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PubMed1990

Lipid peroxidation as the mechanism of modification of brain 5'-nucleotidase activity in vitro.

The effect of lipid peroxidation on the Mg2(+)-independent and Mg2(+)-dependent activity of brain cell membrane 5'-nucleotidase was determined and the affinity of the active sites of Mg2(+)-dependent enzyme for 5'-AMP (substrate) and Mg2+ (activator) was examined. Brain cell membranes were peroxidized at 37 degrees C in the presence of 100 microM ascorbate and 25 microM FeCl2 (resultant) for 10 min. The activity of 5'-nucleotidase and lipid peroxidation products (thiobarbituric acid reactive substances) were determined. At 10 min, the level of lipid peroxidation products increased from 0.20 +/- 0.10 to 17.5 +/- 1.5 nmoles malonaldehyde/mg membrane protein. The activity of Mg2(+)-independent 5'-nucleotidase increased from 0.201 +/- 0.020 in controls to 0.305 +/- 0.028 mumol Pi/mg protein/hr in peroxidized membranes. In the presence of 10 mM Mg2+, the activity increased by 5.8-fold in the peroxidized membrane preparation in comparison to 14-fold in control. In peroxidized preparation, the affinity of active site of Mg2(+)-dependent 5'-nucleotidase for 5'-AMP tripled, as indicated by a significant decrease in Km (Km = 95 +/- 2 microM AMP for control; Km = 32 +/- 2 microM AMP for peroxidized). Vmax was significantly reduced from 3.35 +/- 0.16 in control to 1.70 +/- 0.9 mumoles Pi/mg protein in peroxidized membranes. The affinity of the active site for Mg2+ significantly increased (Km = 6.17 +/- 0.37 mM Mg2+ for control; Km = 4.0 +/- 0.31 peroxidized).(ABSTRACT TRUNCATED AT 250 WORDS)

5'-Nucleotidase↗
PubMed1998

Hydrogen peroxide-enhanced transanal ultrasound in the assessment of fistula-in-ano.

UNLABELLED: Appropriate classification of the fistulous tracts in patients with fistula-in-ano may be of value for the planning of proper surgery. Conventional transanal ultrasound has limited value in the visualization of fistulous tracts and their internal openings. Hydrogen peroxide can be used as a contrast medium for ultrasound to improve visualization of fistulas. PURPOSE: This prospective study evaluates hydrogen peroxide-enhanced ultrasound in comparison with physical examination, standard ultrasound, and surgery in the assessment of fistula-in-ano. METHODS: Twenty-one consecutive patients (4 women; mean age, 42 years) with fistula-in-ano were evaluated by local physical examination (inspection, probing, and digital examination), conventional ultrasound, and hydrogen peroxide-enhanced ultrasound before surgery. Ultrasound was performed using a B&K Diagnostic Ultrasound System with a 7-MHz rotating endoprobe. Hydrogen peroxide (3%) was infused via a small catheter into the fistula. The results of physical examination, ultrasound, and hydrogen peroxide-enhanced ultrasound were compared with surgical data as the criterion standard. The additive value of standard ultrasound and hydrogen peroxide-enhanced ultrasound compared with physical examination was also determined. RESULTS: At surgery, 8 intersphincteric and 11 transsphincteric fistulas and 2 sinus tracts (without an internal opening) were found. During physical examination, probing was incomplete in 13 patients, the diagnosis being correct in the other 8 patients (38%) as a low (intersphincteric or transsphincteric) fistula. With conventional ultrasound, the assessment of fistula-in-ano was correct in 13 patients (62%); defects in one or both sphincters could also be found (n = 8). With hydrogen peroxide-enhanced ultrasound, the fistulous tract was classified correctly in 20 patients, the overall concordance with surgery being 95%. The internal opening was found at physical examination in 15 patients (71%), with hydrogen peroxide-enhanced ultrasound in 10 patients (48%), and during surgery in 19 patients (90%). Secondary extensions, confirmed during surgery, were found in five cases. In two patients, a secondary extension with hydrogen peroxide-enhanced ultrasound was not confirmed during surgery. Both patients developed a recurrent fistula. CONCLUSION: Hydrogen peroxide-enhanced ultrasound is superior to physical examination and standard ultrasound in delineating the anatomic course of perianal fistulas. It makes accurate preoperative assessment of the fistula possible and may be of value for the surgeon in planning therapeutic strategy.

Adult↗
PubMed1982

Influence of vitamin E and nitrogen dioxide on lipid peroxidation in rat lung and liver microsomes.

Rat lung and liver microsomes were used to examine the effects of dietary vitamin E deficiency on membrane lipid peroxidation. Microsomes from vitamin-E-deficient rats displayed increased lipid peroxidation in comparison to microsomes from vitamin-E-supplemented controls. The extent of lipid peroxidation, as determined by measurement of thiobarbituric acid reacting materials, was enhanced by addition of reduced iron and ascorbate (or NADPH). Rats fed a vitamin-E-supplemented diet and exposed to 3 ppm NO2 for 7 days did not exhibit increases in microsomal lipid peroxidation compared to air-breathing controls. However, increase were found in microsomes prepared from rats fed a vitamin-E-deficient diet and exposed to NO2. Lung microsomes from vitamin-E-fed rats contained almost 10 times as much vitamin E as liver microsomes when expressed in terms of polyunsaturated fatty acid content. The extent of lipid peroxidation was, in turn, considerably less in lung than in liver microsomes. Lipid peroxidation in lung microsomes from vitamin-E-deficient rats comparable to liver microsomes from vitamin-E-supplemented rats as was the content of vitamin E in these respective microsomal samples. A combination of vitamin E deficiency and NO2 exposure resulted in the greatest increases in lung and liver microsomal lipid peroxidation with the largest relative increases occurring in lung microsomes. An inverse relationship was found between the extent of lipid peroxidation and vitamin E content. Most of the peroxidation in lung microsomes appeared to proceed nonenzymatically whereas peroxidation in liver was largely enzymatic. Vitamin E appears to be assimilated by the lung during oxidant inhalation, but with dietary vitamin E deprivation, the margin for protection in lung may be less than in liver.

Animals↗
PubMed1992

Fluorospectroscopic analysis of the fluorescent substances in peroxidized microsomes of rat liver.

The fluorescent substances formed in rat liver microsomes in the course of lipid peroxidation were investigated by fluorescence techniques. The fluorescence emitted from peroxidizing microsomes continuously increased as lipid peroxidation progressed, while the steady-state fluorescence anisotropy increased and then reached a plateau. A similar increase was observed in the steady-state fluorescence anisotropy of 1,6-diphenyl-1,3,5-hexatriene in peroxidizing microsomes. The fluorescence from peroxidized microsomes consisted of at least three species having short, middle or long fluorescence lifetimes. The lifetimes and relative amplitudes of fluorescence were unaffected by the extent of lipid peroxidation. Both fluorescence of the chromolipids extracted and the proteins isolated from peroxidized microsomes had the same characteristics in fluorescence lifetimes as the fluorescence from whole peroxidized microsomes. Thus, these lipids and proteins appear to be the major biological substances responsible for the fluorescence emanating from whole peroxidized microsomes. Furthermore, fluorescent substances formed in microsomes seem to increase in quantity rather than change in quality as lipid peroxidation progresses.

Animals↗
PubMed1991

Mechanism of cobalt (II) ion inhibition of iron-supported phospholipid peroxidation.

Co2+ inhibited nonenzymatic iron chelate-dependent lipid peroxidation in dispersed lipids, such as ascorbate-supported lipid peroxidation, but not iron-independent lipid peroxidation. Histidine partially abolished the Co2+ inhibition of the iron-dependent lipid peroxidation. The affinity of iron for phosphatidylcholine liposomes in Fe(2+)-PPi-supported systems was enhanced by the addition of an anionic lipid, phosphatidylserine, and Co2+ competitively inhibited the peroxidation, while the inhibiting ability of Co2+ as well as the peroxidizing ability of Fe(2+)-PPi on liposomes to which other phospholipids, phosphatidylethanolamine, or phosphatidylinositol had been added was reduced. Co2+ inhibited microsomal NADPH-supported lipid peroxidation monitored in terms of malondialdehyde production and the peroxidation monitored in terms of oxygen consumption. The inhibitory action of Co2+ was not associated with iron reduction or NADPH oxidation in microsomes, suggesting that Co2+ does not affect the microsomal electron transport system responsible for lipid peroxidation. Fe(2+)-PPi-supported peroxidation of microsomal lipid liposomes was markedly inhibited by Co2+.

Animals↗
PubMed1992

Bactericidal activity of alkyl peroxyl radicals generated by heme-iron-catalyzed decomposition of organic peroxides.

To clarify the nature of cytocidal molecular species among the radicals generated in the iron-catalyzed reactions of peroxides (ROOH), we examined the cytocidal effects of these radicals against gram-positive and gram-negative bacteria in the presence or absence of various radical scavengers. Three organic peroxides, t-butyl hydroperoxide (t-BuOOH), methyl ethyl ketone peroxide (MEKOOH), and cumene hydroperoxide, were used. Each radical generated from these peroxides was identified and quantitated by electron spin resonance (ESR) spin trapping with 5,5-dimethyl-1-pyrroline-N-oxide (DMPO). The major cytotoxic radical species generated in the mixtures of various peroxides and heme iron, especially methemoglobin, metmyoglobin, or hemin, was the alkyl peroxyl radical (ROO.). Strong bactericidal action against gram-positive bacteria was observed in the peroxide-heme iron system, especially in the case of t-BuOOH and MEKOOH. Killing curves for gram-positive bacteria showed an initial lag period, which may indicate the multihit/multitarget kinetics of cell killing. When the diethylenetriamine pentaacetic acid (DTPA)-Fe2+ complex was used as a catalyst for decomposition of various peroxides, alkyl, alkoxyl, and alkyl peroxyl radicals were identified by spin-trapping analysis. However, study of the time course of alkyl peroxyl radical production in the DTPA-Fe2+ complex system revealed that radical species generated in this system were very short lived: a maximal level was achieved within 1 min and then declined sharply, and no bactericidal activity was observed after 10 min. In contrast, the alkyl peroxyl radical level generated by the organic peroxide-heme iron system remained high for 30 min or longer. The generation of alkyl peroxyl radicals quantified by ESR correlated quite well with the bactericidal effect of the system of peroxide plus iron. In addition, bactericidal activity was completely inhibited by the addition of the spin trap DMPO, as well as of other various radical scavengers (alpha-tocopherol and L-ascorbic acid), into the peroxide-heme iron system, but this effect was not observed with superoxide dismutase, beta-carotene, dimethyl sulfoxide, diphenylamine, or butylated hydroxyltoluene. In view of these results, it is assumed that alkyl peroxyl radicals are the potent molecular species that are cytotoxic against bacteria, whereas alkoxyl radicals (RO.) generated in this system do not affect bacterial viability.

Benzene Derivatives↗
PubMed1983

Effect of paraquat on cytochrome P-450-dependent lipid peroxidation in bovine adrenal cortex mitochondria.

We have investigated the effect of paraquat (methyl viologen) on lipid peroxidation in bovine adrenal cortex mitochondria. Incubation of a buffered aerobic mixture of mitochondria in the presence of Fe2+ or NADPH resulted in the formation of lipid peroxides whose accumulation could be followed at 532 nm as malondialdehyde. Fe2+ stimulates lipid peroxidation in normal mitochondria and those in which enzymes have been inactivated with heat. In contrast, NADPH has a stimulatory effect only in normal mitochondria, but not in heat-treated mitochondria. These results indicate that NADPH-dependent lipid peroxidation is an enzymatic process. Paraquat strongly inhibits this enzymatic lipid peroxidation, but has no effect on the non-enzymatic Fe2+-dependent process. The chemiluminescence that accompanies the NADPH-dependent lipid peroxidation is also markedly decreased in the presence of paraquat. Superoxide dismutase, which removes superoxide anion efficiently, does not inhibit malondialdehyde production. The mechanism of the inhibition of the lipid peroxidation by paraquat has been examined. Paraquat has no effect on NADPH-2,6-dichlorophenolindophenol reductase and on NADPH-cytochrome c reductase activities in bovine adrenal cortex mitochondria. However, paraquat strongly inhibits the NADPH-dependent reduction of cytochrome P-450. These results suggest that the inhibitory effect of paraquat on NADPH-dependent lipid peroxidation in adrenal cortex mitochondria is due to a decrease in the level of reduced cytochrome P-450 probably by diverting electrons from cytochrome P-450. Cytochrome c, which can compete with P-450 for available electrons from adrenodoxin, like paraquat had an inhibitory effect on NADPH-dependent lipid peroxidation. Lipid peroxidation was also strongly inhibited by steroid hydroxylase inhibitors, e.g., amphenone B, aminoglutethimide and metyrapone.

Adrenal Cortex↗
PubMed1986

Lipid peroxidation in rat uterus.

Lipid peroxidation in rat uterus has been studied using NADPH- and ascorbate-induced systems. Lipid peroxidation in rat uterus is low as compared to rat liver. Uterus is more sensitive to ascorbate-induced lipid peroxidation than that induced by NADPH. Uterus contains lower amounts of phospholipids and has a lesser degree of unsaturation in lipids. Co-factor studies show that Fe2+ is more important for ascorbate-induced lipid peroxidation. Endometrium is more sensitive to ascorbate-induced lipid peroxidation than myometrium. It also contains more total lipids and phospholipids besides having a higher degree of unsaturation in the lipids as compared to myometrium. Among the subcellular fractions, mitochondria are more prone to ascorbate-induced lipid peroxidation, whereas microsomes are more sensitive to NADPH-induced lipid peroxidation. Uteri from old rats (24 months) and pregnant rats are more resistant to lipid peroxidation than those from 3-month-old control rats. Uterus of pregnant rats contains more factors which inhibit lipid peroxidation and also has a lesser degree of unsaturation in lipids compared with uterus of control rats. The possible consequences of the resistance of uterus to lipid peroxidation, especially during pregnancy and senescence, are discussed.

Animals↗
PubMed1987

Lipid peroxidation, protein thiols and calcium homeostasis in bromobenzene-induced liver damage.

The mechanisms of bromobenzene hepatotoxicity in vivo were studied in mice. The relationships among glutathione (GSH) depletion, lipid peroxidation, loss of protein thiols, disturbed calcium homeostasis and liver necrosis were investigated. Liver necrosis (as estimated by the serum glutamate-pyruvate transaminase (SGPT) level) appeared between 9 and 12 hr and increased at 18 hr. Lipid peroxidation which was already detectable at 6 hr in some animals, increased thereafter showing a good correlation with the severity of liver necrosis. Despite a quite fast depletion of hepatic GSH, a significant decrease in protein thiols could be observed at 12-18 hr only. Loss of protein thiols in both whole liver and subcellular fractions (microsomes and mitochondria) was correlated with lipid peroxidation. Also a good inverse correlation was seen between lipid peroxidation and the calcium sequestration activity of liver microsomes and mitochondria. The treatment of mice with desferrioxamine (DFO) after bromobenzene-intoxication completely prevented lipid peroxidation, loss of protein thiols and liver necrosis in the animals sacrificed 15 hr after poisoning. When, however, the animals were examined at 24 hr, although the general correlation between lipid peroxidation and liver necrosis was held, in some animals (about 30% of the survivors) elevation of SGPT was observed in the virtual absence of lipid peroxidation. It seems likely therefore that the liver damage seen during the first phase of bromobenzene-intoxication is strictly related to lipid peroxidation. It is, however, possible that in some animals in which for some reason lipid peroxidation does not develop, another mechanism of liver necrosis unrelated to lipid peroxidation occurs at later times.

Animals↗
PubMed1987

NADPH- and linoleic acid hydroperoxide-induced lipid peroxidation and destruction of cytochrome P-450 in hepatic microsomes.

Temporal aspects of the effects of inhibitors on hepatic cytochrome P-450 destruction and lipid peroxidation induced by NADPH and linoleic acid hydroperoxide (LAHP) were compared. In the absence of added Fe2+, NADPH-induced lipid peroxidation in hepatic microsomes exhibited a slow phase followed by a fast phase. The addition of Fe2+ eliminated the slow phase, thus demonstrating that iron is a rate-limiting component in the reaction. EDTA, which complexes iron, and p-chloromercurobenzoate (pCMB), which inhibits NADPH-cytochrome P-450 reductase, inhibited both phases of the reaction. Catalase as well as scavengers of hydroxyl radical, inhibited NADPH-induced lipid peroxidation almost completely. GSH also inhibited the NADPH-dependent reaction but only when added at the beginning of the reaction. In contrast with NADPH-dependent lipid peroxidation, the autocatalytic reaction induced by LAHP was not biphasic, NADPH-dependent or iron-dependent, nor was it inhibited by hydroxyl radical scavengers, catalase or GSH. A synergistic effect on lipid peroxidation was observed when both NADPH and LAHP were added to microsomes. It is concluded that both the fast and slow phases of NADPH-dependent microsomal lipid peroxidation are catalyzed enzymatically and are dependent upon Fe2+, whereas LAHP-dependent lipid peroxidation is autocatalytic. Since the fast phase of enzymatic lipid peroxidation occurred during the fast phase of destruction of cytochrome P-450, it is postulated that iron made available from cytochrome P-450 is sufficient to promote optimal lipid peroxidation. Since catalase and hydroxyl radical scavengers inhibited NADPH-dependent but not LAHP-dependent lipid peroxidation, it is concluded that the hydroxyl radical derived from H2O2 is the initiating active-oxygen species in the enzymatic reaction but not in the autocatalytic reaction.

Animals↗
PubMed1992

Lipid peroxides in blood from patients with atherosclerosis of coronary and peripheral arteries.

Lipid peroxides in plasma were determined in 100 patients with coronary artery disease, in 100 patients with peripheral artery disease and in 100 persons without any clinical symptoms of coronary or peripheral artery disease. The concentrations of lipid peroxides were significantly higher in patients with atherosclerosis (both coronary and peripheral arteries) than in controls. There was no difference between lipid peroxides in patients with coronary and peripheral artery disease. Lipid peroxides in plasma were similar in subgroups of patients with coronary artery disease without a history of myocardial infarct and those who had had myocardial infarct. In subgroups of patients with peripheral artery disease divided according to the severity of peripheral atherosclerosis a positive association between the concentration of lipid peroxides in plasma and the severity of disease was observed. In all groups there was a significant correlation between the age of examined persons and lipid peroxides in plasma; however, the concentration of lipid peroxides in plasma was statistically higher in patients with atherosclerosis than in the control age matched group. The correlation between lipid peroxides and total cholesterol as well as triglycerides were weak and not statistically significant in most of the examined groups. The results of this study provide clinical support for experimental data indicating that peroxidation of lipids is an important factor in the formation of atherosclerotic changes. They also indicate that determination of plasma lipid peroxides may give important supplementary information in monitoring patients with clinical symptoms of atherosclerosis.

Adult↗
PubMed1989

Lipid peroxidation in developing fetal guinea pig brain during normoxia and hypoxia.

Lipid peroxidation in the fetal guinea pig brain was studied at 30, 35, 40, 45, 50, and 60 days of gestation. Conjugated dienes and fluorescent compounds, indices of lipid peroxidation, peaked at 35 days of gestation, decreased by 45 days, and remained at that level until birth. The higher levels of peroxidation products in early gestational periods (30-40 days) suggest that either the anti-oxidant mechanisms for scavenging oxygen free-radicals and further metabolizing oxidation products are underdeveloped, or the rate of peroxidation is higher than periods near term. Prenatal hypoxia increased the levels of conjugated dienes and fluorescent products in the brains of preterm (50 days) and term (60 days) fetuses. Brain homogenates incubated in air at 37 degrees C underwent rapid lipid peroxidation as measured by the level of thiobarbituric acid (TBA)-reactive substances. However, term brain showed a higher rate of peroxidation and attained higher steady state levels of TBA-reactive substances than preterm brain. This may be due to the higher levels and degrees of unsaturation in fatty acids in term brain. Following hypoxia, term brain showed 5 times the rate of lipid peroxidation and a 3-fold increase in total TBA-reactive substances over controls. These studies show that a significant degree of lipid peroxidation is occurring in the fetal brain during gestation and that the developing brain is more susceptible to lipid peroxidation near term. Furthermore, prenatal hypoxic stress further increases the susceptibility of the brain to peroxidative reactions.

Animals↗
PubMed1985

Peroxidation of linolenic acid promoted by human polymorphonuclear leucocytes.

Human polymorphonuclear leucocytes were found to promote peroxidation linolenic acid micelles. The peroxidation was markedly enhanced by addition of ferric iron, either in the form of chloride, ADP-complex or EDTA to the phosphate-buffered reaction mixture. The leucocyte oxygen burst was induced by the addition of the lipid micelles, and no other stimulatory agent was therefore required. Pretreatment of the leucocytes with cytochalasin B did not inhibit t.e lipid peroxidation which indicates that phagocytosis was not part of the peroxidative mechanism. Lipid peroxidation was inhibited by alpha-tocopherol acetate, butylated hydroxytoluene, manganese ions and desferrioxamine but not by superoxide dismutase, catalase or the hydroxyl radical scavenger dimethylsulfoxide. Lipid peroxidation promoted by xanthine oxidase, was studied for comparison. This was inhibited by superoxide dismutase, indicating that xanthine oxidase, in contrast to leucocytes, promotes lipid peroxidation via a superoxide-dependent mechanism. Manganese ions and butylated hydroxytoluene, and to a lesser extent alpha-tocopherol, were also inhibitors. The leucocyte promoted lipid peroxidation is similar to the well-known peroxidation promoted by microsomal NADPH-cytochrome P450 reductase, which also is not induced by superoxide radicals. Peroxidation of lipids may be a mechanism whereby granulocytes express tissue damage in for example inflammation and ischaemia.

Catalase↗
PubMed1985

Peroxidation of liposomes promoted by human polymorphonuclear leucocytes.

Human polymorphonuclear leucocytes were found to promote peroxidation of phospholipid liposomes upon stimulation by phorbol myristate acetate. Peroxidation required the presence of either pyrophosphate-chelated or ADP-chelated iron, whereas iron chelated to EDTA or ATP had no effect. Peroxidation was also catalyzed by ferritin, but not by transferrin. Superoxide dismutase abolished the peroxidation, whereas catalase and apparently also the hydroxyl radical scavenger dimethyl sulphoxide were inactive, indicating that the peroxidation was mediated by superoxide radicals but not by hydrogen peroxide or hydroxyl radicals. Xanthine oxidase-promoted peroxidation was studied for comparison and showed similar characteristics except that transferrin catalyzed the peroxidation. Peroxidation of membrane lipids may be a mechanism whereby granulocytes cause tissue damage in inflammation. The drugs paracetamol, gentisic acid and 5-aminosalicylic acid inhibited lipid peroxidation, probably through their ability to react with the superoxide anion.

Cytochrome c Group↗
PubMed1996

A possible mechanism for initiation of lipid peroxidation by ascorbate in rat liver microsomes.

The mechanism by which lipid peroxidation progresses has been known for years, but there is disagreement regarding the mode of its initiation. The aim of this study was to examine: (a) the role of endogenous iron in the initiation of ascorbate-induced lipid peroxidation in microsomal and liposomal membranes; (b) the role of oxygen-free radicals in this process; and (c) the redox state of ascorbate during the course of lipid peroxidation. Ascorbate-induced lipid peroxidation was assessed by measuring hydroperoxide and thiobarbituric acid reactive substances (TBARS) formation in membranes after incubation in Tris-HCl buffer (pH 7.4) for 15 min. To confirm the role of endogenous iron and oxygen-free radicals, the effect of iron chelating agents (EDTA and thiourea) and radical scavengers (benzoate, mannitol, catalase and SOD) on lipid peroxidation was examined. Spectrophotometric measurements and ESR spectra have made it possible to determine ascorbate concentration and its redox state. Ascorbate promoted lipid peroxidation in both rat liver microsomes and liposomes without addition of exogenous iron. Iron chelating agents such as EDTA and thiourea inhibited lipid peroxidation, while SOD, catalase, mannitol and benzoate had no effect. The addition of 5 microM Fe2+ (or Fe3+) to the incubation mixture did not significantly alter hydroperoxide production, but that of TBARS was increased. Lipid peroxidation significantly altered the fatty acid profile in microsomes and liposomes, the most affected being the C20:4 and C22:6 species. Ascorbate in Tris-HCl buffer (pH 7.4) autoxidized very slowly. Its oxidation was catalyzed by Fe3+ ions at a rate determined by incubation time and iron concentration. In contrast, no ascorbate oxidation occurred in the presence of microsomes when lipid peroxidation was proceeding at a maximal rate. Under these conditions a typical ascorbyl radical ESR spectrum signal greater than that arising from ascorbate alone was obtained and the magnitude of this signal was unchanged by variations of microsome or ascorbate concentrations. A ferrous ion ascorbyl radical complex was responsible for this signal. These results suggest that an ascorbate-microsomal iron complex is responsible for the initiation of lipid peroxidation, and that during this process ascorbate remains in its reduced form.

Animals↗
PubMed2006

Hydrogen peroxide producing lactobacilli in women with vaginal infections.

OBJECTIVE: Hydrogen peroxide producing lactobacilli are isolated from the vaginas of a majority of healthy reproductive age women. Their toxic and inhibitory effect against the overgrowth of pathogens in the vagina is documented by in vitro studies. Clinical studies concerning the role of hydrogen peroxide producing lactobacilli in vaginal infections are controversial. STUDY DESIGN: The aim of this study was to isolate lactobacilli from women with major vaginal infections: bacterial vaginosis (BV), vulvovaginal candidiasis (VVC) and trichomoniasis (TV), and from women with normal flora (NF), to test their ability to produce hydrogen peroxide, to quantitate lactobacilli and to evaluate factors related to the colonization of vagina with hydrogen peroxide producing lactobacilli. The study group comprised 108 women: 27 with VVC, 26 with BV, 20 with TV and 35 with NF. Data was analysed with Fisher exact test, chi2-test, and ANOVA. RESULTS: Lactobacilli were isolated from 81.5% of women with VVC, 58% of women with BV (p=0019), 55% of women with TV (p=0.015) and from 86% of women with NF. The majority of isolates of lactobacilli from women with VVC, TV and NF produced hydrogen peroxide (77%, 63.5% and 80%, respectively), compared with women with BV where only 26.5% of isolates produced hydrogen peroxide (p=0.01). Quantitative analysis showed that in an overwhelming majority of women colonized with lactobacilli, their count was >10(7) CFU/ml. Upon evaluation of behavioural and demographic characteristics, we found that smokers had a lower incidence of isolation of hydrogen peroxide producing lactobacilli (p=0.018). Our results showed that women with BV lack lactobacilli, especially hydrogen peroxide producing ones. Women with TV had a lower rate of lactobacilli. In women with VVC, there was neither significant difference in the isolation of lactobacilli, nor in their ability to produce hydrogen peroxide, compared to women with NF. CONCLUSION: Our results point out that hydrogen peroxide producing lactobacilli could protect against the development of BV, but not against VVC and TV.

Adolescent↗
PubMed2004

Protective mechanisms against peptide and protein peroxides generated by singlet oxygen.

Reaction of certain amino acids, peptides, and proteins with singlet oxygen yields substrate-derived peroxides. Recent studies have shown that these species are formed within intact cells and can inactivate key cellular enzymes. This study examines potential mechanisms by which cells might remove or detoxify such peroxides. It is shown that catalase, horseradish peroxidase, and Cu/Zn superoxide dismutase do not react rapidly with these peroxides. Oxymyoglobin and oxyhemoglobin, but not the met (Fe3+) forms of these proteins, react with peptide but not protein, peroxides with oxidation of the heme iron. Glutathione peroxidase, in the presence of reduced glutathione (GSH) rapidly removes peptide, but not protein, peroxides, consistent with substrate size being a key factor. Protein thiols, GSH, other low-molecular-weight thiols, and the seleno-compound ebselen react, in a nonstoichiometric manner, with both peptide and protein peroxides. Cell lysate studies show that thiol consumption and peroxide removal occur in parallel; the stoichiometry of these reactions suggests that thiol groups are the major direct, or indirect, reductants for these species. Ascorbic acid and some derivatives can remove both the parent peroxides and radicals derived from them, whereas methionine and the synthetic phenolic antioxidants Probucol and BHT show little activity. These studies show that cells do not have efficient enzymatic defenses against protein peroxides, with only thiols and ascorbic acid able to remove these materials; the slow removal of these species is consistent with protein peroxides playing a role in cellular dysfunction resulting from oxidative stress.

Animals↗
PubMed2003

Determination of organic peroxides by liquid chromatography with on-line post-column ultraviolet irradiation and peroxyoxalate chemiluminescence detection.

A HPLC method was developed for the simultaneous determination of organic peroxides and hydrogen peroxide with peroxyoxalate chemiluminescence (PO-CL) detection following on-line UV irradiation. Organic peroxides [i.e., benzoyl peroxide (BP), tert.-butyl hydroperoxide (BHP), tert.-butyl perbenzoate (BPB), cumene hydroperoxide (CHP)] were UV irradiated (254 nm, 15 W) to generate hydrogen peroxide, which was determined by PO-CL detection. The conditions for UV irradiation and PO-CL detection were optimized by a flow injection analysis (FIA) system. Generation of hydrogen peroxide from peroxides with on-line UV irradiation also was confirmed by the FIA system by incorporating an enzyme column reactor immobilized with catalase. The separation of four organic peroxides and hydrogen peroxide by HPLC was accomplished isocratically on an ODS column within 30 min. The detection limits (signal-to-noise ratio=3) were 1.1 microM for hydrogen peroxide, 6.8 microM for BP, 31.3 microM for BHP, 7.5 microM for BPB and 1.3 microM for CHP. The proposed method was applied to the determination of BP in wheat flour.

Calibration↗