The photogeneration of superoxide by isolated photoreaction center from Rhodospirillum rubrum.
Explore the source record for details and available documents.
Aerobiosis↗
Biomedical subjects
F Boucher
Publications and source records attributed to F Boucher.
Monolayer studies of retinyl polyenes. I. Spectroscopic properties.
Explore the source record for details and available documents.
Isomerases↗
Ischemia and reperfusion injury in isolated rat heart: effect of reperfusion duration on xanthine oxidase, lipid peroxidation, and enzyme antioxidant systems in myocardium.
The aim of this work was to assess the catalytic activity of xanthine oxidase, the level of lipid peroxides and enzymic antioxidant systems in isolated rat heart muscle subjected to a globally partial ischemia followed by varying durations of reperfusion. After 40 min of globally partial ischemia (residual perfusion flow rate: 0.1 ml/min), four different durations of reperfusion were investigated (0, 20, 40, and 60 min). After each experimental ischemia/reperfusion sequence, the heart was frozen in liquid nitrogen. Lipid peroxides were assayed in the cardiac homogenate and the catalytic activity of xanthine oxidase and enzymic antioxidant systems (glutathione peroxidase, superoxide dismutase and catalase) were determined in the centrifuged supernatant. In the different experimental protocols studied in this work, there was no significant increase in the activity of cardiac xanthine oxidase or in the level of lipid peroxides when compared to the non reperfused or to the continuously perfused hearts. Indeed, enzymic antioxidant systems were also not significantly modified in the different periods of reperfusion when compared to control hearts (continuously perfused hearts). These results suggest that xanthine oxidase is apparently not a major source of free radicals in the course of an ischemia-reperfusion sequence in heart muscle, in particular, if we consider the early phases of reperfusion. The process of lipid peroxidation, assessed by assaying thiobarbituric acid reactants, is not a predominant phenomenon of reperfusion-induced injury, at least in the experimental model used here. However, enzymic antioxidant systems investigated in this study do not seem modified. This could mean that the small quantity of oxygen free radicals produced does not overwhelm the enzymic antioxidant systems of myocardium which is in agreement with peroxidatized lipid results.
Animals↗
Chronic administration of allopurinol fails to exert any cardioprotective effect in rats submitted to permanent coronary artery ligation.
It has been shown that allopurinol, an inhibitor of xanthine oxidase, may limit the extent of myocardial infarction in dogs. In the present work, we studied the effect of a chronic administration of allopurinol on myocardial infarct size measured histochemically 48 h after in situ left coronary artery ligation in the rat. Our results indicate that allopurinol pretreatment does not produce any limitation of the extent of necrosis, but induces a significant increase in the volume of the non-ischemic portion of the myocardium, accompanied by an increase in protein content. This phenomenon, which could be due to the development of an edema in the non-ischemic portion of the myocardium, may well explain some discrepancies reported in previous experimental studies in which the infarct size was conventionally expressed as a percentage of the total volume of ventricular tissue. We have also shown that allopurinol pretreatment failed to improve the residual cardiac function in rats after left coronary artery ligation. We conclude that the enzyme xanthine oxidase is probably not involved in the pathophysiology of myocardial infarction in the rat because of the absence of collateral vasculature in this species which prevents any oxygen supply to the ischemic zone. In most other mammals such as the dog, the existence of a collateral system maintains a residual blood flow and oxygen supply to the ischemic portion of ligated hearts, allowing the xanthine oxidase-induced production of superoxide anions to be activated, thereby initiating peroxidative lesions in membrane lipids.
Allopurinol↗
Effect of ischemia/reperfusion sequence on cytosolic iron status and its release in the coronary effluent in isolated rat hearts.
The hypothesis that oxygen-derived free radicals play an important role in myocardial ischemic and reperfusion injury has received a lot of support. In the presence of catalytic amounts of transition metals such as iron, superoxide anions, and hydrogen peroxide can be transformed into a highly reactive hydroxyl radical .OH (Haber-Weiss reaction). In view of this, we have undertaken this study to investigate whether iron is involved in the reperfusion syndrome and therefore could aggravate free radicals injury. Coronary effluent iron concentrations and cardiac cytosolic iron levels were evaluated in rat hearts subjected to an ischemia/reperfusion sequences. In the case of total ischemia, iron concentration in coronary effluents peaked immediately in the first sample collected upon reperfusion. However, in the case of partial ischemia, iron concentration in coronary effluents peaked rather exclusively during ischemia period. Cardiac cytosolic iron level augmented significantly after 30 min of total ischemia and non significantly in the other ischemia protocols compared to perfused control hearts. It also appears that the iron released is not protein-bound, and could therefore have a marked catalytic activity. The results of the present study suggest that in the oxygen paradox, iron plays an important role in inducing alterations during reoxygenation.
Animals↗
The interaction between halogenated anaesthetics and bacteriorhodopsin in purple membranes as examined by intrinsic ultraviolet fluorescence.
In the presence of halogenated general anaesthetics such as enflurane and halothane, the spectral properties of the bacteriorhodopsin pigment contained in the purple membranes of Halobacterium halobium are strongly modified. It is reversibly transformed into a red-coloured species absorbing maximally at 480 nm, at the expense of its characteristic 570-nm absorption band. The ultraviolet fluorescence of bacteriorhodopsin has been used to probe the structural modifications that are reflected by this spectral change. Our results show that they are very small and do not perturb the energy transfer dynamics which take place between the aromatic amino acid residues and the retinyl chromophore. The fluorescence properties of anaesthetic-treated bacteriorhodopsin are dominated by the quenching properties of the halogenated hydrocarbon, which are obvious even at anaesthetic concentrations under those needed to induce a spectral change in the bacteriorhodopsin chromophore. This does not rule out direct interaction between anaesthetics and bacteriorhodopsin, but it indicates that the chromophoric site might well not be their primary target.
Bacteriorhodopsins↗
Halogenated general anesthetics in visual photoreceptor membranes as examined by static and dynamic properties of rhodopsin.
The visual pigment rhodopsin was used as an intrinsic probe to measure the effect of incorporation of enflurane into bovine rod outer segment disk membranes. At moderately low enflurane concentration, we find that, while extrinsic probes show little membrane perturbation, rhodopsin may experience large changes with respect to the native lipid-protein interactions which modulate some of its properties. Enflurane induces a small blue shift in the pigment lambda max and a strong inhomogeneity in its photochemical behavior. As a function of enflurane concentration, there appears to be an increasing population of rhodopsin molecules for which the metarhodopsin I-->II transition is blocked, while it is accelerated in the remaining population. Under these conditions, electrophoresis and partial membrane solubilization indicate that an increasing amount of rhodopsin does not behave like a free monomeric species. These results are all consistent with a reduction of the membrane order accompanied by lateral aggregation of rhodopsin in the presence of enflurane. By comparison with the perturbation probed by a spin label, the large molecular environment change experienced by the rhodopsin molecule suggests that enflurane may concentrate at the lipid-protein interface.
Animals↗
Vasodilatory effects of a salen-manganese complex with potent oxyradical scavenger activities.
The effects on rat aorta of EUK-8, a salen-manganese complex with high superoxide dismutase and catalase activities, were investigated. EUK-8 protected the acetylcholine-induced relaxation of rat aortic rings from inhibition by superoxide anions and reduced H2O2-induced relaxation. Moreover, EUK-8 dose-dependently relaxed rat aorta precontracted with phenylephrine (10(-6) M) and decreased the vascular tone of noncontracted aortic rings. The relaxant effect of EUK-8 was significantly potentiated by endothelium abrasion and/or preincubation with N-nitro-L-arginine methyl ester (10(-5) M and 5 x 10(-4) M), an inhibitor of nitric oxide synthase. Indomethacin (10(-5) M) had no effect on the action of EUK-8, showing that it was not dependent on prostacyclin synthesis. Methylene blue (10(-5) M), an inhibitor of soluble guanylate cyclase, partly abolished relaxation induced by EUK-8. Incubation of rat aorta with EUK-8 (10(-4) M) induced an increase in vascular cyclic AMP content. The lack of inhibition by dl-propranolol showed that adenylate cyclase activation by EUK-8 was not mediated through beta-adrenergic receptors. The inhibition of the effects of EUK-8 by tetraethylammonium (10(-2) M) and glibenclamide (10(-5) and 2 x 10(-5) M) showed the implication of potassium channels in the intracellular cascade triggered by EUK-8. The vasorelaxant activity of EUK-8 was neither affected by xanthine oxidase inhibition (incubation with oxypurinol 25 microM) nor by superoxide anion scavenging (incubation with oxypurinol 125 microM). Finally, the ligand for EUK-8 (EUK-8 without manganese), which has the same aromatic structure as EUK-8 without its antioxidant activities because of the absence of manganese, conversely potentiated phenylephrine-induced contraction of aortic rings. We conclude that the vasorelaxant effect of EUK-8 observed under our experimental conditions is essentially mediated through an activation of adenylate cyclase and soluble guanylate cyclase of smooth muscle cells and is different from a classical antioxidant effect of protection of nitric oxide.
Animals↗
[The effect of argan oil on heart function during ischemia and reperfusion].
The aim of this study was to evaluate the effect of organ oil on isolated heart function before and after ischemia and on the activity of cardiac antioxidant enzymes. 16 Wistar rats were divided into 2 groups; control group and treated group receiving 5 mL/kg/day of organ oil. After 8 weeks of treatment, hearts were perfused and subjected to a global ischemia followed by reperfusion. Activity of cardiac antioxidant enzymes was assessed in freeze-clamped hearts at the end of reperfusion. Results showed that organ oil induces: 1--damage to heart function during the preischemic period, 2--decreased functional recovery during reperfusion and 3--significant increase in catalase activity. It seems that, in our experimental conditions, organ oil increases heart sensitivity to ischemia and reperfusion. However, the mechanism involved has yet to be understood.
Animals↗
[Contribution to the study of Mexican marihuana. Preliminary studies: cannabinoids and essential oil (author's transl)].
Explore the source record for details and available documents.
Cannabinoids↗
Modulation by selenium supplementation of lipid peroxidation induced by chronic administration of adriamycin in rats.
Adriamycin (doxorubicin) is an antineoplastic drug used to treat various cancers; however, its chronic use is accompanied by cardiotoxicity. Previous results suggested that free radical formation may contribute to Adriamycin toxicity. Adriamycin-induced cardiotoxicity was examined in rats maintained on either standard or selenium-supplemented diets. Adriamycin was administered intraperitoneally; the cumulative dose was 15 mg/kg body weight. Selenium status, glutathione peroxidase activities, vitamin E, and MDA contents were determined on red blood cell (RBC) and cardiac homogenates. RBC selenium levels and selenium glutathione peroxidase activity were significantly increased in selenium-supplemented animals compared with control or placebo groups. However, Adriamycin-treated rats showed a significant decrease in RBC selenium and selenium glutathione peroxidase compared with the placebo group. Moreover, treatment with Adriamycin increased RBC MDA content, which was attenuated by the selenium supplementation. In parallel, RBC vitamin E decreased markedly in the Adriamycin-treated group and was totally restored by selenium supplementation. Cardiac biochemical analyses confirmed the blood results. Thus, a free radical mechanism does contribute to Adriamycin cardiotoxicity, and shows the importance of balancing selenium levels in Adriamycin-treated subjects to limit Adriamycin's action. A decrease in Adriamycin cardiotoxicity with no concomitant decrease in its antineoplastic activity would considerably improve the therapeutic benefit of the drug.
Animals↗
Protective effect of the superoxide scavenger EUK8 against ultrastructural alterations induced by ischemia and reperfusion in isolated rat hearts.
We have recently shown that iron overload may increase the susceptibility of isolated rat hearts to ischemia and reperfusion, an effect that could be related to an iron-dependent activation of the Fenton reaction, thus producing cytotoxic hydroxyl radicals. The purpose of our study was to investigate the influence of EUK8, a new catalytic scavenger of superoxide anions that is similar to superoxide dismutase, on cardiac ultrastructural alterations associated with reperfusion. Experiments were carried out ex vivo in iron-overloaded rat hearts perfused at a constant flow rate (11 ml/min) with (EUK8) or without (control) EUK8 (50 mumol/L) throughout the perfusion. Hearts were submitted to 15 min global normothermic no-flow ischemia and then reperfused for 15 min before examination. For each heart, six micrographs at a magnification of x 11,300 were used to quantitate ultrastructural alterations. In our experimental model, EUK8 prevented some of the ultrastructural modifications associated with ischemia and reperfusion in iron-overloaded rat hearts. This beneficial effect could be related to the limitation of reperfusion-induced oxygen free radical production under the effect of EUK8.
Animals↗
Oral selenium supplementation in rats reduces cardiac toxicity of adriamycin during ischemia and reperfusion.
The aim of the present study was to assess whether an 8-wk oral selenium supplementation (standard food enriched with 2500 micrograms Se/kg) in rats might prevent the cardiotoxicity of adriamycin (ADR) treatment. ADR was administered at a dose of 2.5 mg/kg body wt intraperitoneally twice weekly for 3 wk. One week after the end of ADR treatment, rats (n = 10 per group) were killed and their hearts were perfused on a Langendorff mode and subjected to a 30-min period of low-flow ischemia (residual flow = 0.1 ml/min) followed by reperfusion (15 min). The results were as follows: 1) selenium supplementation significantly increased the activity of cardiac mitochondrial glutathione peroxidase (GPx) in ADR-treated rats (control: 206 +/- 17.4 IU/g protein; Se: 277 +/- 24.5 IU/g protein, p < 0.05); 2) selenium supplementation reduced myocardial malondialdehyde content in ADR-treated rats (control: 1220 +/- 49.1 nmol/g protein; Se: 1010 +/- 75.9 nmol/g protein; p < 0.05); and 3) ADR treatment significantly increased the degree of reperfusion-induced structural alterations to sarcomeres compared to untreated hearts. Again, this phenomenon was abolished by selenium supplementation. In conclusion, this study demonstrates that selenium supplementation is able to limit ADR cardiotoxicity in isolated rat hearts submitted to a sequence of ischemia/reperfusion.
Animals↗