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At least 145 records · Page 8Linked to original sources

A combination benzoyl peroxide and clindamycin topical gel compared with benzoyl peroxide, clindamycin phosphate, and vehicle in the treatment of acne vulgaris.

A topical gel combining 5% benzoyl peroxide and 1% clindamycin as phosphate was evaluated in a 10-week randomized double-blind trial involving 287 patients with moderate to moderately severe acne. The combination agent demonstrated significantly greater reductions in inflammatory lesions than either of its active constituents (5% benzoyl peroxide and 1% clindamycin) or vehicle when used alone. Significantly greater reductions in comedos and improvements, as measured by both physicians' and patients' global evaluations, were obtained with the combination agent than with clindamycin or vehicle. The reduction in comedos and the global improvements were similar between the combination agent and benzoyl peroxide. The combination agent was well tolerated; the incidence of dry skin was similar to that found with benzoyl peroxide, and other adverse events were similar to that with vehicle. The improved efficacy obtained with combination therapy was accompanied by a safety profile similar to that of either constituent used alone.

Acne Vulgaris↗

Superoxide, hydrogen peroxide, and singlet oxygen in lipid peroxidation by a xanthine oxidase system.

1. Xanthine oxidase acting aerobically upon acetaldehyde was found to cause the peroxidation of linolenate. This was demonstrated by increased absorbance at 233 nm due to diene conjugation and by the detection of a lipid peroxide spot on the thin layer chromatograms. 2. Superoxide dismutase inhibited this lipid peroxidation, as did catalase, thus indicating that both O2- and H2O2 were essential intermediates. Scavengers of singlet oxygen also inhibited the peroxidation of linolenate, whereas scavengers of hydroxyl radical did not. These effects, which were observed in the absence of iron salts, led to the proposal that O2- and H2O2 can directly give rise to a singlet oxygen, as follows: O2- + H2O2 leads to OH- + OH. + O2. 3. This proposal was further supported through the use of 2,5-dimethylfuran, as an indicating scavenger of singlet oxygen. Thus, when this compound was exposed to a known source of singlet oxygen, it gave a product which was detectable by thin layer chromatography. This product was also observed when 2,5-dimethylfuran was exposed to the xanthine oxidase system, in which case its accumulation was prevented by superoxide dismutase or by catalase, but not by scavengers of hydroxyl radical.

Acetaldehyde↗

A randomized clinical trial comparing a novel 5.3% hydrogen peroxide whitening strip to 10%, 15%, and 20% carbamide peroxide tray-based bleaching systems.

A randomized and controlled, parallel-group clinical trial compared the whitening benefits of a novel 5.3% hydrogen peroxide bleaching strip to 10%, 15%, and 20% carbamide peroxide tray-based bleaching systems. A total of 36 healthy adults were randomized to a 14-day regimen in which both arches were whitened for 1 hour per day in the whitening-strip group or 2 hours per day in the tray groups. Efficacy was measured objectively using digital images of the anterior teeth at baseline and after 14 days of treatment. Overall tooth color (L*a*b*) was derived from individual pixel values, and then mean levels of delta b*, delta L*, and composite color (delta E*) were compared using analysis of covariance. After 14 days of treatment, all groups experienced a greater than 1-unit mean improvement in delta b*, delta L*, and delta E* relative to baseline. For the primary study variable, reduction of yellow (delta b*) outcomes after 14 hours of using the experimental strip were comparable to those observed with the 10% tray group after 28 hours of use. These two treatment groups did not differ statistically with respect to any of the color measurements used in this study. For the tray groups, there was a reasonable dose relationship for the primary end point, delta b*, with the 15% and 20% tray groups averaging 17% and 68% improvements in yellow, respectively, over the 10% group. Except for the 20% carbamide peroxide system, where sensitivity was relatively common, all test products were well tolerated. In this first comparative evaluation vs marketed controls, use of the whitening strips twice daily for 14 days yielded a highly significant improvement in tooth color vs baseline.

Adult↗

At-home vital bleaching: a comparison of hydrogen peroxide and carbamide peroxide treatments.

Tray bleaching of vital teeth performed at home by the patient under the dentist s supervision, whether alone or in combination with any of the in-office techniques, provides an interesting alternative to other methods employed in this type of dental treatment. This bleaching procedure applies low-concentration peroxides to the enamel by means of a custom-made mouth tray specifically designed for this purpose. The aim of this study is to examine and compare two commercially-available bleaching products, at equivalent concentrations, for use in this technique: VivaStyle (Vivadent) and FKD (Kin); the former is a 10% carbamide peroxide and the latter a 3.5% hydrogen peroxide formulation. It examines the parameters that must be monitored during the application of this type of procedure and presents 6 cases (3 treated with one of the above-mentioned products and the other 3 with the other), establishing the bleaching power of the products and the appearance and intensity of post-operatory hypersensitivity. The results obtained show that both products are effective for the purpose for which they were designed. In general, dental hypersensitivity was minimal.

Carbamide Peroxide↗

Rat hepatic cytosolic glutathione-dependent enzyme protection against lipid peroxidation in the NADPH-microsomal lipid peroxidation system.

Dialyzed rat liver cytosol (105 000 X g supernatant), when added along with 2.5 mM glutathione, blocked malonaldehyde formation in the NADPH-microsomal lipid peroxidation system, thus protecting against lipid peroxidation. Preheating the cytosol for 10 min at 60 degrees C destroyed its protective ability. Ammonium sulfate fractionation and Sephadex G-100 gel filtration of cytosol indicated that more than one glutathione-dependent protective enzyme was present. Fractions from the G-100 column containing the selenoenzyme glutathione peroxidase failed to protect, but fractions containing the glutathione S-transferases, which have non selenium-dependent glutathione peroxidase activity, did protect. The glutathione S-transferases were purified further with ion exchange chromatography and shown to have protective activity. Thus the rat hepatic cytosolic glutathione-dependent enzyme protection against lipid peroxidation in the NADPH-microsomal lipid peroxidation system is in part due to some of the glutathione S-transferases. The selenium-dependent glutathione peroxidase appears to have no protective effect in this system.

Animals↗

Placental and decidual lipid peroxidation and antioxidant defenses in preeclampsia. Lipid peroxidation in preeclampsia.

We evaluated lipid peroxidation in serum, placenta and decidua basalis and antioxidant defenses in preeclampsia and normal pregnancy. The study group consisted of 70 women with preeclampsia and 72 healthy pregnant women. Lipid peroxides in serum, placenta and decidua basalis, and serum vitamin E and total carotene were measured by spectrophotometric methods. Unpaired Student's t-test, chi(2)-test and Pearson correlation test were used for the statistical analyses. Levels of lipid peroxides in serum, placenta and decidua basalis were markedly higher; and serum vitamin E, total carotene, bilirubin, albumin levels were markedly lower in preeclamptic pregnants compared with healthy pregnant women. Our findings demonstrated that both placenta and decidua basalis tissues may be a source of lipid peroxides in preeclamptic pregnancies. Prophylactic antioxidant therapy may abate the disease process. Further studies are needed to clarify the pathophysiology of preeclampsia and effectiveness of prophylactic antioxidant therapy in preeclampsia.

Journal Article↗

Time course of hydrogen peroxide induced changes in the lipid peroxidation of human sperm membranes.

The present study evaluates the changes in sperm motility due to H202 induced membrane damage. Washed human sperm suspended in HAM's F-10 (20-30 x 10 6/ml) were incubated (37 degrees Celsius) with varying concentrations (0-0.05%) of H202 for up to 15 minutes. Sperm were analyzed for % motility, % viability, the ratio of cholesterol to phospholipids (C/PL), and the degree of lipid peroxidation (LPO). Motility was monitored manually and viability was evaluated by the Eosin Y staining method. Total lipids were extracted with chloroform:methanol (1:2) and used in colorimetric determination of cholesterol and phospholipid contents (mcmol/106 sperm). Lipid peroxidation was measured by the production of malondialdehyde (nmol MDA/108 sperm). The results (mean +or- SEM, n=8) indicate a dose a time-dependent effect on % motility during the 15 minute incubation period. In comparison to control (8 +or- 4%), samples incubated with 0.01% H202 exhibited a 25 +or- 3% decrease in % motility, while a complete loss of motility was observed with 0.05% H202. No significant differences in decrease in sperm viability were observed between control (211 +or- 4) and H202 (0.01%) treated samples (14 +or- 2%). An increase of (54 +or- 5%) in lipid peroxidation was observed with 0.01% H202, as compared with an 18 +or- 1% increase in control samples at 15 minutes. The C/PL ratio increased by 46 +or- 4% at 15 minutes in H202 treated samples while showing a 34.3% decrease in control samples. H202 inhibited sperm motility while increasing membrane LPO and C/PL, without altering sperm viability. It would appear that lipid peroxidation and alteration of sperm membrane composition lead to the loss of sperm motility.

Biology↗

Studies on lipid peroxidation using isolated rat liver cells: the role of singlet oxygen in the propagation of lipid peroxidation ADP-Fe3+ or CCl4 induced.

The separation of lipid peroxidation reactions in two sequential parts, initiation and propagation, has been proposed. Furthermore, it has been shown that some of the propagation reactions following the peroxidative breakdown of membrane lipids may produce singlet oxygen, a highly excited, energetic species of molecular oxygen. To investigate whether singlet oxygen is involved in the propagation of ADP-Fe3+ or CCl4-induced lipid peroxidation, hepatocytes in single cell suspension were treated with the two mentioned drugs in the presence or in the absence of 1,4-diazabicyclo-[2,2,2]octane (DABCO), a known scavenger of singlet oxygen. Only the stimulation of malonaldehyde production due to ADP-Fe3+ was partially prevented by high concentrations of the scavenger, while the CCl4-induced increase of malonaldehyde was not influenced. The results reported here suggest that ADP-iron complex stimulates lipid peroxidation in a way that is somehow different from that occurring in the case of CCl4 poisoning.

Adenosine Diphosphate↗

Spontaneous lipid peroxidation and production of hydrogen peroxide and superoxide in human spermatozoa. Superoxide dismutase as major enzyme protectant against oxygen toxicity.

Spontaneous lipid peroxidation in washed human spermatozoa was induced by aerobic incubation at 32 C and measured by malonaldehyde production; loss of motility during the incubation was determined simultaneously. Malonaldehyde production at the point of complete loss of motility, defined as the lipoperoxidative lethal endpoint (LLE), was 0.10 +/- 0.03 nmol/10(8) cells (mean +/- SD, n = 40), and was independent of the time to complete loss of motility. Human spermatozoa produced both H2O2 and O2-. during aerobic incubation. Inhibition of superoxide dismutase in these cells with KCN showed that all the H2O2 production is due to action of the dismutase. The superoxide dismutase activity of individual human sperm samples varied between 1 and 10 U/10(8) cells, variations between samples from a single donor being nearly as great as those between different donors. The time to complete motility loss (tL) showed equal variation of 1 to 10 hours among samples. The rate of spontaneous lipid peroxidation, calculated as LLE/tL, for a given sperm sample and the superoxide dismutase activity of the same sample, determined prior to aerobic incubation, gave a good linear correlation (r = 0.97). Glutathione reductase, glutathione peroxidase, and glutathione were found to be present in human spermatozoa, but showed little variation among samples. These results suggest that superoxide dismutase plays the major role in protecting human spermatozoa against lipid peroxidation. In addition, the superoxide dismutase activity of a fresh sperm sample appears to be a good predictor of the lifetime (up to the complete loss of motility) of that particular sample, and so may prove useful in semen analysis.

Humans↗

Constitutive hsp70 attenuates hydrogen peroxide-induced membrane lipid peroxidation.

Thermal pretreatment improves cardiac recovery from subsequent ischemia/reperfusion. Induction of heat shock proteins (hsps) may contribute to this protection. We have demonstrated that augmentation of the constitutive hsp70 (hsc70) in H9c2 heart myoblasts promotes oxidative resistance. We employed a model oxidant to explore potential target(s) of protection by hsc70. Upon exposure to 54 microM of hydrogen peroxide (H(2)O(2)), hsc70-overexpressing cells exhibited a lower lipid peroxidation than the sham-transfected control. Constitutive hsc70 overexpression, however, did not protect against H(2)O(2)-induced depletion of ATP and glutathione (GSH). Lipid protection also occurred in cells preconditioned at 39 degrees C (selectively induces hsc70) during H(2)O(2) exposure. Interestingly, the protection conferred by hsc70 was comparable in magnitude to that provided by alpha-tocopherol, and was followed with a reduced release of lactate dehydrogenase and a unaltered calcium uptake during H(2)O(2) challenge. Collectively, our observations suggest that hsc70 may preserve membrane function via attenuation of lipid peroxidation during oxidative insult.

Animals↗

Antiinflammatory effects of free radical scavengers and antioxidants: further support for proinflammatory roles of endogenous hydrogen peroxide and lipid peroxides.

Scavengers of reactive oxygen species were tested by local administration during granulomatous inflammation in the rat, induced by the subdermal implantation of carrageenin-soaked sponges. Drugs were administered either in a single dose immediately after sponge implantation, or in daily doses on days 3-6 of inflammation. The effects of the injected drugs were assessed using the day 7 granuloma. When given at the moment of sponge implantation, catalase showed antiinflammatory effects, whereas superoxide dismutase did not. However, the addition of superoxide dismutase to catalase, prior to injection, markedly potentiated the inhibition of granuloma formation by catalase alone. Negative results obtained with scavengers of hydroxyl radicals and singlet molecular oxygen suggest that protection of superoxide dismutase by catalase from inactivation by hydrogen peroxide, is a likely explanation for the observed potentiation. When administered at the moment of the induction of inflammation, alpha-tocopherol and propyl gallate, both antioxidants, also inhibited granuloma formation. All drugs tested were either ineffective or even enhanced granuloma weight following administration into a preformed granuloma. An inhibitor of both pathways of arachidonate metabolism, phenidone, inhibited granuloma formation irrespective of the moment of administration. The results presented in this paper suggest proinflammatory roles for hydrogen peroxide and lipid peroxides and a possible involvement of hydroxyl radicals and singlet oxygen in the breakdown of collagen.

Animals↗

Cumene peroxide and Fe(2+)-ascorbate-induced lipid peroxidation and effect of phosphoglucose isomerase.

Malondialdehyde (MDA) is one of cytotoxic aldehydes produced in cells as a result of lipid peroxidation and further MDA metabolism in cytoplasm is not known. In our experiments the liver fraction 10,000 g containing phosphoglucose isomerase and enzymes of the glyoxalase system was used and obtained experimental data shows that in this fraction there is an aggregate of reactions taking place both in membranes (lipid peroxidation) and outside membranes. MDA accumulation is relatively slow because MDA is a substrate of aldehyde isomerase (MDA <--> methylglyoxal). The well known enzyme phosphoglucose isomerase acts as an aldehyde isomerase (Michaelis constant for this enzyme Km = 133 +/- 8 microM). MDA conversion to methylglyoxal and further to neutral product D-lactate (with GSH as a cofactor) occurs in cytoplasm and D-lactate should be regarded as the end product of two different parametabolic reactions: lipid peroxidation or protein glycation.

Animals↗

Activity of rat liver microsomal glutathione transferase toward products of lipid peroxidation and studies of the effect of inhibitors on glutathione-dependent protection against lipid peroxidation.

Rat liver microsomal glutathione transferase displays glutathione peroxidase activity with linoleic acid hydroperoxide, linoleic acid ethyl ester hydroperoxide, and dilinoleoyl phosphatidylcholine hydroperoxide, with rates of 0.2, 0.3, and 0.3 mumol/min/mg, respectively. The activities are increased between three- and fourfold when the enzyme is activated with N-ethylmaleimide. Microsomal glutathione transferase can also conjugate 4-hydroxynon-2-enal with a specific activity of 0.5 mumol/min/mg. These findings show that the enzyme can remove harmful products of lipid peroxidation and thereby possibly protect intracellular membranes against oxidative stress. A set of glutathione transferase inhibitors (rose bengal, tributyltin acetate, S-hexylglutathione, indomethacin, cibacron blue, and bromosulfophtalein) which abolish the glutathione-dependent protection against lipid peroxidation in liver microsomes have been characterized. These inhibitors were found to be effective in the micromolar range and could prove valuable in studying the factor responsible for glutathione-dependent protection against lipid peroxidation.

Animals↗

Solid state and solution 43Ca NMR of calcium peroxides involved in the disproportionation of hydrogen peroxide by calcium hydroxide.

In order to get some insight into the mechanism of the disproportionation of hydrogen peroxide catalyzed by calcium hydroxide, 43Ca NMR spectra of enriched samples of calcium peroxides and of their precursors have been studied in both solution and solid state. This study demonstrates that no well-defined peroxidized calcium species are formed in solution, showing that the catalytic role of calcium is likely restricted to the solid state. Most of the calcium compounds that could be involved in the catalytic process have been investigated with solid state NMR. The shift and quadrupolar parameters of Ca(OH)2, CaO2.8H2O and CaO2.2H2O2 are reported for the first time. These parameters are different enough to allow the quantitative analysis of a complex mixture of these compounds by NMR.

Calcium Hydroxide↗

Influence of bile acids on stimulated lipid peroxidation and hydrogen peroxide production in rat liver microsomes.

Bile acids were found to be effective antioxidants in bile and intestine. The influence of different bile acids on the NADPH-Fe(++)-stimulated lipid peroxidation (LPO) and cytochrome P-450 dependent hydrogen peroxide production (H2O2) in rat liver microsomes was investigated in vitro. LPO was determined as production of thiobarbituric acid reactants (TBAR). Different tri-, di- and monohydroxylated bile acids and cholesterol were given to the incubation mixture in concentrations ranging from 10(-5) to 10(-3) M. Sodium salts of cholic, tauroglycocholic and deoxycholic acids as well as cheno-deoxycholic, ursodeoxycholic, lithocholic acids and cholesterol did not alter the microsomal production of TBAR. H2O2 formation was significantly decreased by sodium deoxycholate whereas cholesterol increased H2O2 production up to 4 times. These results show that bile acids were not able to protect microsomal membrane lipids against peroxidative damage. Cholesterol mediated H2O2 formation as a source of hydroxyl radicals had no toxic effect concerning LPO, TBAR were not enhanced significantly.

Animals↗

Bcl-2 protects isolated plasma and mitochondrial membranes against lipid peroxidation induced by hydrogen peroxide and amyloid beta-peptide.

The bcl-2 protooncogene product possesses antiapoptotic properties in neuronal and nonneuronal cells. Recent data suggest that Bcl-2's potency as a survival factor hinges on its ability to suppress oxidative stress, but neither the subcellular site(s) nor the mechanism of its action is known. In this report electron paramagnetic resonance (EPR) spectroscopy analyses were used to investigate the local effects of Bcl-2 on membrane lipid peroxidation. Using hydrogen peroxide (H2O2) and amyloid beta-peptide (A beta) as lipoperoxidation initiators, we determined the loss of EPR-detectable paramagnetism of nitroxyl stearate (NS) spin labels 5-NS and 12-NS. In intact cell preparations and postnuclear membrane fractions, A beta and H2O2 induced significant loss of 5-NS and 12-NS signal amplitude in control PC12 cells, but not PC12 cells expressing Bcl-2. Cells were subjected to differential subcellular fractionation, yielding preparations of plasma membrane and mitochondria. In preparations derived from Bcl-2-expressing cells, both fractions contained Bcl-2 protein. 5-NS and 12-NS signals were significantly decreased following A beta and H2O2 exposure in control PC12 mitochondrial membranes, and Bcl-2 largely prevented these effects. Plasma membrane preparations containing Bcl-2 were also resistant to radical-induced loss of spin label. Collectively, our data suggest that Bcl-2 is localized to mitochondrial and plasma membranes where it can act locally to suppress oxidative damage induced by A beta and H2O2, further highlighting the important role of lipid peroxidation in apoptosis.

Amyloid beta-Peptides↗

Lipid peroxidation and the reactions of superoxide and hydrogen peroxide in mouse spermatozoa.

Mouse spermatozoa released from the cauda epididymidis underwent spontaneous lipid peroxidation during aerobic incubation at 37 degrees C in medium containing 113 mM NaCl, 0.4 mM EDTA, and 15 mM sodium phosphate ( NTPC ). The rate of lipid peroxidation, as measured by malonaldehyde production, was 0.045 nmol malonaldehyde/h per 10(3) cells. The motility of these cells declined with time in medium NTPC ; the percent spermatozoa showing no motility increased linearly with production of malonaldehyde. All flagellar activity stopped at 0.80 nmol malonaldehyde/10(8) cells, independent of the malonaldehyde production rate. Spermatozoa suspended in NTPC at 24 degrees C produced O(2), with an intrinsic rate of 1.96 nmol/min per 10(8) cells; this increased to 3.80 nmol/min per 10(8) cells in 10 mM cyanide. Mouse sperm contain 3.5 U/10(8) cells of superoxide dismutase activity, 91% of which is sensitive, and 9% of which is insensitive, to cyanide inhibition. Mouse sperm also produce H2O2, all of which can be attributed to the action of superoxide dismutase on O(2) produced. Mouse sperm contain high levels of glutathione and of glutathione reductase and peroxidase activities, implicating the glutathione system as the major protective enzyme system against cell damage by autoxidation. This is in contrast to rabbit spermatozoa, which have little endogenous glutathione and rely on superoxide dismutase as protective enzyme against peroxidative damage.

Animals↗

Benzoyl peroxide in the treatment of acne vulgaris: a double-blind, multi-centre comparative study of 'Quinoderm' cream and 'Quinoderm' cream with hydrocortisone versus their base vehicle alone and a benzoyl peroxide only gel preparation.

A double-blind, multi-centre general practice study was carried out to compare the effectiveness of benzoyl peroxide/potassium hydroxyquinoline sulphate cream, with or without hydrocortisone, its aqueous astringent cream base alone, and a benzoyl peroxide alcoholic gel in the treatment of 107 patients with acne vulgaris. Patients on entry were allocated at random to one of four treatment groups and instructed to apply the medication twice daily to all affected areas for 12 weeks. Assessments of the severity of acne on the face, chest and back, and response to treatment were made at 2, 4, 8 and 12 weeks. Acceptability of the treatment, i.e. 'greasiness', was also assessed by patients. The results showed that the combination cream preparation produced a greater reduction in acne scores than did the base or benzoyl peroxide alone. The addition of 1% hydrocortisone eliminated the flare reaction to benzoyl peroxide seen in patients in the other two active treatment groups. The majority of patients found the preparations cosmetically acceptable.

Acne Vulgaris↗