomyocytes, but they did not examine the function and state of the sarcoplas-mic reticulum (SR) as a regulator of intracellular calcium. The SR is one of the major target organelles injured by oxygen radicals [14][15][16] and most experiments investigating the SR have been conducted in vitro. To our knowledge, there have been no reported studies in which both the generation of oxygen radicals and the function of SR were measured during the same experimental conditions in vivo.…”

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confidence: 99%

Generation of Free Radicals and the Damage Done to the Sarcoplasmic Reticulum During Reperfusion Injury Following Brief Ischemia in the Canine Heart

et al. 1999

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Free radical generation was studied by the electron spin resonance (ESR) technique using -phenyl N tert butyl nitrone (PBN) in a brief ischemia-reperfusion model of the canine heart, and correlated with biochemical changes of the sarcoplasmic reticulum (SR). ESR spectra (aH = 0.3-0.4 mT, aN = 1.43-1.58 mT) were observed as PBN spin adducts, which peaked at levels 5-fold above the control levels at 5 min after reperfusion. The simulated coupling constants of PBN spin adducts suggested that the sample should contain at least 2 carbon-centered radicals at 5 min after reperfusion (radical A: aH = 0.350 mT, aN = 1.485 mT; radical B: aH = 0.370 mT, aN = 1.615 mT). At this time point, a significant reduction in Ca-ATPase activity of the SR was found without degradation of the major ATPase protein. Superoxide dismutase (SOD) significantly reduced the intensity of the PBN spin adduct signals and preserved the Ca-ATPase activity of the SR to 80% of the control level. Reperfusion injury after brief ischemia may be the result of inactivation of intracellular Ca-ATPase by free radicals generated during reperfusion, and SOD contributes to the protective effect by scavenging the radicals. (Jpn Circ J 1999; 63: 373 -378)

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Oxygen radical-mediated lipid peroxidation and inhibition of Ca2+-ATPase activity of cardiac sarcoplasmic reticulum

Cited by 143 publications

References 34 publications

Mechanisms of the Hypolipidemic Effect of NIP-200 in Rats

Mechanisms of the Hypolipidemic Effect of NIP-200 in Rats

Oxygen radicals generated at reflow induce peroxidation of membrane lipids in reperfused hearts.

Generation of Free Radicals and the Damage Done to the Sarcoplasmic Reticulum During Reperfusion Injury Following Brief Ischemia in the Canine Heart

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