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PubMed1995

Direct measurement of lipid peroxidation in submitochondrial particles.

The susceptibility of the polyunsaturated fatty acid parinaric acid (cis-PnA) to peroxidative damage with concomitant loss of its fluorescent character can be used to detect lipid peroxidation in a direct and sensitive way. The procedure, originally developed to measure peroxidation in lipid vesicles and erythrocyte membranes, has been adapted for the study of submitochondrial particles. Optimal conditions for the concentrations of cis-PnA (0.8 mol %), mitochondrial membrane (100 microM membrane phospholipid), and the radical generating system (50 microM NADH and 10 microM:1 mM Fe(III)-ADP) were established. In the absence of peroxidation inducing compounds, a stable fluorescent signal can be detected. Upon addition of NAD(P)H and ADP-Fe(III), lipid peroxidation starts, and the observed fluorescence decrease is a measure of peroxidation. Both NADH and NADPH were able to induce lipid peroxidation in submitochondrial particles in the presence of an iron chelate. The use of NADH resulted in higher rates of peroxidation compared with NADPH at the same concentration. Whereas the rate of NADH-induced lipid peroxidation was maximal at very low NADH concentrations (2.5 microM) and decreased when the concentration became higher, the NADPH-induced lipid peroxidation reaches saturation at 100 microM. NADH-induced lipid peroxidation in submitochondrial particles from different rat tissues (heart, skeletal muscle, and liver) resulted in a clear difference in peroxidation rates. The highest rates were observed in heart submitochondrial particles, while the lowest rates were obtained in submitochondrial particles derived from liver. Skeletal muscle submitochondrial particles showed intermediate rates of lipid peroxidation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Diphosphate↗
PubMed1983

Studies on the role of reactive oxygen species in mediating lipid peroxide formation in epidermal microsomes of rat skin.

The role of superoxide, hydrogen peroxide, and singlet oxygen in mediating nonenzymic and NADPH-supported enzymic lipid peroxidation in skin microsomes was investigated. Incubation of skin microsomes with NADPH and/or Fe+3-ADP or ascorbate resulted in the formation of lipid peroxides. The epidermis was the major target site for microsomal lipid peroxide formation in skin. Enzymic peroxidation of epidermal microsomes required NADPH and was oxygen-dependent. Addition of the nonenzymic catalysts, Fe+3 and ADP, to the enzymic peroxidation system had an additive effect on the generation of lipid peroxide in epidermal microsomes. Epidermal microsomal lipid peroxidation was inhibited by singlet oxygen quenchers such as dimethylfuran, histidine, and beta-carotene. Hydroxyl ion scavengers such as mannitol, benzoate, or ethyl alcohol and the enzymic scavenger of superoxide, superoxide dismutase, were all ineffective in this respect. Addition of EDTA, Mn+2, cytochrome c+3, and catalase to the NADPH-supported enzymic peroxidation system resulted in strong inhibition of lipid peroxide formation in skin. Glutathione or epidermal cytosol added alone or in combination to the NADPH-supported incubation system enhanced peroxidation of microsomal lipids. Vitamin E (alpha-tocopherol) inhibited lipid peroxidation. These results indicate that singlet oxygen may mediate lipid peroxide formation in epidermal microsomes.

Adenosine Diphosphate↗
PubMed2000

Mechanisms of cerebral arterial relaxations to hydrogen peroxide.

BACKGROUND AND PURPOSE: The role of hydrogen peroxide in the regulation of cerebral arterial tone is not completely understood. Previous studies have demonstrated that hydrogen peroxide causes vasodilation of small cerebral arteries. The present study was designed to determine the mechanisms responsible for relaxations of large cerebral arteries to hydrogen peroxide. METHODS: Rings of canine middle cerebral arteries without endothelium were suspended for isometric force recording in modified Krebs-Ringer bicarbonate solution bubbled with 94% O(2)/6% CO(2) (37 degrees C, pH 7.4). Radioimmunoassay technique was used to determine the levels of cAMP and cGMP. RESULTS: During contraction to UTP (3 x 10(-6) or 10(-5) mol/L), hydrogen peroxide (10(-6) to 10(-4) mol/L) caused concentration-dependent relaxations. Catalase (1200 U/mL) abolished the relaxations to hydrogen peroxide. Inhibition of cyclooxygenase by indomethacin (10(-5) mol/L) significantly reduced relaxations to hydrogen peroxide. In arteries contracted by KCl (20 mmol/L), the relaxations to hydrogen peroxide were significantly reduced. In the presence of a nonselective potassium channel inhibitor, BaCl(2) (10(-4) mol/L), a delayed rectifier potassium channel inhibitor, 4-aminopyridine (10(-3) mol/L), or a calcium-activated potassium channel inhibitor, charybdotoxin (3 x 10(-8) mol/L), the relaxations to hydrogen peroxide were also significantly reduced. An ATP-sensitive potassium channel inhibitor, glyburide (5 x 10(-6) mol/L), did not affect the relaxations to hydrogen peroxide. Hydrogen peroxide produced concentration-dependent increase in levels of cAMP. Indomethacin (10(-5) mol/L) inhibited the stimulatory effect of hydrogen peroxide on cAMP production. In contrast, hydrogen peroxide did not affect the levels of cGMP. CONCLUSIONS: These results suggest that hydrogen peroxide may cause relaxations of large cerebral arteries in part by activation of arachidonic acid metabolism via cyclooxygenase pathway with subsequent increase in cAMP levels and activation of potassium channels.

Animals↗
PubMed1990

Antigonadotropic and antisteroidogenic actions of peroxide in rat granulosa cells.

Reactive oxygen species are produced in the ovary. In luteal cells, peroxide abruptly inhibits LH-sensitive cAMP and progesterone production, and may serve a role as a mediator of luteolysis by such mechanisms. The objective of the present studies was to evaluate the acute actions of peroxide in rat granulosa cells. Peroxide at concentrations in the low micromolar range produced a marked and dose-dependent inhibition of FSH-sensitive cAMP accumulation and progesterone production, and depleted cell levels of ATP within 1 min. Longer treatment with peroxide (60 min) caused complete abrogation of the actions of FSH. Peroxide-induced depletion of ATP was prevented by 3-aminobenzamide, an inhibitor of DNA repair, but maintenance of cell levels of ATP did not prevent the anti-FSH effects of peroxide. Peroxide also abrogated cAMP accumulation and progesterone production in response to LH in granulosa cells. Unlike that seen with LH, inhibition of FSH-sensitive cyclic AMP accumulation by peroxide was partially reversed with isobutylmethyl xanthine, an inhibitor of cyclic AMP phosphodiesterase. Although peroxide inhibited cAMP accumulation in response to cholera toxin, it did not inhibit this same response to forskolin, which indicates that peroxide may interfere with G-protein-dependent activation of adenylate cyclase. Peroxide inhibited steroidogenesis in response to cholera toxin, forskolin, and 8-bromo-cAMP. The marked inhibitory actions of peroxide on gonadotropic hormone action and steroidogenesis in granulosa cells raise the possibility that peroxide may mediate events associated with loss of follicular function.

1-Methyl-3-isobutylxanthine↗
PubMed2000

[Studies on membrane factors in iron-supported lipid peroxidation].

Lipid peroxidation in biomembranes is mediated by free radical reactions. It leads to membrane damage and has been proposed to be associated with the pathogenesis to tissue injuries. Iron is known as a catalyst of lipid peroxidation. Microsomal lipid peroxidation by both NADPH and iron-chelate, such as Fe(3+)-ADP or Fe(3+)-PPi, is believed to be enzymatically associated with iron reduction. On the other hand, the addition of free Fe2+ to microsomes or liposomes produces a lag phase before the maximal rates of lipid peroxidation. We examined the interaction of iron with membrane in iron-supported lipid peroxidation and microsomal membrane components associated with iron reduction in NADPH-supported lipid peroxidation. Iron-supported lipid peroxidation was affected by the surface charges of liposomal membrane. Liposomes containing phosphatidylserine (PS) were most sensitive to iron-supported lipid peroxidation. The effect of PS on iron-supported lipid peroxidation indicates that iron participates in binding to membrane surface charges and also indicates that Fe2+ at high level bound to membranes plays a role in producing a lag phase. The mechanism producing a lag phase in Fe(2+)-PPi-supported lipid peroxidation is discussed. In NADPH-supported lipid peroxidation in microsomes, it seemed unlikely that superoxide may be involved in iron reduction. Alternatively, under anaerobic conditions, NADPH-supported iron reduction in microsomes was not dependent on cytochrome P450 content and not inhibited by CO. A cholate-solubilized fraction of microsomes was applied to a laurate-Sepharose column and an active fraction for lipid peroxidation was obtained. Involvement of a heat-labile component, distinct from cytochrome P450, responsible for iron reduction in microsomal lipid peroxidation was demonstrated.

Animals↗
PubMed1997

Admixture of a multivitamin preparation to parenteral nutrition: the major contributor to in vitro generation of peroxides.

BACKGROUND: Peroxides have been reported to contaminate lipid emulsions and amino acid solutions used in total parenteral nutrition (TPN). This is particularly disturbing in newborn infants who are prone to several diseases related to immature defense mechanisms against oxidative challenges. It is not clear whether the antioxidants in multivitamins help protect parenteral nutrients against the hazards of oxidation. OBJECTIVE: To evaluate the role of a multivitamin preparation (MVI) on the actual peroxide load received by patients on TPN. METHODOLOGY: The generation of peroxides in parenteral nutrition was tested first using test solutions. We compared the relative contribution of commercially available amino acid solutions, a lipid emulsion, and MVI on the level of peroxides in clinically relevant TPN solutions. Second, we measured the level of peroxides actually infused at the bedside. In both circumstances, the effects of time and light exposure were isolated. The level of peroxides was determined by a colorimetric technique and expressed as microM equivalents tert-butyl hydroperoxide (microM = TBH). RESULTS: Even when protected from light, the addition of MVI produced a 10-fold increase in peroxides (mean +/- SEM, n = 3, 19 +/- 4 to 189 +/- 8 microM = TBH at 4 h) in the fat-free TPN solution and a fourfold increase (64 +/- 6 to 244 +/- 8 microM = TBH at 4 h) in the lipid-containing TPN solution. A dose-response relationship was found between the concentration of MVI and peroxide levels. The effect of light was the strongest in the presence of multivitamins. The amino acid solutions had a relative inhibitory effect on the generation of peroxides by MVI, which varied (from 54 +/- 1% to 72 +/- 1%) all according to the amino acid blend. In parenterally fed premature infants, protecting the intravenous set from light decreased the load of infused peroxides (146 +/- 15 vs 215 +/- 24 microM = TBH). CONCLUSIONS: The lipid emulsion had a significant but minor additive effect compared with the multivitamin preparation, which was the major contributor to the generation of peroxides. Protection from photooxidation is not sufficient to prevent peroxidation of TPN solutions. Contrary to what one would expect, increasing the concentration of MVI will lead to a greater generation of peroxides, suggesting that the essential antioxidants in MVI do not have antiperoxide properties.

Amino Acids↗
PubMedDate not supplied

[Hydrogen peroxide as an inductor of uncultivable state of Vibrio cholerae eltor in an experiment].

The influence of hydrogen peroxide on the dynamics of transition into uncultivable state (UCS) and on the reversion of V. cholerae and their subcultures, resistant to hydrogen peroxide, was studied. The transition of the initial cultures in river and distilled water into UCS took place earlier than that in resistant to hydrogen peroxide variants. The capacity for reversion to hydrogen peroxide resistant subcultures preserved, on the average, 2 - 3 times longer. An increase in the level of hydrogen peroxide in uncultivable populations was found to be 2.7 - 4.4 times. Subcultures, resistant to hydrogen peroxide, in the vegetative form had lower characteristics of peroxide concentrations than in uncultivable form (UCF), but somewhat higher than in initial variants. In revertants the concentration of hydrogen peroxide was lower in UCF, but somewhat higher than in vegetative cultures. The dynamics of the formation of UCF by cholera vibrios, with different degree of stability to the action of hydrogen peroxide, the accumulation of hydrogen peroxide in uncultivable populations, the deceleration of transition into uncultivable forms, an accumulation of hydrogen peroxide and an increase in the time of the reversion of clones, resistant to hydrogen peroxide, made it possible to suggest that the accumulation of hydrogen peroxide was possible to make an essential contribution to the formation of UCF of cholera vibrios in an experiment.

Adaptation, Physiological↗
PubMed1996

Biological properties of peroxide-containing tooth whiteners.

Peroxides have been used in tooth whitening for more than 100 years. Current peroxide-containing whiteners can be classified into three categories: (1) those containing high concentrations of peroxides for professional use only; (2) materials dispensed by dentists and used by patients at home; and (3) over-the-counter products available directly to consumers for home use. Hydrogen peroxide (H2O2) and carbamide peroxide are the most commonly used active ingredients in these whiteners. Both peroxides have long been used safely in oral health products and are accepted by the US Food and Drug Administration. However, questions have been raised regarding the safety of at-home whiteners because the peroxides appear to constitute a new use. Substantial differences exist in the manner of application between at-home whiteners and oral health products. In addition, tooth whiteners are a mixture of various ingredients; possible interactions may occur because of the active nature of peroxides. Therefore, the safety evidence for peroxide-containing whiteners is considered inadequate. This paper will review the history of using peroxides for tooth whitening, the toxicology of H2O2 and carbamide peroxide, and available information on the safety of whiteners. The rationale and approaches for evaluating biological properties of peroxide containing whiteners are also discussed.

Carbamide Peroxide↗
PubMed2004

A new approach to strip-based tooth whitening: 14% hydrogen peroxide delivered via controlled low dose.

Professionally dispensed, take-home whitening products originally consisted of tray systems into which the patient dispensed a peroxide-containing gel. Because the process of inserting peroxide-containing gels into the trays is patient controlled, the resulting exposure of the gingiva to peroxide can be variable, and often high. In addition to concentration, soft tissue irritation is a function of the amount, or dose, of peroxide with which the tissue is challenged. All other things being equal, higher-concentration products will whiten faster because of the peroxide concentration gradient, but they also will lead to poorer soft tissue tolerability because of a higher peroxide challenge. Consequently, take-home trays are somewhat limited with respect to the concentration of hydrogen peroxide that they can safely use. In 2000, strip-based whitening technology was introduced that allowed a controlled, uniform, low dose of peroxide to be applied to the teeth. An execution of this strip-based technology that contained 6.5% hydrogen peroxide, Crest Professional Whitestrips, was launched in 2001. A new professionally dispensed strip product, Crest Whitestrips Supreme, recently has been introduced. A 14% hydrogen-peroxide gel is incorporated onto these strips, but the amount of gel is half of what is on the 6.5% strips. The net result is that the dose, or amount, of peroxide on each strip is essentially the same as for the Professional Whitestrips product. Therefore, the 14% hydrogen-peroxide strip product whitens faster and better than previous strip products, while still being well tolerated by the soft tissue.

Carbamide Peroxide↗
PubMed1993

Xanthine oxidase- and iron-dependent lipid peroxidation.

Xanthine oxidase and iron-dependent lipid peroxidation has been studied extensively in many model systems, yet several details of this process remain unclear. Because redox reactions of iron are important parameters of iron-catalyzed lipid peroxidation, we have examined the roles of superoxide and hydrogen peroxide, produced by xanthine oxidase, to oxidize and reduce iron and thereby affect iron-catalyzed lipid peroxidation. Thus, we compared lipid peroxidation catalyzed by xanthine oxidase and ADP:Fe(III) to that catalyzed by xanthine oxidase and ADP:Fe(II). An examination of the action of superoxide on iron oxidation and reduction revealed that superoxide is a better oxidant of ADP:Fe(II) than a reductant of ADP:Fe(III). A superoxide generating system (composed of xanthine oxidase and catalase) and ADP:Fe(II) also resulted in a greater amount of lipid peroxidation than superoxide and ADP:Fe(III). Hydrogen peroxide, as expected, only served as an Fe(II) oxidant. A comparison of the oxidant activities of either superoxide or hydrogen peroxide on ADP:Fe(II) and the corresponding effects on lipid peroxidation revealed that both oxidants were roughly equivalent. We conclude that superoxide and hydrogen peroxide, produced from xanthine oxidase, support iron-catalyzed lipid peroxidation through their participation in redox reactions of iron, that is, they facilitate Fe(II) oxidation or Fe(III) reduction necessary for lipid peroxidation. The relevance of the reactions of O2-. and H2O2 on physiological chelates of iron are discussed.

Adenosine Diphosphate↗
PubMed2002

Multivitamin solutions for enteral supplementation: a source of peroxides.

OBJECTIVE: We investigated whether solutions of enteral vitamin supplementation are involved in the generation of peroxides and whether that contamination is biologically significant. METHODS: Peroxide contents of oral multivitamin preparations were measured over 3 wk after the initial opening of the containers. In selected premature infants (younger than 35 wk gestation), urinary peroxides were measured after initiating oral multivitamin supplementation. RESULTS: Peroxides in multivitamin solutions for enteral use are predominantly organic peroxides because they resist catalase. After the initial opening of the containers, there was a two-fold increase in total peroxides levels (P < 0.05) even in the preparation without riboflavin, a catalyst for the generation of peroxides. Initiation of oral vitamin supplementation was associated with increased (P < 0.05) urine peroxide levels. The high organic peroxide load did not correlate with its urinary excretion, mostly in the form of H(2)O(2). The excretion of H(2)O(2) corresponded to its oral intake from the multivitamin solution. CONCLUSIONS: Compared with parenteral multivitamin solutions, the enteral preparations contained higher organic peroxide levels starting with the initial opening of the bottles. The increased urinary excretion of H(2)O(2) after enteral multivitamin supplementation suggested a systemic diffusion of peroxides or of components of the multivitamin preparation responsible for the generation of peroxides. This oxidant load was not quenched by the immature antioxidant defenses of premature infants.

Drug Contamination↗
PubMed2002

Higher-concentration carbamide peroxide effects on surface roughness of composites.

BACKGROUND: Ten percent carbamide peroxide has been used extensively within the dental profession for the purpose of bleaching teeth. Although this method has been successful, the use of higher-concentration carbamide peroxides (20-35%) for home bleaching has increased substantially in the past few years. The purpose of this study was to evaluate changes in surface roughness of a hybrid and a microfilled composite after exposure to bleaching agents containing higher concentrations of carbamide peroxide. MATERIALS AND METHODS: Sixty-eight circular, resin-based composite specimens (8 mm x 2 mm) were prepared against a Mylar surface. Half of the specimens were fabricated from a hybrid composite material and the other half with a microfilled composite. Specimens were polished with aluminum oxide finishing disks, divided into four groups, and then exposed either to 20% carbamide peroxide for 3 hours per day for 14 days or to 35% carbamide peroxide for 1 hour per day for 14 days. The mean surface roughness (Ra) was determined for each specimen before and after exposure to bleaching agents, using mechanical profilometry. Data were analyzed by two-way analysis of variance (ANOVA) for differences between composite type, carbamide peroxide concentrations, and interaction of the two factors with respect to average surface roughness. All data analysis was performed at alpha = 0.05. RESULTS: Mean change from baseline of surface roughness (Ra) of microfilled composite and 20% carbamide peroxide was -0.03 microm +/- 0.10 microm; microfilled composite and 35% carbamide peroxide: 0.01 microm x 0.02 microm; hybrid composite and 20% carbamide peroxide: -0.43 microm x 0.91 microm; hybrid composite and 35% carbamide peroxide: -0.19 microm x 0.43 microm. Surface roughness of hybrid or microfilled composite did not change significantly from baseline with either concentration of carbamide peroxide (p = .300). CLINICAL SIGNIFICANCE: Higher-concentration carbamide peroxide bleaching agents, used as intended by the manufacturer, pose no significant risk to resin composite restoration surfaces.

Aluminum Oxide↗
PubMed2002

Safety issues when using a 16% carbamide peroxide whitening solution.

BACKGROUND: The scientific literature is lacking on the occurrence of side effects and other safety issues when using carbamide peroxide whitening solutions of concentrations greater than 10%. This double-blind nightguard vital bleaching study compares safety issues when using 16% carbamide peroxide against a placebo or 10% carbamide peroxide (Nite White Classic by Discus Dental Inc.). Evaluated were changes in gingival index, plaque index, nonmarginal gingival index, nongingival oral mucosal index, tooth vitality, and the patients' perceptions of tooth sensitivity and gingival irritation. MATERIALS AND METHODS: Twenty female dental hygiene students participated in the study. Each participant wore a maxillary treatment tray for 1 week without any solution and then for 8 to 10 hours per night for 14 nights, filling each quadrant with placebo, 10% carbamide peroxide, or 16% carbamide peroxide, using a split tray design. RESULTS: With respect to gingival index, plaque index, nonmarginal gingival index, nongingival oral mucosa index, tooth vitality, and tooth sensitivity, there were no statistically significant differences between the 16% carbamide peroxide solution and the other two solutions (p > .05). Quadrants receiving the 16% carbamide peroxide solution experienced more gingival irritation than quadrants receiving placebo or 10% carbamide peroxide solution (p > .05). CONCLUSIONS: When evaluating the above-mentioned safety issues, except for gingival irritation, there were no statistically significant differences between a 16% carbamide peroxide solution and 10% carbamide peroxide solution or a placebo when used as described here. CLINICAL SIGNIFICANCE: Among the 20 participants whose data were analyzed, it was found that a 16% carbamide peroxide whitening solution (Nite White Classic), when used as described in this study, can be effective in nightguard vital bleaching with no statistical differences in gingival index, plaque index, nonmarginal gingival index, nongingival oral mucosa changes, tooth vitality, or tooth sensitivity, compared with a 10% whitening solution (Nite White Classic). More gingival irritation was experienced with 16% carbamide peroxide. Additionally, 20% of the participants in this study self-reported sensitivity when wearing their treatment tray without any solution, and 36% of the participants reported sensitivity to the placebo solution.

Adult↗
PubMed1992

Effect of exogenous hydrogen peroxide on myocardial function and structure in isolated rat heart.

A time- and dose-dependent effect of exogenous hydrogen peroxide was determined on myocardial function, structure, high energy phosphate and lipid peroxidation in the isolated perfused rat heart. Hydrogen peroxide induced a dose-dependent decrease in cardiac function whereas 200 microM hydrogen peroxide reduced +dP/dt to 50% of control value after 10 mins. The effect of 300 microM hydrogen peroxide was more severe after 15 mins; changes observed with this dose were reversible within 10 mins of perfusion, becoming irreversible after 15 mins. Lipid peroxidation and severe morphological damage were observed after 10 mins of perfusion with 300 microM hydrogen peroxide. When 16 mEq potassium ions were added in the perfusion buffer during hydrogen peroxide perfusion, the degree of tissue damage and loss of ATP were attenuated. However, lipid peroxidation was not inhibited by high potassium ions. When 0.25 microM N,N'-diphenyl-1,4-phenylenediamine, a potent antioxidant, was added to the perfusate, lipid peroxidation was totally inhibited and the degree of tissue damage was decreased. However, depletion of tissue ATP and functional deterioration were not influenced. These results suggest that hydrogen peroxide-mediated ATP loss was independent of lipid peroxidation.

Adenosine Triphosphate↗
PubMed1991

Perhydroxyl radical (HOO.) initiated lipid peroxidation. The role of fatty acid hydroperoxides.

It is demonstrated that the perhydroxyl radical (HOO., the conjugate acid of superoxide (O2-], initiates fatty acid peroxidation (a model for biological lipid peroxidation) by two parallel pathways: fatty acid hydroperoxide (LOOH)-independent and LOOH-dependent. Previous workers (Gebicki, J. M., and Bielski, B. H. J. (1981) J. Am. Chem. Soc. 103, 7020-7025) demonstrated that HOO., generated by pulse radiolysis, initiates peroxidation in ethanol/water fatty acid dispersions by abstraction of the bis-allylic hydrogen atom from a polyunsaturated fatty acid. Addition of O2 to the fatty acid radicals forms peroxyl radicals (LOO.s), the chain-propagating species of lipid peroxidation. In this work it is demonstrated that HOO., generated either chemically (KO2) or enzymatically (xanthine oxidase), is a good initiator of fatty acid peroxidation in linoleic acid ethanol/water dispersions; O2- serves only as the source of HOO., and HOO. initiation can be observed at physiologically relevant pH values. In contrast to the previous results, the initiating effectiveness of HOO. is related directly to the initial concentrations of LOOHs in the lipids to be peroxidized. This defines a LOOH-dependent mechanism for fatty acid peroxidation initiation by HOO., which parallels the previously established LOOH-independent pathway. Since the LOOH-dependent pathway is much more facile than the LOOH-independent pathway, LOOH is the kinetically preferred site of HOO. attack in these systems. Experiments comparing HOO./LOOH-dependent fatty acid peroxidation with transition metal- and peroxyl radical-initiated peroxidation rule out the participation of the latter two species as initiators, which defines the HOO./LOOH initiation system as mechanistically unique. LOOH product studies are consistent with either a direct or indirect hydrogen atom transfer between LOOH and HOO. to yield LOO.s, which propagate peroxidation. The LOOH-dependent pathway of HOO.-initiated fatty acid peroxidation may be relevant to mechanisms of lipid peroxidation initiation in vivo.

Chromatography, High Pressure Liquid↗
PubMed1982

Effects of peroxides on rodent skin: epidermal hyperplasia and tumor promotion.

Free radical generating peroxides are potent skin irritants. After a single topical application of either 10, 20, or 40 mg of lauroyl peroxides or benzoyl peroxide on the dorsal skin of Sencar mice, the epidermal thickness increased markedly. No major inflammatory or vascular alterations were noted. On the other hand, 15 or 30% hydrogen peroxide produced an extensive epidermolysis, as well as inflammation and vascular injury, followed by quick regeneration and epidermal hyperplasia. Both lauroyl peroxide- and benzoyl peroxide-induced hyperplasias were characterized by a sustained production of dark basal keratinocytes, which constituted approximately 10% of the basal cell population during the first week after single topical application. Hydrogen peroxide-induced epidermal hyperplasias also exhibited numerous dark cells, but their presence was less sustained. Although all these peroxides were inactive either as initiators or as complete carcinogens, lauroyl peroxide was as effective as benzoyl peroxide when used as a skin tumor promoter in a two-stage carcinogenesis protocol. In a similar experimental protocol, hydrogen peroxide proved to be a very weak skin tumor promoter.

Administration, Topical↗
PubMed2001

Relative efficacies of indole antioxidants in reducing autoxidation and iron-induced lipid peroxidation in hamster testes.

Increased iron stores are associated with free radical generation and carcinogenesis. Lipid peroxidation is involved in DNA damage, thus indirectly participating in the early steps of tumor initiation. Melatonin and structurally related indoles are effective in protecting against oxidative stress. The aim of the study was to compare the relative efficacies of melatonin, N-acetylserotonin (NAS), indole-3-propionic acid (IPA), and 5-hydroxy-indole-3-acetic acid (5HIAA) in altering basal and iron-induced lipid peroxidation in homogenates of hamster testes. To determine the effect of the indoles on the autoxidation of lipids, homogenates were incubated in the presence of each agent in concentrations of 0.0, 0.01, 0.05, 0.1, 0.25, 0.5, 0.75, 1.0, 2.0, 2.5, or 5.0 mM. To study their effects on induced lipid peroxidation, homogenates were incubated with FeSO(4) (30 microM + H(2)O(2) (0.1 mM) + each of the indoles in the same concentrations as above. The degree of lipid peroxidation was expressed as concentrations of malondialdehyde + 4-hydroxyalkenals (MDA + 4-HDA) per mg protein. The indoles decreased both basal and iron-related lipid peroxidation in a concentration-dependent manner. Melatonin reduced basal MDA + 4-HDA levels when used at the concentrations of 0.25 mM or higher, and prevented iron-induced lipid peroxidation at concentrations of 1.0, 2.0, 2.5, or 5.0 mM. The lowest effective concentrations of NAS required to lower basal and iron-related lipid peroxidation were 0.05 mM and 0.25 mM, respectively. IPA, only when used in the highest concentrations of 2.5 mM or 5 mM inhibited basal lipid peroxidation levels and it was ineffective on the levels of MDA + 4-HDA due to iron damage. 5HIAA reduced basal lipid peroxidation when used at concentrations of 0.25 mM or higher, and it prevented iron-induced lipid peroxidation only at the highest applied concentration (5 mM). In conclusion, melatonin and related indoles at pharmacological concentrations protect against both the autoxidation of lipids as well as induced peroxidation of lipids in testes. In doing so, these agents would be expected to reduce testicular cancer that is initiated by products of lipid peroxidation.

Animals↗
PubMed1989

Free radicals mediate peroxidative damage in guinea pig hippocampus in vitro.

Previous studies have shown that peroxide caused electrophysiological damage. The present study investigates the action of agents that interfere with a free radical process in an effort to define the mechanism of peroxide damage. Deferoxamine chelates iron, making it unavailable for the Fenton reaction and thereby preventing the formation of hydroxyl free radicals from peroxide. Dimethylsulfoxide (DMSO) scavenges hydroxyl free radicals. Trolox-C, a water soluble Vitamin E analog, is an antioxidant that can scavenge peroxy radicals. Slices of hippocampus were removed from brains of euthanized guinea pigs. Electrical stimulation of an orthodromic pathway to CA1 region evoked a synaptic response and a population spike. Input-output curves were generated to evaluate the protection by deferoxamine, Trolox-C, and DMSO on the synaptic damage and impaired spike generation caused by peroxide. Lipid peroxidation was measured by the thiobarbituric acid test. Peroxide was found to increase lipid peroxidation. Deferoxamine and Trolox-C protected against the peroxide-induced synaptic damage, impaired spike generation, and lipid peroxidation. DMSO was ineffective synaptically but reduced peroxide damage to spike generating mechanisms and further lipid peroxidation. The data support the hypothesis that peroxide causes damage through a free radical mechanism.

Action Potentials↗