Using online in vivo chemiluminescence (CL), we studied for the first time continuously the production of reactive oxygen species (ROS) after global cerebral ischemia and the relationship of ROS production to CBF. In anesthetized rats equipped with a closed cranial window, the CL enhancer, lucigenin (1 mM), was superfused onto the brain topically. CL was measured through the cranial window with a cooled photomultiplier, and CBF was measured simultaneously with laser-Doppler flowmetry. Reperfusion after 10 min (n = 8) of global cerebral ischemia led to a CL peak to 188 +/- 77% (baseline = 100%) within 10 +/- 4 min. After 2 h of reperfusion, CL had returned to 102 +/- 28%. Reperfusion after 20 min (n = 8) of ischemia increased CL to 225 +/- 48% within 12 +/- 3 min. After 2 h, CL was still increased (150 +/- 44%, p < 0.05 compared with 10 min of ischemia). CL after 10 min of ischemia was neither affected by brain topical free CuZn-superoxide dismutase (SOD) (100 U/ml, n = 3) nor by i.v. administration of free CuZn-SOD (104 U/kg, followed by 104 U/kg/h, n = 3). The CBF hyperfusion peak on reperfusion preceded the CL peak in all experiments by several minutes. In additional in vitro experiments we investigated the source of CL: Intracellular loading of lucigenin was demonstrated in cultured CNS cells, and a very similar pattern of CL as in the in vivo preparation after ischemia developed in rat brain slices after 15 min of hypoxia, which was unaffected by free CuZn-SOD (100 U/ml) but strongly attenuated by liposome-entrapped CuZn-SOD. We conclude that lucigenin-enhanced CL is a promising tool to study ROS production continuously from the in vivo brain of experimental animals and brain slices, and that the CL signal most likely derives from the intracellular production of superoxide. The production of ROS is preceded by reperfusion, is burst-like, and is dependent on the duration of the ischemic interval.

https://journals.sagepub.com/doi/pdf/10.1038/jcbfm.1995.118

Global cerebral ischemia in the rat: Online monitoring of oxygen free radical production using chemiluminescence in vivo

https://www.gastrojournal.org/article/S0016-5085(99)70568-8/pdf

Glutathione protects the rat liver against reperfusion injury after hypothermic preservation

Preface. Acknowledgments. Evaluation of Mitochondrial Function in Living Cells. 1. Flow Cytometric Analysis of Mitochondrial Function H. Rottenberg. 2. Confocal Microscopy of Mitochondrial Function in Living Cells J.L. Lemasters, et al. 3. Primary Disorders of Mitochondrial DNA and the Pathophysiology of mtDNA-related Disorders E.A. Schon, S. DiMauro. 4. Transmission and Segregation of Mammalian Mitochondrial DNA E.A. Shoubridge. 5. Cardiac Reperfusion Injury: Aging, Lipid Peroxidation, and Mitochondrial Function L.I. Szweda, et al. Mitochondrial Ion Homeostatis and Necrotic Cell Death. 6. Ca2+-Induced Transition in Mitochondria: A Cellular Catastrophe? R.A. Haworth, D.R. Hunter. 7. Physiology of the Permeability Transition Pore M. Zoratti, F. Tombola. 8. Control of Mitochondrial Metabolism by Calcium-dependent Hormones P. Burnett, et al. 9. The Permeability Transition Pore in Myocardial Ischemia and Reperfusion A.P. Halestrap, et al. 10. Mitochondrial Calcium Dysregulation during Hypoxic Injury to Cardiac Myocytes E.J. Griffiths. Apoptosis. 11. Mitochondrial Implication in Cell Death P.X. Petit. 12. Role of Mitochondria in Apoptosis Induced by Tumor Necrosis Factor-alpha C.A. Bradham, et al. 13. The ATP Switch in Apoptosis D.J. McConkey. Mitochondria, Free Radicals and Disease. 14. Reactive Oxygen Generation by Mitochondria A.J. Kowaltowski, A.E. Vercesi. 15. The Role of the Permeability Transition in Glutamate-mediated Neuronal Injury I.J. Reynolds, T.G. Hastings. 16. Mitochondrial Dysfunction in the Pathogenesis of Acute Neural Cell Death G. Fiskum. 17. Varied Responses of CNS Mitochondria to Calcium N. Brustovetsky, J.M. Dubinsky. 18. Mitochondrial Dysfunction in Oxidative Stress, Excitotoxicity, and Apoptosis A.-L. Nieminen, et al. 19. Mitochondria in Alcoholic Liver Disease J.C. Fernandez-Checa, et al. 20. Mitochondrial Depolarization and Permeability Changes after Acute Alcohol H. Higuchi, H. Ishii. 21. Mitochondrial Dysfunction in Chronic Fatigue Syndrome B. Chazotte. Chemical Toxicity. 22. Bile Acid Toxicity G.J. Gores. 23. Reye's Related Chemical Toxicity L.C. Trost, J.J. Lemasters. 24. Purinergic Receptor-mediated Cytotoxicity J.F. Nagelkerke, J.P. Zoetewey. 25. Doxorubicin-induced Mitochondrial Cardiomyopathy K.B. Wallace. 26. Drug-induced Microvesicular Steatosis and Steatohepatitis D. Pessayre, et al.

Mitochondria in Pathogenesis

https://www.gastrojournal.org/article/0016-5085(95)90216-3/pdf

Hepatic free radical production after cold storage: Kupffer cell-dependent and -independent mechanisms in rats.

Low-intensity light therapy (LILT) is showing promise in the treatment of a wide variety of medical conditions. Concurrently, our knowledge of LILT mechanisms continues to expand. We are now aware of LILT's potential to induce cellular effects through, for example, accelerated ATP production and the mitigation of oxidative stress. In clinical use, however, it is often difficult to predict patient response to LILT. It appears that cellular reduction/oxidation (redox) state may play a central role in determining sensitivity to LILT and may help explain variability in patient responsiveness. In LILT, conditions associated with elevated reactive oxygen species (ROS) production, e.g. diabetic hyperglycemia, demonstrate increased sensitivity to LILT. Consequently, assessment of tissue redox conditions in vivo may prove helpful in identifying responsive tissues. A noninvasive redox measure may be useful in advancing investigation in LILT and may one day be helpful in better identifying responsive patien...

Biophoton detection and low-intensity light therapy: a potential clinical partnership.

The influx of extracellular Ca2+ has been postulated to be one of the mediators of ischemia-reperfusion injury. A possible link between Ca2+ influx and oxygen radical generation has also been suggested. In the present study, using the isolated perfused rat liver, we evaluated the role of extracellular Ca2+ on oxygen radical generation, liver damage, and lipid peroxidation during 30 min ischemia and 60 min of reperfusion. Oxygen radical generation in the liver was continuously monitored by lucigenin-enhanced chemiluminescence. Liver damage and lipid peroxidation were evaluated by measuring lactate dehydrogenase (LDH) and thiobarbituric acid reactive substances (TBARS) release into the effusate, respectively. In the absence of extracellular Ca2+ (much less than 30 microM) oxygen radical generation from the liver increased gradually over 2 hr and there were concomitant increases in LDH and TBARS release. When livers were made ischemic and then reperfused, oxygen radical generation increased at the onset of reperfusion and then decreased over 30 min of reperfusion. After 30 min of reperfusion, livers reperfused with low Ca2+ buffer showed a linear increase in oxygen radical generation as well as progressive increases in LDH and TBARS release. On the other hand, livers reperfused with Ca2+ containing (1.25 mM) buffer showed no further increase in oxygen radical generation and no evidence of progressive liver damage and lipid peroxidation. These results suggest that Ca2+ overload is not a primary cause of liver ischemia-reperfusion injury and that the presence of extracellular Ca2+ during reperfusion is necessary to maintain normal liver function.

Role of extracellular Ca2+ in ischemia-reperfusion injury in the isolated perfused rat liver.

Using luminol- and lucigenin-enhanced chemiluminescence (Lm-CL and Lg-CL), we monitored oxygen radical generation during ischemia-reperfusion in the isolated perfused rat liver. Both enhanced chemiluminescence levels decreased during 30 min of ischemia and increased markedly at the onset of reperfusion. When the liver was subjected to another 30 min of ischemia, reperfusion caused a progressive increase in both types of enhanced chemiluminescence. Administration of superoxide dismutase (SOD) into the perfusate strongly attenuated Lm-CL, but had a limited effect on Lg-CL. Catalase (CAT) and allupurionol (ALP) failed to attenuate both types of enhanced chemiluminescence. Thus the predominant oxygen radicals in the liver during reperfusion is superoxide and the lack of effect of ALP on oxygen radical generation indicates that hypoxanthine-xanthine oxidase reaction is unlikely to be a primary source of oxygen radicals. The different response to SOD in Lm-CL and Lg-CL is considered to be based on the diffusion space of luminol and lucigenin in the tissue. The relationship between oxygen radical levels and tissue damage, and the site of oxygen radical detection are discussed.

Oxygen radical generation during ischemia-reperfusion in the isolated perfused rat liver monitored by enhanced chemiluminescence.

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Role of extracellular Ca2+ in ischemia-reperfusion injury in the isolated perfused rat liver.

Oxygen radical generation during ischemia-reperfusion in the isolated perfused rat liver monitored by enhanced chemiluminescence.