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PubMed1993

The role of cytochrome c and mitochondrial catalase in hydroperoxide-induced heart mitochondrial lipid peroxidation.

The role of cytochrome c and catalase in hydroperoxide-induced lipid peroxidation of rat heart mitochondria was investigated. Mitoplasts were prepared from hearts of aminotriazole-treated rats which displayed both an 80-90% reduction in matrix catalase activity and rate of H2O2 consumption. Catalase-depleted mitochondria were more susceptible to H2O2-dependent lipid peroxidation and had similar extents of tert-butyl hydroperoxide (t-BuOOH)-induced lipid peroxidation compared with control mitochondria. The magnitude of lipid peroxidation induced by H2O2 was greater than that for t-BuOOH in catalase-depleted mitochondria, while t-BuOOH induced soybean phosphatidylcholine (PC) liposome lipid peroxidation to a greater extent than H2O2. The t-BuOOH- and H2O2-dependent mitochondrial lipid peroxidation was inhibited 50 and 7%, respectively, by cytochrome c3+ depletion of mitochondria. Similar relative sensitivities to t-BuOOH- and H2O2-dependent peroxidation occurred for cytochrome c(3+)-supplemented soybean PC liposomes. These data show a critical role for cytochrome c3+ in hydroperoxide-induced mitochondrial lipid peroxidation and demonstrate the importance of matrix catalase in protecting heart mitochondria from the toxicity of H2O2.

Animals↗
PubMed1996

The limitations of an iodometric aerobic assay for peroxides.

A technique recommended for the assay of lipid and other organic peroxides based on the use of a commercial color reagent (El-Saadani et al., J. Lipid Res. 30, 627-630, 1989) has the advantage over other iodometric methods of being insensitive to oxygen. Although tested so far with a limited range of peroxides, this aerobic method has found popular use with complex biological systems, such as plasma. We have examined the ability of this assay to provide accurate estimates of peroxides in H2O2, tert-butanol, and cumene hydroperoxides, and in oxidized linoleate, low-density lipoprotein, and human blood plasma. The results were compared with values obtained with an anaerobic iodometric peroxide method taken as the standard peroxide assay. We found that the published protocol gave correct peroxide values for H2O2 solutions. Correct values could also be obtained for oxidized low-density lipoprotein, provided that the incubation period was extended from 30 to 60 min. All the other peroxides tested gave much lower values than those of the standard iodometric method. Incubation at 50 degrees C to increase the velocity of the reaction for some of the slowly reacting peroxides did not improve the accuracy of the aerobic method. We recommend that the color reagent should be used as originally specified only for the assay of H2O2, or for oxidized lipoprotein with the incubation extended to 60 min.

Humans↗
PubMed2004

An in vitro comparison of the bleaching efficacy of 35% carbamide peroxide with established intracoronal bleaching agents.

AIM: To evaluate the bleaching efficacy of 35% carbamide peroxide, 35% hydrogen peroxide and sodium perborate for intracoronal bleaching of root filled discoloured teeth. METHODOLOGY: Extracted premolars were artificially stained using whole blood then root canal treatment was performed. After obturation, a 2 mm intermediate base was placed 1 mm below the buccal amelo-cemental junction. Intracoronal bleaching was performed in 11 teeth per group, using either 35% carbamide peroxide gel (group CP), 35% hydrogen peroxide gel (group HP) or sodium perborate mixed with distilled water (group SP). The bleaching agents were replaced after 7 days. The shade of the teeth was evaluated at day 0, 7 and 14. The results were analysed using Kruskal-Wallis one-way analysis of variance and Mann-Whitney U-test. RESULTS: At the end of 7 days, both groups CP and HP lightened by 8 +/- 3 Vita tab positions, respectively, whereas group SP lightened by 5 +/- 3 tab positions (P < 0.05). At the end of the second bleaching period at day 14, group CP and HP lightened by a further 2 +/- 2 and 2 +/- 3 tab positions, respectively, whereas group SP lightened by a further 3 +/- 4 tab positions. There were no statistical differences between groups at day 14. CONCLUSIONS: Thirty-five per cent carbamide peroxide and 35% hydrogen peroxide were equally effective for intracoronal bleaching, and significantly better than sodium perborate after 7 days. After 14 days, there were no significant differences between the groups. Thirty-five per cent carbamide peroxide can be recommended as an equally effective alternative to hydrogen peroxide for intracoronal bleaching.

Adolescent↗
PubMed2005

In vitro peroxide penetration into the pulp chamber from newer bleaching products.

AIM: To investigate peroxide penetration from newer bleaching products into the pulp chamber. METHODOLOGY: Fifty extracted human maxillary central incisor teeth were separated into five groups (n = 10). All the teeth were sectioned 3 mm apical to the cemento-enamel junction; the intracoronal pulp tissue was removed, and the pulp chamber filled with acetate buffer. Buccal crown surfaces of teeth in the experimental groups were subjected to either a whitening strip (containing 5.3% hydrogen peroxide-G1) or one of three paint-on liquid whiteners (containing 19% sodium percarbonate peroxide-G2, 18% carbamide peroxide-G3 and 8.7% hydrogen peroxide-G4). The teeth in the control group (G5) were exposed only to distilled water. The acetate buffer solution in each tooth was then transferred to a glass test tube after 30 min and leuco-crystal violet and enzyme horseradish peroxidase were added, producing a blue solution. The optical density of the resultant blue colour in the tubes was measured by a UV-visible spectrophotometer at a wavelength of 596 nm. The values were converted into microgram equivalents of HP using a spectrophotometric calibration curve. Data were analysed statistically using the Kruskal-Wallis Analysis of Variance and the Mann-Whitney U-test. RESULTS: Statistically significant differences were found between all of the groups (P < 0.05). Pulpal peroxide was not observed in the control group. The amount of hydrogen peroxide (microg) found in the pulp chamber of G1 (0.726 +/- 0.024) > G4 (0.443 +/- 0.017) > G3 (0.231 +/- 0.011) > G2 (0.175 +/- 0.012). CONCLUSIONS: The peroxides from the whitening strip and paint-on whiteners penetrated into the pulp chamber to varying degrees.

Carbamide Peroxide↗
PubMed1999

In vitro penetration of the pulp chamber by three brands of carbamide peroxide.

PURPOSE: Vital tooth bleaching has become a popular procedure for whitening teeth. Most home bleaching products contain 10% carbamide peroxide. The purpose of this in vitro study was to measure the quantity of hydrogen peroxide that reaches the pulp chamber from three carbamide peroxide products: Opalescence, Sparkle, and Rembrandt. MATERIALS AND METHODS: Seventy roots of extracted premolars were amputated approximately 3 mm apical to the cementoenamel junction, and the pulp tissues were removed. They were divided into three experimental groups (n = 20) and a control group of 10 teeth. An acetate buffer solution was placed in the pulp chamber before the crown was exposed to the bleaching agent at 37 degrees C for 25 minutes. The buffer solution was removed and reacted with leukocrystal violet and horseradish peroxidase. The optical density of blue color that developed was measured at a wavelength of 596 nm and read from a standard curve for hydrogen peroxide quantity. RESULTS: The measured amounts of hydrogen peroxide were 3.605 +/- 1.405, 1.282 +/- 0.762, and 0.339 +/- 0.251 micrograms for the Opalescence, Sparkle, and Rembrandt groups, respectively. A statistically significant difference in the hydrogen peroxide levels was observed by analysis of variance (p < .05) among the three groups. It was concluded that the penetration of commercial bleaching products was different even though the products were labeled as having the same 10% carbamide peroxide. CLINICAL SIGNIFICANCE: Carbamide peroxide penetration to the pulp varies significantly for various commercial bleaching products. This may result in different levels of tooth sensitivity or bleaching efficacy.

Carbamide Peroxide↗
PubMed2005

[Lipid peroxidation product as prognostic factors in acute necrotizing pancreatitis].

UNLABELLED: The aim of the study is the assessment of the role of oxygen free radicals (OFRs) in the pathology of acute pancreatitis (AP). MATERIAL AND METHODS: It has been accomplished based on the analysis of lipid peroxidation products' and hydrogen peroxide blood concentration in 60 patients with AP. Spectrometric and spectrofluorometric methods were used. Patients were divided into 2 groups. Group 1 consisted of 42 patients, who survived the 30 day observation period. Group 2 included patients, with a systematic deterioration resulting in death. All patients were subjected to surgery between the 15th and 30th day of observation because of septic syndrome signs. On 1st, 5th, 10th, and 15th day of treatment we measured concentrations of lipid peroxidation products such as: conjugated dienes (CD), malonyl dialdehyde (MDA), Schiff's bases, lipid peroxides (LOOH), and hydrogen peroxide. RESULTS: We observed high levels of CDs and MDA throughout the entire observation period as well as increase in lipid and hydrogen peroxide serum concentrations in patients with poor prognoses. Shiff's bases serum concentrations presented a non-characteristic pattern of changes. CONCLUSIONS: Lipid peroxidation products' metabolism path observed in our study suggests a substantial role of oxygen free radicals in acute pancreatitis pathology. Authors claim, that the assessment of lipid peroxidation product serum concentrations may be a useful marker for prognosing in most severe forms of acute pancreatitis.

Adult↗
PubMed2003

Protective effect of green tea polyphenol (-)-epigallocatechin gallate and other antioxidants on lipid peroxidation in gerbil brain homogenates.

The aim of this study was to compare the protective effects of green tea polyphenol (-)-epigallocatechin gallate (EGCG) and other well-known antioxidants on the lipid peroxidation in gerbil brain homogenates. Oxidative stress was induced by H2O2 (10 mM) or ferrous ammonium sulfate (5 microM) and lipid peroxidation was studied. Hydrogen peroxide and ferrous ions are capable of oxidizing a wide range of substrates and causing biological damage. The reaction, referred to as the Fenton process, is complex and can generate both hydroxyl radicals and higher oxidation states of the iron. Thiobarbituric acid-reactive substances (TBA-RS) were used as a marker of lipid peroxidation. EGCG, trolox, lipoic acid, and melatonin reduced H2O2- or ferrous ion-induced lipid peroxidation in a concentration-dependent manner. In reducing the H2O2-induced lipid peroxidation, IC50 values of antioxidants were as follows: EGCG (0.66 microM), trolox (37.08 microM), lipoic acid (7.88 mM), and melatonin (19.11 mM). In reducing the ferrous ion-induced lipid peroxidation, IC50 values of antioxidants were as follows: EGCG (3.32 microM), trolox (75.65 microM), lipoic acid (7.63 mM), and melatonin (15.48 mM). Under the in vitro conditions of this experiment, EGCG was the most potent antioxidant in inhibiting H2O2 or ferrous ion-induced lipid peroxidation in the gerbil brain homogenates.

Animals↗
PubMed1993

Myeloperoxidase-dependent loss of malondialdehyde: a limitation for detecting neutrophil-mediated lipid peroxidation.

Lipid peroxidation is commonly measured using the thiobarbituric acid (TBA) assay. We have examined how this assay is affected by hypochlorite, which is generated by the neutrophil enzyme myeloperoxidase. The TBA reactivity of phospholipid liposomes that had been partially peroxidized with iron/ascorbate was destroyed by low concentrations of sodium hypochlorite. Since most of the TBA reactivity in peroxidized liposomes is due to malondialdehyde, its reactivity was investigated. Addition of sodium hypochlorite destroyed the uv absorbance of malondialdehyde with a 2:1 stoichiometry and eliminated its TBA reactivity. The TBA reactivity of malondialdehyde and peroxidized liposomes was also lost after treatment with myeloperoxidase. The reaction with myeloperoxidase required chloride and was inhibited by catalase and methionine, indicating the involvement of hypochlorite. Neutrophils stimulated with phorbol myristate acetate or N-formyl-methionyl-leucyl-phenylalanine destroyed the TBA reactivity of malondialdehyde and peroxidized liposomes by a hypochlorite-dependent mechanism. The ability of hypochlorite to break down malondialdehyde explains why lipid peroxidation by stimulated neutrophils, as measured with TBA, is apparently inhibited by myeloperoxidase. Myeloperoxidase may not, however, inhibit the peroxidation process. The TBA assay and other assays of malondialdehyde may be of limited value, therefore, for assessing lipid peroxidation in systems where neutrophils or myeloperoxidase are involved.

Chlorides↗
PubMed1997

Myeloperoxidase-dependent generation of a tyrosine peroxide by neutrophils.

It has recently been shown that tyrosyl radicals react with superoxide to form a peroxide adduct of tyrosine. Since myeloperoxidase oxidizes tyrosine to its radical, and neutrophils and monocytes contain myeloperoxidase as well as produce superoxide, we have investigated whether tyrosine peroxide could be a significant product of tyrosine oxidation by these cells. Oxidation of tyrosine by purified myeloperoxidase and a superoxide-generating system, and by stimulated human neutrophils, was found to generate peroxide adducts as detected in the xylenol orange (FOX) assay and by HPLC. Superoxide, hydrogen peroxide, and myeloperoxidase were required for formation of the peroxide. Dityrosine was also formed in each system, and in the presence of superoxide dismutase, suppression of tyrosine peroxide formation gave elevated formation of dityrosine. Quantitative estimates indicate that at physiological tyrosine concentration the peroxide is likely to be formed in preference to dityrosine and to be a significant product of neutrophils. This metastable peroxide therefore has the potential to contribute to neutrophil- or monocyte-mediated tissue injury.

Chromatography, High Pressure Liquid↗
PubMed1985

The fatty acid composition of red cells deficient in glucose-6-phosphate dehydrogenase and their susceptibility to lipid peroxidation.

Oxidant damage to red cell membranes could play a part in the pathogenesis of acute and chronic haemolysis in glucose-6-phosphate dehydrogenase deficiency. Therefore, we studied the substrate for red cell membrane lipid peroxidation, i.e. the content of various polyunsaturated fatty acids in ghosts, and the susceptibility of red cells to lipid peroxidation in normal subjects and in subjects deficient in glucose-6-phosphate dehydrogenase. The fatty acid composition of red cell membranes and plasma was analysed by capillary column gas chromatography. The sensitivity of red cells to lipid peroxidation was evaluated after hydrogen-peroxide-induced oxidant stress. The degree of lipid peroxidation was monitored by measuring the release of pentane and ethane formed during the breakdown of n-6 and n-3 fatty acids. The red cell sensitivity to lipid peroxidation was found to be higher in subjects with glucose-6-phosphate dehydrogenase deficiency than in normal subjects. In the former, saturated fatty acids, in particular palmitic and stearic acid, were found to be decreased, whereas the proportion of arachidonic acid showed a clear increase. Fatty acid analysis of plasma did not reveal significant abnormalities in enzyme-deficient patients, which could explain the alteration of membrane fatty acids. Our results suggest that the increased content of substrate for lipid peroxidation, particularly arachidonic acid, in red cell membranes of subjects deficient in glucose-6-phosphate dehydrogenase, should be considered in an evaluation of an enhanced sensitivity to red cell lipid peroxidation.

Erythrocyte Membrane↗
PubMed1987

Hydrogen peroxide-induced glutathione depletion and aldehyde dehydrogenase inhibition in erythrocytes.

To study relationships between lipid peroxidation and aldehyde dehydrogenase (ALDH) inhibition, the Stocks and Dormandy model of H2O2-induced lipid peroxidation in erythrocytes was employed. Hydrogen peroxide treatment of erythrocytes and erythrocyte lysates caused a dose-dependent inhibition and depletion of ALDH and reduced glutathione (GSH) respectively. Complete ALDH inhibition and glutathione depletion occurred before significant lipid peroxidation was detected by HPLC analysis of malondialdehyde-thiobarbituric acid adducts. Hydroxyl radical scavengers did not antagonize the hydrogen peroxide-induced enzyme inhibition. Studies with the iron chelator desferrioxamine suggested that the hydrogen peroxide-induced ALDH inhibition was mediated by iron in erythrocyte lysates but not in semi-purified (and Chelex-treated) ALDH preparations. Glutathione peroxidase reduction of H2O2 exhibited an anomalous GSH dependence which was not in agreement with the accepted reaction mechanism. Reduced glutathione also antagonized the hydrogen peroxide-induced ALDH inhibition by possible complex formation with the enzyme. A hypothetical model is presented which accounts for the observed responses to hydrogen peroxide.

Aldehyde Dehydrogenase↗
PubMed1991

Free radical scavenging and inhibition of lipid peroxidation by beta-blockers and by agents that interfere with calcium metabolism. A physiologically-significant process?

It has been proposed that beta-blockers and agents affecting Ca2+ metabolism might exert cardioprotective actions because of their ability to act as antioxidants in vivo. The feasibility of this proposal was tested by examining the reaction of a series of such compounds with various oxygen-derived species. None of the compounds tested was sufficiently reactive with superoxide radical, hydrogen peroxide or hypochlorous acid for scavenging of these species to be feasible in vivo at the drug concentrations present in patients given the usual therapeutic doses. All the drugs tested were powerful scavengers of hydroxyl radical except for flunarizine, which stimulated iron ion-dependent hydroxyl radical generation from hydrogen peroxide. However, none of the drugs significantly inhibited production of hydroxyl radicals in this system. Propranolol, verapamil and flunarizine had significant inhibitory effects on the peroxidation of rat liver microsomes in the presence of iron ions and ascorbic acid. All three compounds exerted weaker inhibitory effects on peroxidation of arachidonic acid caused by a mixture of myoglobin and H2O2: pindolol stimulated peroxidation in this system. It is concluded that the ability of beta-blockers and "Ca(2+)-blockers" to inhibit lipid peroxidation varies with the lipid substrate used and the mechanism by which peroxidation is induced. We conclude that suggestions that beta-blockers and "Ca(2+)-blockers" exert antioxidant effects in vivo are not well founded, although there is a possibility that verapamil and propranolol might have some inhibitory effects against peroxidation if they accumulate in membranes to a sufficiently-high concentration in vivo. We could not confirm the reported ability of propranolol to inhibit the enzyme xanthine oxidase.

Adrenergic beta-Antagonists↗
PubMed1989

NADPH-dependent drug redox cycling and lipid peroxidation in microsomes from human term placenta.

1. NADPH-dependent iron and drug redox cycling, as well as lipid peroxidation process were investigated in microsomes isolated from human term placenta. 2. Paraquat and menadione were found to undergo redox cycling, catalyzed by NADPH:cytochrome P-450 reductase in placental microsomes. 3. The drug redox cycling was able to initiate microsomal lipid peroxidation in the presence of micromolar concentrations of iron and ethylenediaminetetraacetate (EDTA). 4. Superoxide was essential for the microsomal lipid peroxidation in the presence of iron and EDTA. 5. Drastic peroxidative conditions involving superoxide and prolonged incubation in the presence of iron were found to destroy flavin nucleotides, inhibit NADPH:cytochrome P-450 reductase and inhibit propagation step of lipid peroxidation. 6. Reactive oxo-complex formed between iron and superoxide is proposed as an ultimate species for the initiation of lipid peroxidation in microsomes from human term placenta as well as for the destruction of flavin nucleotides and inhibition of NADPH:cytochrome P-450 reductase as well as for impairment of promotion of lipid peroxidation under drastic peroxidative conditions.

Female↗
PubMed1991

Effect of chronic ethanol treatment on the t-butyl hydroperoxide-dependent lipid peroxidation in rat liver.

1. The effect of chronic ethanol consumption on the level of the t-butyl hydroperoxide (Bu'OOH)-induced lipid peroxidation in rat liver homogenate and subcellular fractions was measured using chemiluminescence technique and malondialdehyde formation. 2. It was shown that under the action of ethanol the rate of lipid peroxidation was decreased in the whole and "postnuclear" liver homogenates. 3. Ethanol significantly decreased the intensity of lipid peroxidation in microsomes, but did not affect the Bu'OOH-dependent process in mitochondria. 4. The level of lipid peroxidation was reduced after incubation of the total particulate fraction (mitochondria plus microsomes) with the undialysed cytosol from ethanol-treated rat liver. Dialysis of the cytosol prevented depressive effect of ethanol treatment on lipid peroxidation. 5. Reduced glutathione (0.1-1.0 mM) was shown to decrease the rate of lipid peroxidation in rat liver microsomes, but did not affect its level in mitochondria. 6. Pyrazole injections to rats reduced and phenobarbital treatment increased the level of the Bu'OOH-dependent lipid peroxidation in liver microsomes. 7. The data obtained indicate that the Bu'OOH-dependent lipid peroxidation is not an appropriate marker of the ethanol-induced oxidative stress in rat liver cells.

Animals↗
PubMed1995

Lipid peroxidation of circulating low density lipoproteins with age, smoking and in peripheral vascular disease.

In this study, lipid peroxides in plasma and the low density lipoprotein (LDL) fraction and plasma concentrations of vitamin E, lipids and lipoproteins were measured in 22 smokers (mean age 35 years), 26 non-smoking patients with peripheral vascular disease (PVD), mean age 66 years), and 23 younger (ages < or = 55 years) and 26 older (ages > 55 years) healthy subjects. Plasma lipid peroxide concentrations in the PVD patients (105.9 +/- 20.6 vs. 91.8 +/- 15.8 ng malondialdehyde (MDA)/ml plasma, mean +/- S.D.) and the smokers (94.1 +/- vs. 74.0 +/- 13.9 ng MDA/ml plasma) were significantly elevated compared with levels in the appropriate control subjects and levels were significantly higher in older compared with younger control subjects. Plasma LDL lipid peroxides were also significantly raised in patients with PVD and smokers compared with control values (PVD): 37.1 +/- 7.7 vs. 26.3 +/- 4.1 ng MDA/ml plasma; smokers: 30.4 +/- 6.9 vs 24.9 +/- 7.5 ng MDA/ml plasma). The ratio of LDL lipid peroxides: LDL-cholesterol was significantly higher in the smokers, and plasma cholesterol and LDL-cholesterol were significantly higher in patients with PVD compared with other groups of subjects. The ratio of vitamin E: total lipid was not significantly different between the study groups. These data show that lipid peroxide levels in the plasma LDL fraction are elevated along with raised circulating levels in patients with PVD and smokers but that LDL lipid peroxide concentrations were independent of age in the healthy subjects. Elevated LDL lipid peroxide concentrations may may be mainly due to abnormally high LDL levels in PVD patients, whereas in smokers, the concentration of lipid peroxides in the LDL particles is raised and might render the lipoprotein more atherogenic.

Adult↗
PubMed1981

Lipid peroxidation and hemoglobin degradation in red blood cells exposed to t-butyl hydroperoxide. Dependence on glucose metabolism and hemoglobin status.

Changes in hemoglobin status and lipid peroxidation were followed in red cells containing either oxy-met-, or carbonmonoxyhemoglobin, incubated with t-butyl hydroperoxide in a medium with or without glucose. Loss of intact hemoglobin (the sum of oxyhemoglobin and methemoglobin) was inversely proportional to the degree of lipid peroxidation in red cells containing either oxy- or methemoglobin. When glucose was added to the medium, lipid peroxidation increased while there was a decreased loss of intact hemoglobin in red cells containing either oxy- or methemoglobin, while both lipid peroxidation and changes in hemoglobin decreased in red cells containing carbonmonoxyhemoglobin. Methemoglobin formation and loss of intact hemoglobin were directly proportional to the degree of lipid peroxidation in red cells containing carbonmonoxyhemoglobin. The greatest amount of lipid peroxidation occurred in red cells containing carbonmonoxyhemoglobin, incubated without glucose. These results indicate that methemoglobin and non-intact hemoglobin may protect the membrane against lipid peroxidation. We propose that, depending on the availability of glucose and the liganded state of hemoglobin, lipid peroxidation and hemoglobin alterations represent extremes of a spectrum of oxidative damage.

Adult↗
PubMed1991

Change of lipid peroxide levels in rat tissues after cisplatin administration.

cis-Diamminedichloroplatinum(II) (cisplatin) is one of the most effective antitumor agents currently available for cancer chemotherapy. Unfortunately, its clinical use is severely limited by its dose-dependent nephrotoxicity. Recently, it has been reported that this nephrotoxicity is associated with an increase in lipid peroxides in the rat kidney. However, it is not clear if the specific nephrotoxicity is related to the increase in lipid peroxides induced by cisplatin since the increase in lipid peroxides in the kidney has not been compared with that in other tissues. We examined the changes in lipid peroxide levels in rat tissues after cisplatin administration to clarify the relationship between lipid peroxides and cisplatin nephrotoxicity. After cisplatin administration (5 mg/kg i.p.), the relative weight of the rat liver decreased, but that of the kidney increased. The increase in lipid peroxide levels in the kidney and liver of cisplatin-treated rats was significant. The percent change from control was greatest in the kidney on the 5th day after administration among all tissues examined. Cisplatin did not affect enzymatic or non-enzymatic lipid peroxidation in microsomes of rat kidney or liver in vitro. It appears that the increase in lipid peroxides in the kidney was not a direct consequence of cisplatin administration.

Animals↗
PubMed1995

Oxidative stress aspects of the cytotoxicity of carbamide peroxide: in vitro studies.

Carbamide peroxide is the active ingredient in many at-home patient-applied tooth whiteners. The cytotoxicity of carbamide peroxide, as related to oxidative stress, was evaluated in vitro with several human cell lines, including Smulow-Glickman (S-G) gingival epithelial cells. The potency of carbamide peroxide was related to its hydrogen peroxide component rather than to carbamide, was eliminated in the presence of exogenous catalase, and was enhanced in the presence of aminotriazole, an inhibitor of cellular catalase. The intracellular level of glutathione, a scavanger of toxic oxygen metabolites, was decreased in cells exposed to carbamide peroxide; at higher concentrations of carbamide peroxide, leakage of lactic acid dehydrogenase was also evident. Cells pretreated with the glutathione-depleting agents, buthionine sulfoximine, chlorodinitrobenzene, and bis(chloroethyl) nitrosourea, were hypersensitive to subsequent challenge with carbamide peroxide. Conversely, pretreatment with the iron chelator, deferoxamine, protected the cells against subsequent exposure to carbamide peroxide.

Carbamide Peroxide↗