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PubMed2000

Contribution of multivitamins, air, and light in the generation of peroxides in adult and neonatal parenteral nutrition solutions.

OBJECTIVE: To compare the concentrations of peroxides between adult and neonatal total parenteral nutrition (TPN) solutions in response to protection against inducers of peroxidation such as multivitamins and exposure to light or air. METHODS: Peroxide concentrations were measured in freshly prepared adult and neonatal solutions of fat-free TPN in four settings: with or without an air inlet, and protected or unprotected from ambient light. An oxygen washout was performed by exposing a fat-free neonatal TPN solution to a continuous flow of nitrogen. RESULTS: Globally, light was the main inducer of peroxides in adult and neonatal solutions. However, in adult solutions the concentration of peroxides remained <15 micromol/L, while in neonatal solutions the peroxide concentration was as high as 300 micromol/L in ambient light. Although the oxygen washout did prevent the generation of peroxides, avoiding air inlet was not as effective as was photoprotection in decreasing the important peroxide load in the neonatal TPN solution. CONCLUSIONS: The higher concentration of peroxides found in neonatal solutions compared with adult solutions is explained by the differences in nutrient composition between the two solutions. Contamination of parenteral solutions by air during compounding accounts for the photoinduced generation of peroxides in TPN solutions. It is more convenient to protect TPN solutions from light exposure after the admixture of the multivitamin solution than to avoid contact with oxygen.

Adult↗
PubMed2003

Light augments tooth whitening with peroxide.

BACKGROUND: The authors tested the adjunctive use of light with a 15 percent peroxide gel as a single-visit, in-office tooth whitening system. METHODS: Subject (N = 87) with stained (> shade D4, Vita Zahnfabrik, Bad Säckingen, Germany) anterior teeth were randomly assigned to test (peroxide and light), peroxide control (peroxide gel) or light control (placebo gel and light) groups and were treated for one hour. The researchers evaluated tooth shade, color and subject response at baseline and posttreatment and at three and six months posttreatment. RESULTS: The initial shade unit reduction of combined light and peroxide treatment (8.4) was greatest compared with that of peroxide alone (5.9) and of light alone (4.9). Approximately 88 percent of these effects persisted for six months. Lightness was increased and yellowness decreased to a significantly greater extent in the test group than in either control. These findings were corroborated by subject evaluation. One week after treatment, moderate to greatly increased tooth sensitivity occurred in 20 percent of test subjects, 21.7 percent of peroxide control subjects and none of the light control subjects. Neither tooth sensitivity nor gingival redness was present at the three- and six-month visits. CONCLUSIONS: Peroxide and light treatment significantly lightened the color of teeth to a greater extent than did peroxide or light alone, with a low and transient incidence of tooth sensitivity. CLINICAL IMPLICATIONS: Light can increase the tooth-whitening effect of peroxide, thereby increasing the effectiveness of tooth-whitening procedures.

Adolescent↗
PubMed1996

Potentiating effect of hydrogen peroxide on the serotonin-induced vasocontraction in human umbilical artery.

BACKGROUND: Our objective was to investigate the role of hydrogen peroxide in the vasocontraction induced in the human umbilical artery by serotonin. METHODS: Umbilical arteries collected from healthy women at term were cut helically and suspended in an organ bath to record isometric mechanical activity. In Study I, we measured the concentration-contraction response to serotonin with or without pretreatment with hydrogen peroxide (0.01-10 microM). In Study 2, vessels were pre-incubated with L-arginine (0.1-10mM), or with hydrogen peroxide (10 mM) and L-arginine (1 mM), then serotonin was added cumulatively. In Study 3, vessels were suspended in a calcium-free solution containing potassium chloride 20 mM, and a cumulative concentration-response curve to calcium chloride (10(-5)-10(-3) M) was constructed for vessels pretreated with hydrogen peroxide (10 microM). In Study 4, vessels were pre-treated with M1, an inhibitor of 5-HT2 serotoninergic receptors, and hydrogen peroxide (10 microM), and then prostaglandin F2 alpha (9.0 x 10(-7) M). Finally, we measured the 5-HT1 receptor-mediated relaxation induced by serotonin. RESULTS: Hydrogen peroxide (1 or 10 microM) significantly potentiated the contractile response to serotonin (p < 0.04, p < 0.005). L-arginine (1 or 10 mM) significantly reduced the contractile response to serotonin (p < 0.02, p < 0.0002). Pretreatment with L-arginine significantly suppressed the potentiating effect of hydrogen peroxide on the serotonin-induced contraction. The sensitivity of the arteries to calcium chloride in the presence of hydrogen peroxide did not differ from that in the control group. Pretreatment with hydrogen peroxide significantly reduced the 5-HT1 serotoninergic receptor-mediated relaxation at higher concentrations of serotonin (1.23 x 10(-4) M, 2.47 x 10(-4) M, 2.47 x 10(-4) M). CONCLUSION: Hydrogen peroxide potentiated the umbilical artery contraction induced by serotonin. This action may be mediated by suppression of endogenous nitric oxide activity.

Arginine↗
PubMed1991

Hydrogen peroxide stimulates phospholipase A2-mediated arachidonic acid release in cultured intestinal epithelial cells (INT 407).

The mechanisms by which hydrogen peroxide and, for comparison, 4-beta-phorbol-12-myristate-13-acetate (PMA) stimulate release of radiolabeled arachidonic acid (14C-AA) in cultured intestinal epithelial cells (INT 407) were investigated. Both hydrogen peroxide and PMA caused a rapid (3 min) and dose-related intracellular release of free 14C-AA, followed by a dose- and time-dependent release of 14C-AA into the extracellular medium, but hydrogen peroxide was about 50,000 times less effective than PMA in releasing 14C-AA. No 14C-AA was released on stimulation with 4-alpha-phorbol-12,13-di-decanoate (PDD), a phorbol ester that does not activate protein kinase C. The 14C-AA release was reduced by the phospholipase A2 inhibitors nordihydroguaiaretic acid and 4-bromophenacyl bromide and by the calmodulin/protein kinase C inhibitor trifluoperazine and the protein kinase C inhibitor 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine (H-7). However, H-7 was less effective than the other inhibitors in reducing the hydrogen peroxide-stimulated 14C-AA release. The hydrogen peroxide-stimulated, but not the PMA-stimulated, rapid (3 min) 14C-AA release was associated with an increased influx of extracellular calcium. Stimulation of the cells with PMA resulted in phosphorylation of a cellular protein of about 32 kDa, whereas no phosphorylation of this protein was detected after stimulation with hydrogen peroxide. Taken together, these findings indicate that (i) both PMA and hydrogen peroxide may stimulate phospholipase A2-mediated AA release from human intestinal epithelial cells; (ii) this stimulation is brought about via protein kinase C and calmodulin-mediated events; (iii) PMA-stimulated 14C-AA release is associated with phosphorylation of a 32-kDa protein, possibly lipocortin, whereas the hydrogen peroxide-stimulated release is not; and (iv) calmodulin is more important for the hydrogen peroxide-stimulated 14C-AA release than is protein kinase C. The possibility that hydrogen peroxide-evoked AA release may contribute to the mucosal abnormality in Crohn's disease is discussed.

Arachidonic Acid↗
PubMed2006

A multicenter efficacy and tolerability evaluation of benzoyl peroxide in a 10% urea vehicle for the treatment of acne vulgaris.

BACKGROUND: Acne vulgaris is a common skin disease that affects 70 to 96% of individuals. Topical benzoyl peroxide has been used successfully for acne treatment; however, it may be accompanied by drying and or flaking skin. The addition of a 10% urea to the product excipient is theorized to moisturize the skin due to its humectant properties, aid in the efficacy of benzoyl peroxide due to its keratolytic properties, and effectively combat Propionibacterium acnes due to its antibacterial properties. OBJECTIVE: To assess the efficacy and tolerability of the treatment of acne vulgaris with multiple strengths of benzoyl peroxide in a 10% urea vehicle gel or cream and cleanser. METHODS: A multicenter, non-randomized, open-label study in which 1,089 patients with acne vulgaris were enrolled at 133 participating physician office sites. Qualifying and consenting patients were prescribed either 4.5% or 8.5% benzoyl peroxide in a 10% urea vehicle cream or gel and cleanser. Additional medications were permitted during the study with the exception of those containing benzoyl peroxide. The physician assessed lesion counts, both inflammatory and non-inflammatory, at baseline and Week 4. Dryness and erythema were rated by the physician on a scale from 0 (none) to 8 (severe or deep) at baseline and Week 4. RESULTS: Nine hundred sixty-three patients completed the study. The following significant treatment arms were analyzed: patients treated with 4.5%/8.5% benzoyl peroxide in a 10% urea vehicle product only, patients treated with 4.5%/8.5% benzoyl peroxide in a 10% urea vehicle products along with oral doxycycline, and patients treated with 4.5%/8.5% benzoyl peroxide in a 10% urea vehicle products along with oral minocycline. A 44% (n=567) mean reduction in total lesion count was observed after 4 weeks of treatment with 4.5%/8.5% benzoyl peroxide in a 10% urea vehicle products only. Dual therapy using oral doxycycline (n=17) proved to be even more effective with a significant mean reduction in lesion count of 52% after only 4 weeks of treatment. Dual therapy using oral minocycline (n=21) yielded a significant mean reduction in lesion count of 34% after 14 weeks of treatment. The overall tolerability of the treatment illustrated the utility of urea as a moisturizing agent. CONCLUSION: Benzoyl peroxide in a 10% urea vehicle gel or cream and cleanser, used once daily for 4 weeks was found to be both effective and well tolerated for the treatment of symptoms related to acne vulgaris.

Acne Vulgaris↗
PubMed1983

Stimulation of mouse heart and liver microsomal lipid peroxidation by anthracycline anticancer drugs: characterization and effects of reactive oxygen scavengers.

The interaction of adriamycin or several other quinone-containing anthracycline anticancer drugs with mouse heart or liver microsomes resulted in greatly enhanced NADPH oxidation and 5- to 10-fold stimulation of NADPH-dependent, reactive oxygen-mediated microsomal lipid peroxidation. Adriamycin, daunorubicin, desacetyladriamycin and aclacinomycin A all stimulated lipid peroxidation maximally when included at concentrations of 100 to 200 microM, whereas carminomycin and 4-demethoxydaunorubicin produced equivalent enhancement of peroxidation at lower concentrations of 30 to 50 microM. Mitomycin C markedly increased heart microsomal lipid peroxidation, but, interestingly, had little effect when liver microsomes were used. In contrast, 5-imino-daunorubicin and alkylaminoanthracenedione inhibited both heart and liver microsomal lipid peroxidation. NADPH supported anthracycline-stimulated lipid peroxidation, however, an NADPH-generating system provided greater activity. NADH was only about 50% as effective as NADPH and served as cofactor with liver microsomes but not with heart microsomes. Scavengers of reactive oxygen such as superoxide dismutase, reduced glutathione and 1,3-dimethylurea diminished the anthracycline-stimulated heart and liver microsomal lipid peroxidation, indicating that superoxide radical and hydroxyl radical participated in the peroxidation reactions. Ethylenediaminetetraacetic acid was also inhibitory, which suggests trace amounts of iron were also required. Adriamycin, 4-demethoxydaunorubicin, carminomycin, aclacinomycin A and mitomycin C strikingly enhanced peroxidation of unsaturated lipids in mouse lung and kidney microsomes, indicating that anthracycline-mediated enhanced reactive oxyradical generation may have toxic consequences in those organs as well as in the heart. These observations support the proposal that anthracycline-accentuated membrane lipid peroxidation may be relevant to the pathogenesis of anthracycline cardiotoxicity.

Animals↗
PubMed1980

[Comparative properties of mitochondrial and microsomal NAD(P)H-dependent lipid peroxidation].

It was shown that rat liver mitochondria and microsomes contain NADPH- and NADH-dependent systems of enzymatic lipid peroxidation. Activation of the NAD(P)H-dependent process in mitochondria occurs due to inhibition of membrane binding of Fe3+ and Fe2+ by chelators, since the membrane-bound ions of Fe cannot effectively participate in peroxidation. The activity of enzymatic mitochondrial lipid peroxidation decreases at alkaline values of pH. The Michaelis constant for chelated Fe3+ ions under NAD(P)H-dependent mitochondrial peroxidation is by 1,5 order of magnitude more than for microsomal peroxidation. In terms of the chelators' effect on Fe3+ binding by microsomes and peroxidation, as well as pH and Km for Fe3+ the microsomal NADHL-dependent system of lipid peroxidation is similar to mitochondrial NADPH-systems; however, it differs from the latter in the type of dependence of peroxidation on the amount of membranes. Based on the ability of the NADPH-system of microsomes to produce the superoxide radical which participates in initiation of peroxidation together with Fe ions, it is assumed that the decrease of Km for Fe3+ at NAD(P)H-dependent lipid peroxidation in mitochondria and the NADH-process in microsomes can occur in the presence of exogenous sources of active oxygen production.

Animals↗
PubMed1998

Antioxidant and pro-oxidant effects of epinephrine and isoprenaline on peroxidation of LDL and lipid liposomes.

Antioxidant or pro-oxidant properties of epinephrine (EPI) and isoprenaline (ISO) were studied in the absence and presence of Fe2+, Fe3+ and Cu2+ ions. EPI and ISO (>2 micromol/l) inhibited peroxidation of low density lipoprotein (LDL) induced by 2, 2'-azobis(2-amidino-propane) (AAPH). EPI had a similar inhibitory potency as ISO, but their potency was several times higher than the potency of alpha-tocopherol (alpha-TOC). When the LDL peroxidation was induced by 5 micromol/l CuSO4, EPI and ISO enhanced LDL peroxidation at low concentrations (10micromol/l) and decreased peroxidation at higher concentrations (30 micromol/l). The compounds had a similar tendency to inhibit the peroxidation of phosphatidylcholine liposomes. EPI (3-30 micromol/l) inhibited lipid peroxidation of phosphatidylcholine liposomes induced by 2 mmol/l of AAPH, but it was less effective and even increased the peroxidation, when the samples contained 2 mmol/l AAPH with 50 micromol/l FeSO4 or 2 mmol/l AAPH with 20 micromol/l FeCl3. Inhibition of lipid peroxidation by EPI was also observed when studying decreased oxygen consumption, when the peroxidation of linoleic acid was induced by lipoxidase. In conclusion, EPI and ISO reduced lipid peroxidation, but they exhibit pro-oxidant properties in the presence of Fe2+, Fe3+ or Cu2+ ions, depending on the catecholamine and ionic concentration.

Amidines↗
PubMed1998

Nitric oxide inhibits peroxide-mediated endothelial toxicity.

BACKGROUND: Oxidant molecules and nitric oxide (NO) have each been implicated as mediators of endothelial cell damage, but the biologic effect of these molecules acting in concert is incompletely understood. MATERIALS AND METHODS: We studied the effects of an NO donor, S-nitroso-acetyl-D,L-penicillamine (SNAP), in combination with the peroxidants tert-butyl hydroperoxide (TBH) and hydrogen peroxide (H2O2) on rabbit aortic endothelial cells in culture. Cell viability was assessed using Alamar blue, a nontoxic dye indicator of cell metabolism. Lipid peroxidation was assessed using a chemiluminescent single-photon counting technique. RESULTS: After 90 min exposure to test reagents, there was concentration-dependent cytotoxicity for both TBH and H2O2. Peroxidant-induced cytotoxicity was significantly ameliorated by SNAP (10(-4)-10(-3)M). N-Acetylpenicillamine and NO-depleted SNAP failed to demonstrate a cytoprotective effect against peroxidant cellular injury, thus implicating NO as the agent responsible for the protective effect. SNAP reduced lipid peroxidation caused by 10(-3) M TBH in a dose-dependent manner. Preincubation of cells with SNAP before exposure to peroxidants alone had no effect on toxicity. CONCLUSIONS: NO is cytoprotective to the endothelium in the presence of peroxidants through a reduction of lipid peroxidation.

Animals↗
PubMed1989

Inhibitory effect of eugenol on Cu2+-catalyzed lipid peroxidation in human erythrocyte membranes.

1. The effects of eugenol on lipid peroxidation catalyzed by hydrogen peroxide (H2O2) or benzoyl peroxide (BPO) in the presence of copper ions were studied in human erythrocyte membranes. 2. The production of hydroxyl radicals was suggested in the peroxidation system catalyzed by H2O2/Cu2+. 3. H2O2/Cu2+-dependent peroxidation was inhibited by eugenol in a concentration-dependent manner; peroxidation was inhibited 62% by 200 microM eugenol. 4. In the presence of eugenol, the peroxidation catalyzed by BPO/Cu2+ was inhibited in a concentration-dependent manner, and more than 100 microM eugenol completely inhibited peroxidation. 5. The inhibitory effect of eugenol was non-competitive against Cu2+ in H2O2/Cu2+- and BPO/Cu2+-dependent peroxidation. 6. It is suggested that eugenol inhibits formation of hydroxyl radicals.

Benzoyl Peroxide↗
PubMed2002

Lipid peroxidation induced by phenylbutazone radicals.

Lipid peroxidation was investigated to evaluate the deleterious effect on tissues by phenylbutazone (PB). PB induced lipid peroxidation of microsomes in the presence of horseradish peroxidase and hydrogen peroxide (HRP-H2O2). The lipid peroxidation was completely inhibited by catalase but not by superoxide dismutase. Mannitol and dimethylsulfoxide had no effect. These results indicated no paticipation of superoxide and hydroxyl radical in the lipid peroxidation. Reduced glutathione (GSH) efficiently inhibited the lipid peroxidation. PB radicals emitted electron spin resonance (ESR) signals during the reaction of PB with HRP-H2O2. Microsomes and arachidonic acid strongly diminished the ESR signals, indicating that PB radicals directly react with unsaturated lipids of microsomes to cause thiobarbituric acid reactive substances. GSH sharply diminished the ESR signals of PB radicals, suggesting that GSH scavenges PB radicals to inhibit lipid peroxidation. Also, 2-methyl-2-nitrosopropan strongly inhibited lipid peroxidation. R-Phycoerythrin, a peroxyl radical detector substance, was decomposed by PB with HRP-H2O2. These results suggest that lipid peroxidation of microsomes is induced by PB radicals or peroxyl radicals, or both.

Animals↗
PubMed2002

Effect of peroxide concentration and brushing on whitening clinical response.

This clinical trial compared the effects of hydrogen peroxide concentration and toothbrushing on clinical response to vital bleaching. Tooth bleaching was accomplished with a flexible, polyethylene strip coated with a hydrogen peroxide bleaching gel worn for 30 minutes twice daily over a 14-day period. A total of 36 subjects were randomized to 1 of 3 treatment groups: 5.3% hydrogen peroxide strip plus prebrushing, 6.5% hydrogen peroxide strip plus prebrushing, or 6.5% hydrogen peroxide strip without prebrushing. Two groups brushed with regular anticavity toothpaste immediately before bleaching, while the other group performed ad libitum brushing only. Tooth color was measured over a 14-day period using digital images of the anterior dentition. Over the 14-day treatment period, all 3 strip groups experienced highly significant (P < 0.001) whitening as evidenced by decreased yellowness (delta b*) and increased brightness (delta L*), as well as composite color change (delta E*) relative to baseline. Keeping brushing constant, the 6.5% hydrogen peroxide strip plus prebrushing group experienced a 31% to 60% improvement in whitening relative to the 5.3% hydrogen peroxide standard. Keeping concentration constant at 6.5% hydrogen peroxide, the prebrushing group experienced a directional 5% to 33% improvement in whitening relative to no prebrushing. All treatments were generally well tolerated. This study demonstrates that for strip-based delivery, increasing hydrogen peroxide concentration to 6.5% results in a significant improvement in efficacy with few tolerability trade-offs.

Adult↗
PubMed2002

Overview of a professional tooth-whitening system containing 6.5% hydrogen peroxide whitening strips.

Professionally dispensed, at-home tooth whitening began with 10% carbamide peroxide gels applied to the dentition with custom-made trays. In the 1990s, higher-concentration carbamide peroxide gels were introduced to achieve faster results. Today, 15% and 20% carbamide peroxide gels are commonly used. Recently, a new vital tooth-whitening technique that uses a flexible strip rather than a tray to apply a 5.3% hydrogen peroxide whitening gel was introduced. The new strip-based product was shown to provide whitening equivalent to a 10% carbamide peroxide tray with half the wear time. In addition, the strip eliminated the need to custom fabricate trays for each patient. This article provides an overview of a professionally distributed strip-based whitening system and reviews some of the clinical data which supports the efficacy of the product. This new whitening system includes 42 mandibular and 42 maxillary strips at a higher concentration of 6.5% hydrogen peroxide. In addition, the system also includes a novel dual-action whitening dentifrice to prevent future staining postbleaching and an extrasoft toothbrush. Clinically, the professionally distributed strip-based whitening system provided 96% more efficacy than a popular carbamide plus hydrogen peroxide (equivalent to 10% carbamide peroxide) tray system and 52% more whitening than the 5.3% hydrogen peroxide strip system.

Carbamide Peroxide↗
PubMed2004

Clinical response of three whitening products having different peroxide delivery: comparison of tray, paint-on gel, and dentifrice.

OBJECTIVE: Comparative clinical research was conducted to evaluate the efficacy and safety of three peroxide-containing tooth whitening products having different peroxide delivery. METHODOLOGY: A total of 43 healthy adults who met entrance criteria were randomly assigned to either a dual-phase, anticavity, 1% hydrogen peroxide dentifrice with a manganese gluconate activator, an 18% carbamide peroxide paint-on gel, or a 5% carbamide peroxide professional custom tray system. Following manufacturer's instructions, the activated dentifrice was used at least twice daily for two minutes, while the paint-on gel was applied twice daily. The custom tray, a barrier system and the experimental control for this study, was worn continuously for six to eight hours daily. Tooth color (L*a*b*) was measured on the maxillary anterior teeth from standard digital images, while safety was assessed from examination and subject report. RESULTS: At Day 15, the custom tray group had a significant (p < 0.002) reduction in yellowness and increased lightness, with adjusted mean (SE) deltab* of -1.83 (0.210) and deltaL* of 1.45 (0.292). The custom tray group experienced on average greater color improvement compared to either the paint-on gel or activated peroxide whitening dentifrice, differing significantly (p < 0.01) from either of the barrier-free systems with respect to deltab*, deltaL*, deltaE*, and deltaW*. In comparison, 14-days' use of the paint-on gel and activated dentifrice did not result in significant (p > 0.10) color improvements from baseline for deltab*, deltaL*, or deltaW*, with these two barrier-free systems not differing significantly (p > 0.26) with respect to any individual or composite color parameters. Tooth sensitivity and oral irritation were the most common safety findings in the tray and dentifrice groups (there were no adverse events in the paint-on group), and no subject discontinued treatment early because of a treatment-related adverse event. CONCLUSION: In head-to-head 14-day testing, a low concentration (5% carbamide peroxide) barrier-based tray system yielded superior tooth color improvement compared to two barrier-free delivery systems-an 18% carbamide peroxide paint-on gel and a 1% hydrogen peroxide dentifrice with a metal activator.

Adolescent↗
PubMed1976

Effect of glutathione peroxidase activity on lipid peroxidation in biological membranes.

Results are presented indicating that, although glutathione peroxidase activity inhibits lipid peroxidation in membranes, it does not appear to do so by reducing membrane lipid peroxides to lipid alcohols, as has been shown by others to be the case for free fatty acid peroxides in solution. Lipid peroxidation was studied in an enzymic system (microsomal NADPH oxidase) and in a non-enzymic system (mitochondria plus ascorbate). A study of the fatty acids in the phospholipids of microsomes and mitochondria demonstrated that detectable amounts of hydroxy fatty acids were not formed in the membranes when the latter were incubated in the presence of the glutathione peroxidase system even under conditions known to have generated significant levels of lipid peroxides in the membrane. Fatty acid analyses of the microsomal and mitochondrial particles indicated that glutathione peroxidase activity inhibited loss of polyunsaturated fatty acids when these organelles were exposed to peroxidizing conditions. If glutathione peroxidase activity were inhibiting the formation of malondialdehyde (a product of lipid peroxidation) by converting peroxide groups to alcohols, the loss of the constitutive polyunsaturated fatty acids in the membrane should not have been appreciably affected by addition of the peroxidase system. The protective effect cannot be due to quenching of an autocatalytic type of lipid peroxidation (at least in the microsomal system) since it has been established that the microsomal enzyme system (NADPH oxidase) catalyzes a continuous attack on microsomal polyunsaturated fatty acyl groups during the reaction and that the peroxidative process is not autocatalytic in nature. It appears, therefore, that glutathione peroxidase activity must exert its effect on this system by preventing free radical attack on the polyunsaturated membrane lipids in the first place. A possible mechanism for the interruption of a free radical attack on the lipids is proposed.

Animals↗
PubMed1993

Role of lipid structure in the activation of phospholipase A2 by peroxidized phospholipids.

The time course of hydrolysis of a mixed phospholipid substrate containing bovine liver 1,2-diacyl-sn-glycero-3-phosphocholine (PC) and 1,2-diacyl-sn-glycero-3-phosphoethanolamine (PE) catalyzed by Crotalus adamanteus phospholipase A2 was measured before and after peroxidation of the lipid substrate. The rate of hydrolysis was increased after peroxidation by an iron/adenosine diphosphate (ADP) system; the presence of iron/ADP in the assay had a minimal inhibitory effect. The rate of lipid hydrolysis was also increased after the substrate was peroxidized by heat and O2. Similarly, peroxidation increased the rate of hydrolysis of soy PC liposomes that did not contain PE. In order to minimize interfacial factors that may result in an increase in rate, the lipids were solubilized in Triton X-100. In mixtures of Triton with soy PC in the absence of PE, peroxidation dramatically increased the rate of lipid hydrolysis. In addition, the rate of hydrolysis of the unoxidizable lipid 1-palmitoyl-2-[1-14C]oleoyl PC incorporated into PC/PE liposomes was unaffected by peroxidation of the host lipid. These data are consistent with the notions that the increase in rate of hydrolysis of peroxidized PC substrates catalyzed by phospholipase A2 is due largely to a preference for peroxidized phospholipid molecules as substrates and that peroxidation of host lipid does not significantly increase the rate of hydrolysis of nonoxidized lipids.

Adenosine Diphosphate↗
PubMedDate not supplied

Hydroxyl radical formation and lipid peroxidation enhancement by chromium. In vitro study.

Chromium VI compounds have been shown to be carcinogenic in occupationally exposed humans, and to be genotoxic, mutagenic, and carcinogenic in a variety of experimental systems. In contrast, most chromium III compounds are relatively nontoxic, noncarcinogenic, and nonmutagenic. Reduction of Cr6+ leads to reactive intermediates, such as Cr5+, Cr4+, or other radical species. The molecular mechanism for the intracellular Cr6+ reduction has been the focus of recent studies, but the details are still not understood. Our study was initiated to compare the effect of Cr(6+)-hydroxyl radical formation and Cr(6+)-induced lipid peroxidation vs those of Cr3+. Electron spin resonance measurements provide evidence for the formation of long-lived Cr5+ intermediates in the reduction of Cr6+ by glutathione reductase in the presence of NADPH and for the hydroxyl radical formation during the glutathione reductase catalyzed reduction of Cr6+. Hydrogen peroxide suppresses Cr5+ and enhances the formation of hydroxyl radical. Thus, Cr5+ intermediates catalyze generation of hydroxyl radicals from hydrogen peroxide through a Fenton-like reaction. Comparative effects of Cr6+ and Cr3+ on the development of lipid peroxidation were studied by using rat heart homogenate. Heart homogenate was incubated with different concentrations of Cr6+ compounds at 22 degrees C for 60 min. Lipid peroxidation was determined as thiobarbituric acid reacting materiels (TBA-RM). The results confirm that Cr6+ induces lipid peroxidation in the rat heart homogenate. These observations might suggest a possible causative role of lipid peroxidation in Cr6+ toxicity. This enhancement of lipid peroxidation is modified by the addition of some metal chelators and antioxidants. Thus, strategies for combating Cr6+ toxicity should take into account the role of the hydroxy radicals, and hence, steps for blocking its chain propagation and preventing the formation of lipid peroxides.

Animals↗
PubMed2006

Antioxidant effect of bisphosphonates and simvastatin on chondrocyte lipid peroxidation.

The objective of this study was to evaluate the effect of bisphosphonates (BPs) and simvastatin on chondrocyte lipid peroxidation. For this purpose, a flow cytometrical method using C11-BODIPY(581/591) was developed to detect hydroperoxide-induced lipid peroxidation in chondrocytes. Tertiary butylhydroperoxide (t-BHP) induced a time and concentration dependent increase in chondrocyte lipid peroxidation. Addition of a Fe2+/EDTA complex to t-BHP or hydrogen peroxide (H2O2) clearly enhanced lipid peroxidation. The lipophilic simvastatin demonstrated a small inhibition in the chondrocyte lipid peroxidation. None of three tested BPs (clodronate, pamidronate, and risedronate) had an effect on chondrocyte lipid peroxidation induced by t-BHP. However, when Fe2+/EDTA complex was added to t-BHP or H2O2, BPs inhibited the lipid peroxidation process varying from 25% to 58%. This study demonstrates that BPs have antioxidant properties as iron chelators, thereby inhibiting the chondrocyte lipid peroxidation. These findings add evidence to the therapeutic potential of bisphosphonates and statins in rheumatoid arthritis.

Animals↗