Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P06889 (Mol)
630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Leukotrienes formed by the action of 5-lipoxygenase on arachidonic acid are a group of endogenous compounds active in hypersensitivity reactions and inflammation. In this report the formation of LTB4 from LTA4 was measured by incubating lung microsomes from normal and exercised rats to determine whether LTB4 may have a role in the mediation of exercise-induced oxidant stress. Exhaustive exercise in the form of swimming results in the enhanced production of LTB4 in lung microsomes. Further, free radicals measured by ESR spectroscopy were also significantly increased in lung tissue from exercised rats. These results suggest a role for LTB4 in the mediation of lung tissue damage during exercise-induced oxidative stress.
Biochem Mol Biol Int 1997 Mar
PMID:Enhanced production of LTB4 and free radicals in rat lung by exhaustive physical exercise. 909 Apr 73

Alacepril is an inhibitor of the angiotensin converting enzyme (ACE), and is commonly used as an antihypertensive. In this study, the effects of alacepril, its metabolites, desacetylalacepril and captopril, and also lisinopril, which has no sulfhydryl group in the structure, on free radicals were examined in vitro, using an ESR method. Superoxide and hydroxyl radical scavenging activities of alacepril metabolites, desacetylalacepril and captopril, were observed, whereas lisinopril hardly scavenged the superoxide or the hydroxyl radicals. Alacepril and its metabolites did not scavenge nitric oxide, but lisinopril showed slight scavenging activity. These findings suggest that the biological action of alacepril may be partly due to the antioxidant effect of its metabolites, having a sulfhydryl group.
Res Commun Mol Pathol Pharmacol 1997 May
PMID:Free radical scavenging properties of alacepril metabolites and lisinopril. 922 47

The production of radicals was examined in vitro in liver supernatant prepared from LEC rats of different ages before and after the onset of jaundice. Each liver supernatant was subjected to heat-treatment at 90 degrees C for 10 min to remove heat-labile proteins, and then the production of radicals in the resultant supernatant in the presence of hydrogen peroxide and 5,5'-dimethyl-1-pyrroline oxide (DMPO) was studied by ESR. Two sharp ESR signals that completely decayed with time within 5 min after the addition of hydrogen peroxide were observed for the sample prepared from LEC rats before the onset of jaundice, followed by the appearance of four signals of a hydroxyl radical-DMPO adduct after 5 min. On the other hand, in the supernatant prepared from LEC rats after the onset of jaundice, the former two signals were not observed or observed only marginally, and the signals of the hydroxyl radical-DMPO adduct showed a different pattern of decay from that for the supernatant prepared from LEC rats before the onset of jaundice. With the addition of ascorbic acid to the liver supernatant prepared from LEC rats after the onset of jaundice, the former signals of the ascorbate and hydroxyl radicals reappeared. The present results suggest that ascorbate and hydroxyl radicals are produced in the liver of LEC rats with the onset of jaundice, depending on the relative ratio of ascorbic acid and cuprous ions.
Res Commun Mol Pathol Pharmacol 1997 May
PMID:Production of ascorbate and hydroxyl radicals in the liver of LEC rats in relation to hepatitis. 922 48

Three different lipophilic nitroxyl-probes having capability to pass the blood-brain barrier were, for the first time, synthesized to estimate free radical reactions in brain of living animals. Two of the three were designed to be hydrolyzed by esterase and remain in cell. All 3 probes had high n-octanol/buffer partition coefficients and gave 2 signal components in in vivo ESR spectra at head of living mice after intravenous injection. The ESR parameters of 2 components agreed with those of probes dissolved in water and lipidic phases. ESR-CT imaging on the nitroxyl-proves after intravenous injection revealed that all probes presented in both encephalon and extracranial region of head. Tissue distribution of the nitroxyl-probes demonstrated that the newly synthesized lipophilic nitroxyl-probes had capability to pass the blood-brain barrier and accumulated in brain than that of hydrophilic probe.
Biochem Mol Biol Int 1997 Jul
PMID:Synthesis and imaging of blood-brain-barrier permeable nitroxyl-probes for free radical reactions in brain of living mice. 924 22

Chlorella T-1 is a micro algae which carries out highly active photosynthetic carbon fixation. For searching the OH scavenging molecules in this strain, the methanol extract of T-1 was fractionated by RP-HPLC and the fractions were analyzed for DMPO-OH formation by ESR after Fenton reaction. In the course of study, a single chlorella T-1 ingredient was found to enhance the formation of DMPO-OH rather than scavenge in the Fenton system. The OH enhancing chlorella component was further purified by chromatography and finally identified as lactic acid by NMR and LC-MS. From the analysis of the reaction conditions for DMPO-OH, it was found that lactic acid did not serve as direct source of OH but accelerated Fenton reaction.
Biochem Mol Biol Int 1997 Nov
PMID:Identification of Chlorella T-1 ingredient which enhances DMPO-OH adduct formation in Fenton reaction. 938 39

It is now recognized that respiratory muscle fatigue contributes to the development of respiratory failure in some patients with lung disease. This observation has prompted an examination into the mechanisms of development of muscle fatigue, with the understanding that an elucidation of these processes may lead to new therapeutic approaches to the treatment of these patients. A series of recent studies examining this issue have, moreover, discovered that oxygen-derived free radicals generated during strenuous contraction may modulate respiratory muscle contractile function and contribute to the development of muscle fatigue. The data supporting this concept include: (a) direct (e.g. EPR, ESR studies) and indirect (evidence of lipid peroxidation, protein carbonyl formation, glutathione oxidation) evidence that there is heightened free radical production in contracting muscle, (b) evidence that pharmacologic depletion of muscle antioxidant stores increases degree of muscle fatigue present after a period of exercise, and (c) evidence that administration of agents that act as free radical scavengers retard the development muscle fatigue. Free radicals may produce these changes in muscle force generating capacity by interacting with and altering the function of a number of intracellular-biophysical processes (i.e. sarcolemmal action potential propagation, sarcoplasmic reticulum calcium handling, mitochondrial function, contractile protein interactions).
Mol Cell Biochem 1998 Feb
PMID:Free radical induced respiratory muscle dysfunction. 954 53

1. In nonanesthetized rabbits temporal occlusion of the abdominal aorta was used to induce oxidative stress in the lower part of the body including distal segments of the spinal cord. 2. Spinal cord samples were taken from the animals exposed to 25-min aortic occlusion (AO) or to occlusion followed by 1- or 2-hr reperfusion (AO/R1 or AO/R2, respectively) or from sham-operated animals (C). The presence of free radicals (FR) in the spinal cord samples frozen in liquid N2 was assessed by ESR spectroscopy without spin trapping. Moreover, superoxide dismutase (SOD) activity and conjugated diene (CD) levels were measured in the samples. 3. In the AO group FR were detected in the spinal cord regions close to the occlusion (lower thoracic and distal segments) along with a decrease in SOD activity. The calculated g value (g = 2.0291) indicated that the paramagnetic signal recorded might be attributed to superoxide radicals. FR were absent in the AO/R1 group. Concurrently, the SOD activity revealed a significant tendency to return to the control level. FR appeared again in the AO/R2 group, mostly in the upper and middle lumbar regions, along with a decrease in SOD activity. No sample from the C group revealed FR. A significant increase in CD levels was observed in the thoracolumbar region only in the AO/R2 group. The temporary absence of FR in the AO/R1 group suggests activation of defense antioxidant mechanisms (e.g., specific enzymatic systems such as SOD), which might have been exhausted later. 4. Changes in SOD activity similar to those observed in the thoracolumbar region, though less noticeable, occurred in the obviously noncompromised tissue (upper cervical region). This points to a kind of generalized response of the animal to aortic occlusion. 5. Direct ESR spectroscopy revealed the presence of FR as well as their time course in the spinal cord during the early phase of ischemia/reperfusion injury and the inverse relationship between FR and SOD activity.
Cell Mol Neurobiol 1998 Aug
PMID:Free radicals in rabbit spinal cord ischemia: electron spin resonance spectroscopy and correlation with SOD activity. 961 95

The effect of various flavonoids upon the ascorbate radical lifetime was investigated by ESR spectroscopy. The radical was generated via the reaction between ascorbic acid and ascorbate oxidase, the ascorbate radical being detected. The inclusion of the flavonoids in the ascorbic acid-ascorbate oxidase reaction mixture affected both the initial intensity of the ascorbate radical and its lifetime. Of the natural sources tested, Pycnogenol prolonged the ascorbate radical lifetime to the greatest extent, from a control value of 20 min to a maximum of 80 min with 200 micrograms/ml Pycnogenol. The flavonoids could either be regenerating ascorbic acid from ascorbate, or interacting with ascorbate oxidase, thus preventing ascorbic acid binding. When p-cresol, a known ascorbate oxidase inhibitor was added to the ascorbic acid-ascorbate oxidase reaction mixture, the ascorbate radical signal intensity was dramatically reduced and did not display the time-dependent decay observed with the flavonoids. This indicates that a direct interaction between the flavonoids and ascorbate radical occurs. Some of the flavonoids tested; myricetin, polyphenon and theaflavin appeared to compete with ascorbic acid for ascorbate oxidase, as they displayed saturation behaviour. By modifying the experimental conditions the myricetin radical was detected, thus confirming the direct interaction between myricetin and ascorbate oxidase.
Biochem Mol Biol Int 1998 Jul
PMID:ESR studies of vitamin C regeneration, order of reactivity of natural source phytochemical preparations. 967 60

Four dithiocarbamate derivatives of 4-substituted L-proline and N-methyl-L-serine were synthesized, and their iron complexes were prepared in Tris-HCl buffer solution. These complexes were used as spin trapping reagents for nitric oxide in ESR spectrometry, and compared with each other in regard to their spin trapping properties in vivo. When the synthesized complexes were injected to lipopolysaccharide-treated mice intravenously, the nitric oxide adducts were detected both in the liver and in the blood except N-dithiocarboxy-4-(methoxymethyl)oxy-L-proline iron complex, whose nitric oxide adduct was detected mostly in the blood. When the exogenous nitric oxide adduct of this complex was injected, it was not detected in the liver, too. It is considered that this complex can trap nitric oxide in the blood by excluding the accumulation of the nitric oxide adduct in the liver.
Biochem Mol Biol Int 1998 Sep
PMID:Spin trapping for nitric oxide produced in LPS-treated mouse using various new dithiocarbamate iron complexes having substituted proline and serine moiety. 976 11

Post-ischemic reperfusion causes cardiac dysfunction and radical-induced lipid peroxidation (LPO) detectable by ESR spin trapping. This study deals with the applicability of the spin trapping technique to pharmacological investigations during myocardial reperfusion injury. The use of the spin trap phenylbutylnitrone (PBN, 3 mM) in isolated rat hearts demonstrated the release of alkoxyl radicals (aN = 1.39 mT, aHbeta = 0.19 mT) formed particularly within the first 15 min of reperfusion following 30 min of ischemia. The decline of radicals, after 10 min of reperfusion, was accompanied by recovery of function in 80% of the hearts. The radical concentration in the coronary effluent (maximum after 7.5 min) was reduced by the infusion of 1 mM mercaptopropionylglycine (MPG, 2.7+/-0.5 U/ml, p < 0.001) or 5 microM vitamin E (11.7+/-0.8 U/ml, p < 0.001), compared to the (PBN-containing) control (29.7+/-4.3 U/ml). Moreover, functional recovery (left ventricular developed pressure, LVDP 91.6 +/-20% of pre-ischemic level, p < 0.05) was improved by the hydrophilic radical scavenger MPG, compared to the (PBN-containing) control (LVDP 50.5+/-15.7% of baseline). PBN alone led to higher functional recovery (p < 0.05) and reduced VF (duration of ventricular fibrillation; 7.10+/-0.36 min/30 min, p < 0.05), compared to the untreated (PBN-free) control (LVDP 26.6+/-11.8%; VF 19.42+/-3.64 min/30 min). The Ca antagonist verapamil (0.1 microM), MPG, and the lipophilic vitamin E showed cardioprotection in the absence of PBN: post-ischemic recovery of LVDP was 25.4+/-6.8% (p < 0.05), 39.6+/-12.7% (p < 0.05) and 52.4+/-2.6% (p < 0.01), respectively, compared to the corresponding untreated control (13.3+/-6.6%). Whereas verapamil and vitamin E were able to protect the heart when present alone, they offered no additive effect in the presence of PBN. Therefore, PBN can be used to estimate the radical scavenger properties of an agent in the heart. However, because of the protective properties of PBN itself, the results of simultaneous investigations of the effects of other compounds, such as Ca antagonists or lipophilic radical scavengers, on heart function may be limited.
Mol Cell Biochem 1998 Sep
PMID:PBN spin trapping of free radicals in the reperfusion-injured heart. Limitations for pharmacological investigations. 977 91


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