PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Free radicals”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1993

Diabetes mellitus and free radicals. Free radicals, transition metals and oxidative stress in the aetiology of diabetes mellitus and complications.

Diabetes mellitus is a syndrome initially characterized by a loss of glucose homeostasis. The disease is progressive and is associated with high risk of atherosclerosis, kidney and nerve damage as well as blindness. Abnormalities in the regulation of peroxide and transition metal metabolism are postulated to result in establishment of the disease as well as its longer term complications. Diabetes mellitus is associated with oxidative reactions, particularly those which are catalyzed by decompartmentalized transition metals, but their causative significance in diabetic tissue damage remains to be established.

Alloxan↗
PubMed1989

[The role of oxygen free radical and free radical scavenger in septic and hemorrhagic shock].

The roles of oxygen free radical (O2-), lipoperoxide (LPO) and free radical scavenger were clinically and experimentally studied in septic and hemorrhagic shock. The reduction of hepatic tissue blood flow (TBF) were equalized in two groups (40-55% of normal level) and rats were subdivided into 3 groups: untreated, normal saline (NS) continuous IV and superoxide dismutase: SOD + catalase (S/c) continuous IV as free radical scavenger. The change of TBF, destruction of mitochondrial structure and elevation of LPO were prevented by S/c in Et shock. No significant effect by S/c was observed in hemorrhagic shock. The neutrophil derived O2- was markedly elevated in Et shock animals as well as septic shock patients but no significant change was noted in hemorrhagic shock animals or non septic shock patient. SOD and catalase were effective for neutrophil derived O2- in septic shock whereas little beneficial effect was noted in hemorrhagic or non septic shock.

Animals↗
PubMed1996

Influence of oxygen free radicals and free radical scavengers on the growth behaviour and oxidative tissue damage of bovine retinal pigment epithelium cells in vitro.

PURPOSE: This investigation was carried out to ascertain whether oxygen free radicals can influence the growth behaviour and consecutive lipid peroxidation of retinal pigment epithelium (RPE) cells in vitro and whether scavengers can counteract these effects. METHODS: The experimental model was based on calf RPE cells. Hypoxanthine/xanthine oxidase (HX/XO) and superoxide dismutase/ catalase (SOD/CAT) served as the radical generating system and scavengers, respectively. The components were tested alone and in combination. Lipid peroxides were determined in culture supernatants by a thiobarbituric acid assay. RESULTS: Concentrations of up to 100 mumol/l of HX alone and 500/ 1000 microU of XO alone, as well as the application of the scavengers without the radical generating system (HX/XO), had no effect. Dose-related reduction of cell growth and increase of lipid peroxidation were found with HX/XO treatment (single dose of 500 and 1000 microU/ml 24 h after seeding). After application of 500 or 1000 microU/ml of XO, CAT, when given alone (1200 U/ ml), counteracted the effect of the radicals on cell growth and lipid peroxidation; SOD (300 U/ml) had no effect. A combination of SOD and CAT was no better than the effect of CAT alone. CONCLUSION: The prevention of radical-induced reduction of cell growth and lipid peroxidation by scavengers supports trials of therapy using antioxidants and/or free radical scavengers for various ocular syndromes with RPE involvement.

Animals↗
PubMed1988

The significance of free radicals and free radical scavengers in L1210 leukemia.

L1210 leukemia is a murine leukemia which is associated with anemia and marked neutrophilia. In order to determine the significance of free radicals (FR) in this disorder, we determined the presence and localization of free radical scavengers (FRS) and scavenger-like systems in L1210 leukemia cells obtained in vivo and from in vitro cultures. FR are metabolized or detoxified by certain FRS such as glutathione (GSH and GSSG), superoxide dismutase (SOD) and enzymes such as epoxide hydrolase (EH). In all cases specific fractions of L1210 cells, bone marrow and liver were examined for FR/FRS levels. Reduced (GSH) and oxidized (GSSG) glutathione were measured fluorometerically using o-opthalaldehyde (OPT). SOD was determined colorimetrically utilizing pyrogallol by substrate autolysis inhibition, and EH was determined by utilizing [3H] styrene oxide as a substrate. Ratios of GSH/GSSG in fractions prepared from in vivo and in vitro L1210 cells showed a predominance of GSH-reductase with the highest activity in mitochondria (ratio = 15 vs. 10). Normal liver showed a similar pattern whereas, leukemic liver showed altered GSH/GSSG ratios in mitochrondria and microsomes. Leukemic bone marrow showed a predominance of GSH-reductase in all fractions. EH activity was highest in microsomal fractions obtained from L1210 cells grown in vitro and found to become increased in both the mitrochondrial (100%) and microsomal (200%) fractions when cells were exposed to retinoic acid (RA) in culture. SOD activity in the cytosolic (21.2 U SOD/mg) and mitochondrial (12 U SOD/mg) fractions whereas, leukemic liver showed a significant decrease in activity in all fractions compared to normals. SOD was determined in fractions taken from L1210 cells in vivo and in vitro. Results demonstrated detectable but reduced SOD activity in the L1210 cell fractions as contrasted with liver activity. Results from these studies indicate that certain FRS systems are functional in L1210 leukemic animals. Furthermore, variations in the ratios or levels may be of significance in the leukemic and hematological states.

Animals↗
PubMed1988

Plant senescence processes and free radicals.

Free radicals acting at sensitive subcellular sites, appear to play a pivotal role in both the deleterious and beneficial effects of maturation and senescence of various plant organs--leaves, flowers, and fruit. As evidenced by ESR spectrometry, spin trapping, specific membrane phase transition studies and enzyme kinetics, an important factor in the above processes appears to be lipoxygenase activity producing polyunsaturated fatty acid (PUFA) hydroperoxides and subsequently several free radical species and senescence-promoting compounds such as ethylene, malondialdehyde and jasmonic acid. The most intensely investigated are the oxy-free radical species including O2-., .OH, RO., ROO., PUFA and semiquinone free radicals. Higher plants are equipped with ways and means to combat free radicals and these may be classified under two general headings; (a) direct scavengers including SOD, ascorbic acid, and alpha-tocopherol acting in concert (b) incipient preventative mechanisms against radical formation, these include xanthine oxidase inhibitors, strategies based on endogenous H2O2 disposal in the form of peroxidative enzymes and glutathione turnover, and Ca2+ channel blockers. The antisenescence phytohormone cytokinin appears to possess a dual effect and may act in both capacities. The special case of delayed free radical formation in comparatively dry biological systems such as seeds is detailed, and specific free radical-generating photosensitizer compounds are also discussed.

Free Radicals↗
PubMedDate not supplied

Cimetidine as a scavenger of ethanol-induced free radicals.

Free radical generation and the mobilization of catalytic iron are important in the pathogenesis of alcohol-induced liver injury. Cimetidine is a free radical scavenger in thermal skin injury and cobra venom-induced lung injury, and was therefore investigated as a scavenger of ethanol-induced free radicals. In vitro cimetidine inhibited iron-mediated cleavage of DNA as well as the potentiation of such cleavage by bleomycin. Peroxidation of microsomes by xanthine-xanthine oxidase, acetaldehyde-xanthine oxidase, as well as by the addition of low-molecular weight iron chelates were inhibited (17-100%) by cimetidine (0.1-1 mM). Free radical generation due to ethanol in isolated rat hepatocytes was studied by measuring ethane and pentane production. Cimetidine (1 mM) significantly decreased ethane and pentane production due to ethanol: 1 mM (2.2 +/- 0.3 vs. 1.0 +/- 0.2 pmol ethane per 10(6) cells/h; p less than 0.01, 4.2 +/- 0.4 versus 1.6 +/- 0.3 pmole per 10(6) cells/h pentane; p less than 0.001). Similar inhibitions were observed in the isolated perfused liver. Studies of superoxide reduction of ferricytochrome-C as well as hydroxyl radical generation by Fe(+)+/EDTA/ascorbate revealed that cimetidine was an effective hydroxyl radical scavenger. In summary, in a variety of in vitro systems, as well as in isolated hepatocytes and perfused liver, cimetidine inhibits ethanol-induced free radical injury. These findings may warrant its investigation as a therapeutic agent.

Animals↗
PubMed2002

The dopamine agonist cabergoline provides neuroprotection by activation of the glutathione system and scavenging free radicals.

Free radicals are involved in the pathogenesis and/or progression of Parkinson's disease (PD). Several ergot derivative dopamine (DA) agonists have been reported to scavenge free radicals in vitro and to show a neuroprotective effect in vivo. We investigated the in vitro free radical scavenging and antioxidant activities of cabergoline, a long-acting ergot DA agonist, as well as its ability to activate glutathione (GSH), catalase (Cat) and superoxide dismutase (SOD) activating effects and its in vivo neuroprotective properties against 6-hydroxydopamine (6-OHDA) intracerebroventricularly (i.c.v.) in mice. The striatal DA turnover induced by i.c.v. injection of 6-OHDA was completely normalized by pretreatment with cabergoline. Moreover, cabergoline scavenged free radicals in vitro and significantly reduced lipid peroxidation in vitro and in vivo. Furthermore, daily administration of cabergoline to mice significantly increased striatal GSH levels by activation of RNA expressions of GSH-related enzymes, although striatal Cat and SOD activities did not change. In addition, our present results suggest that repeated administration of cabergoline attenuates both 6-OHDA-induced nigrostriatal DAergic dysfunction and DA neuronal cell death, since cabergoline also had a neuroprotective effect in the immunohistochemical experiment. In conclusion, our findings indicate that the multiple antioxidant mechanisms of cabergoline, such as activation of the GSH system and the direct free radical scavenging activity, may explain the neuroprotective effect of this ergot DA agonist.

Aminoacyltransferases↗
PubMed1993

[Free radicals].

Free radicals are continuously threatening living organs. Firstly generated by endogenic pathway during normal and vital metabolic reactions, they can be also produced by environmental factors: atmospheric pollution, radiations... An energetic source ensures the initiation of free radicals reaction. Its expanding is strengthened by oxygen (bi-radical form) and transition metals (chiefly iron). Eyes are very sensitive organs to the deleterious action from the oxygen active species. Protection systems against free radicals action are necessary in living cells. A part the pathologic or ageing conditions, oxygen toxicity doesn't; in fact, neutralised by protection systems coming from enzymes (endogenic way) and food contribution: vitamins, carotenoids, flavonoids... (exogenic way).

Antioxidants↗
PubMedDate not supplied

Free radicals.

Free radicals may be the cause of many neonatal complications, such as chronic lung disease and brain injury. Treatment options for these complications using antioxidants are being evaluated through research. This article begins with a review of the basic science of free radicals. It then discusses neonatal complications potentially caused by free radicals. A brief description of research into potential treatment options is also included.

Asphyxia↗
PubMed1996

Apoptosis and free radicals.

Free radicals that appear during physiological processes may lead to apoptosis in some pathological conditions when antioxidant capacity of the tissue is surpassed. Additionally, free radicals are involved in the control of apoptosis; antioxidant agents suppress apoptosis induced by a variety of stimuli. The possibility that apoptosis is regulated by modulation of the levels of free radicals is discussed.

Animals↗
PubMed1993

Nitrone spin-traps block calcium channels and induce pulmonary artery relaxation independent of free radicals.

Free radicals react with nitrones to form stable nitroxides which can be identified by ESR spectroscopy. Unfortunately, little is known regarding the pharmacological properties of these compounds. In this study, three commonly used nitrones, 5,5-dimethylpyrroline-N-oxide (DMPO), alpha-phenyl-tert-butylnitrone (PBN), and alpha-(4-pyridyl 1-oxide)-N-tert-butylnitrone (POBN), were found to induce relaxation of preconstricted isolated rat pulmonary artery rings. Additional experiments with PBN indicated that vasorelaxation could not be attributed to production of endothelial derived factors, prostaglandins, or free radicals. Patch-clamp techniques revealed reversible calcium channel blockade with PBN at a concentration below that needed to detect free radicals. Calcium channel blockade probably accounts for the vasorelaxation observed in the isolated ring preparations described here, and should be considered when using nitrone spin-traps both in in vivo and clinical studies.

Animals↗
PubMed2002

Effects of simultaneous exposure of surfactant to serum proteins and free radicals.

Free radicals (FRs) and serum proteins have both been implicated in the pathophysiology of surfactant dysfunction during acute lung injury (ALI). This study examines how these 2 distinct mechanisms interact to contribute to altered surfactant function in this setting. Calf lung surfactant (2 mg/mL) was incubated with no additives (C = control), and with low = (LD = 125 microM FeCl2; 250 microM H2O2) and high-dose (HD = 250 microM FeCl2, 500 microM H2O2) Fenton reaction reagents to generate hydroxyl radical. Each condition was studied with (1) no protein (N); and with 25%, 200%, and 800% (weight protein/weight phospholipid) protein added as (2) bovine albumin, (3) bovine fibrinogen, (4) hemoglobin, or (5) calf serum. Lipid (LFR) and protein (PFR) free-radical products, and modifications in the tertiary structure of Surfactant Protein A (SPA) on Western blot, were observed in N LD and N HD samples. Added proteins reduced LFR and PFR changes as well as SPA structural changes. Protection was greatest for fibrinogen, hemoglobin, and serum, and least for albumin. Minimal to no dysfunction, assayed by pulsating surfactometry, was observed in all samples. These findings indicate that addition of serum proteins to surfactant at 2 mg/mL protects against, rather than promotes, FR-mediated chemical changes in surfactant lipid and protein constituents.

Animals↗
PubMed1989

Ischemia-reperfusion injury and histamine release in isolated guinea-pig heart: the role of free radicals.

Free radicals produced by the occlusion and opening of the left anterior descending coronary artery and/or by perfusion of isolated guinea-pig heart with FeCl3/ADP (10 microM/100 microM) induce a differential release of histamine and lactate dehydrogenase (LDH) in the perfusates with a preferential liberation of histamine in the reperfusion phase, associated with an increase of ventricular arrhythmias. The release of histamine has been correlated with malonyldialdehyde (MDA) production and tissue calcium content in left ventricular tissue. MDA increased during ischemia, while the calcium content increased when the tissue was reperfused. Under these conditions, N-t-butyl-alpha-phenylnitrone (BPN), a molecule capable of forming spin adducts with free radicals, and D-mannitol are active in preventing reperfusion-induced arrhythmias.

Animals↗
PubMed1989

[Inhibitory action of tiopronin on free radicals].

Free oxygen radicals are involved in many pathological conditions and particularly in the inflammation which characterizes rheumatic disorders. Tiopronin (Acadione), a new basic treatment for rheumatoid arthritis, and sodium 3-aurothio-2-hydroxypropane-1-sulfonate (Allochrysine), the reference treatment for the disease, have been tested in vitro for their ability to regulate the free radicals produced by inflammatory murine macrophages or granulocytes. The production of free radicals was measured using the technique of luminol-dependent chemoluminescence. Results show that tiopronin causes dose-dependent inhibition of chemoluminescence whereas, under the same experimental conditions, sodium 3-aurothio-2-hydroxypropane-1-sulfonate leads to a stimulation in production of the radicals. Taking into consideration the deleterious effects of free radicals in rheumatic disorders, inhibition of the radicals may be considered as forming part of tiopronin's mode of action.

Acetylcysteine↗
PubMed1993

Modulation of platelet function by free radicals and free-radical scavengers.

Platelets have the capacity to generate oxygen-derived free radicals and are often present at inflammatory foci with other free-radical-generating cells such as white blood cells. Free radicals can modify platelet adhesion and aggregation directly or through effects on the vascular endothelium, which generates prostacyclin and nitric oxide. To defend against the overproduction of free radicals the body manufactures endogenous scavengers, which can be of enzymic or non-enzymic origin. Daniela Salvemini and Regina Botting describe how free-radical scavengers may be used therapeutically to regulate the platelet reactivity involved in many pathological phenomena.

Animals↗
PubMed1983

An approach to free radicals.

Free radicals have become a buzz word in experimental pathology and they are beginning to impinge on clinical practice.

Aging↗