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PubMed1992

[Plasma lipid peroxides in the operation of esophageal cancer].

Lipid peroxides are formed by autooxidation of polyunsaturated fatty acids found primarily in cell membranes. An increase level of lipid peroxides in the tissue therefore reflects membrane damage. We reported that water immersion restraint rats caused significant increase of gastric mucosal lipid peroxide which reflected on gastric mucosal injury. The gastric mucosal injury is also known as the post-operative complication due to physical stress. So we studied plasma lipid peroxide and its related substances in the operation of esophageal cancer. Lipid peroxide levels increased significantly in pre- and post-operation but temporal decrease was found during the operation. Vitamin E is thought to be an important structural component of biologic membranes and is believed to act as a free radical scavenger in lipid peroxidation. Vitamin E also increased in the patients of esophageal cancer and decreased significantly during the operation. Superoxide dismutase changed frequently during the operation but there was no deficit tendency in its changes. Catalase levels also changes frequently and showed temporal but statistical elevation after the operation. These results indicated that lipid peroxidation may contribute to the development of organic damage in the operation of esophageal cancer.

Catalase↗
PubMed1992

Differential effects of transition metal ions on in vitro lipid peroxidation of human serum and protein precipitated from serum.

Elevated concentrations of lipid peroxidation products in serum have been documented in some common human diseases. In addition, several reports indicate that peroxidative damage of tissues in laboratory animals are enhanced in acute toxicity from transition metal ions. We studied the effects of four commonly encountered transition metal ions in human acute toxicity: copper, iron, mercury and lead on in vitro lipid peroxidation of human sera. Cupric and ferric ions caused a significant increase in lipid peroxidation products while mercuric and lead ions had no effects. Lipid peroxidation products in sera incubated with 1 mM cupric ion were increased by 210-248% following 24 h of incubation and 340-480% after 48 h of incubation, while the increases were significantly lower in the aliquots of same serum pools supplemented with same molar concentration of ferric ions (110-115% after 24 h and 137-141% following 48 h). On the other hand the effects were reversed when lipoproteins coprecipitated with other serum proteins were incubated with cupric and ferric ions. Under such conditions increases of lipid peroxidation products were significantly higher with ferric ions (240% after 24 h and 600% after 48 h) compared to cupric ions (20% following 24 h and 25% following 48 h). Such differential behavior of cupric and ferric ions in promoting lipid peroxidation can be explained with a different degree of binding of such ions with serum proteins.

Blood Proteins↗
PubMed2004

[Lipid peroxides concentration in women with intrauterine growth restriction].

OBJECTIVES: Intrauterine growth restriction is connected to high free radicals activity. One of the indices of lipid cell membrane destruction in free radical processes are lipid peroxides. DESIGN: The aim of the study was to find correlation between lipid peroxides products concentration in healthy women and intrauterine growth restriction. MATERIAL AND METHODS: The study was done in Medical University in Lodz in 1999-2002. The study group consist of women with IUGR, the controls of healthy pregnant women. The lipid peroxides were measured by colometric method, using Bioxytech kit for lipid peroxides. RESULTS: In IUGR group concentration of lipid peroxides was 42.17 +/- 11.77 mumol/l. In controls 53.754 +/- 14.07 mumol/l. We found significant difference between two groups and the increase of lipid peroxides in IUGR group. CONCLUSIONS: In women with IUGR the processes of lipid peroxidation increased.

Adult↗
PubMed2004

Lysosomal dysfunction on hydrogen peroxide-induced apoptosis of osteoarthritic chondrocytes.

The purpose of this study was to examine the mechanism of hydrogen peroxide-induced apoptosis in osteoarthritic chondrocytes. We evaluated the reactive oxygen species (ROS) formation, lysosomal staining and dysfunction of the mitochondrial membrane potential in these cells after exposure to hydrogen peroxide. Osteoarthritic chondrocytes were isolated, and divided into 4 dishes in which different concentrations (0.1 mM, 1 mM and 10 mM) of hydrogen peroxide, or no additive (control) was added. The cells were incubated for 1 or 4 h, then assayed for ROS formation, mitochondrial membrane potential and lysosomal staining. ROS formation was detected in chondrocytes after 1 h of exposure to hydrogen peroxide concentrations over 0.1 mM. Lysosomal swelling was detected after 1 h of exposure to hydrogen peroxide concentrations of 0.1 mM and over, possibly revealing lysosomal membrane instability. Moreover, indications of lysosomal rupture, including release of lysosomal enzymes, were apparent 1 h after addition of 10 mM of hydrogen peroxide. The addition of hydrogen peroxide to chondrocytes induces ROS formation and lysosomal dysfunction, revealed by swelling and rupture, prior to dysfunction of the mitochondrial membrane potential. Anti-oxidants may have a therapeutic application in the prevention of lysosomal dysfunction to inhibit chondrocyte apoptosis and degradation of the cartilage matrix.

Antioxidants↗
PubMed2004

Placebo-controlled clinical trial evaluating a 10% hydrogen peroxide whitening strip.

OBJECTIVE: A placebo-controlled clinical trial was conducted to evaluate the effectiveness and safety of a 10% hydrogen peroxide strip-based whitening system in subjects with tooth discoloration and no previous history of tooth whitening. METHODOLOGY: Informed consent was obtained, and 39 healthy adults were randomly assigned to either 10% hydrogen peroxide whitening strips (Crest Whitestrips Premium) or placebo strips with no peroxide. Strips were used unsupervised twice daily for 30 minutes over a seven-day period. At day four and day eight, tooth color (L*a*b*) was measured on the maxillary anterior teeth from standard digital images, and safety was assessed from examinations and subject reports. RESULTS: After three treatment days, the 10% hydrogen peroxide strip group had significant (p < 0.0001) color improvement from baseline, with means (SD) for deltab* and deltaL* of -1.57 (0.472) and 1.72 (0.619), respectively. Continued strip use from day four to day eight resulted in significant (p < 0.002) incremental improvement in both yellowness and lightness. By the end of treatment (day eight), the adjusted mean (SE) color change between groups was -2.20 (0.275) for deltab* and 2.24 (0.254) for deltaL*, a highly significant (p < 0.0001) color improvement for the 10% hydrogen peroxide group relative to placebo, of similar absolute magnitude for deltab* and deltaL*. Treatment with the 10% hydrogen peroxide strips was well-tolerated, with tooth sensitivity and oral irritation representing the most common findings. CONCLUSION: In this double-blind, placebo-controlled clinical trial, statistically significant tooth whitening was evident after three days' treatment with 10% hydrogen peroxide whitening strips, and color improved with continued usage over seven days.

Adult↗
PubMed2005

Effect of changes in plasma vitamin E level of vascular responses and lipid peroxidation in sickle cell anaemia subjects.

The effect of vitamin E supplementation (300 mg/day for 6 weeks) on blood pressure, forearm blood flow, forearm vascular resistance, plasma vitamin E level and lipid peroxidation status was investigated in adult sickle cell anaemia subjects. Ten adults whose ages ranged from 19.0 to 25.0 years (mean 22.8+/-0.8 years) were studied. Vitamin E supplementation had little or no effect on arterial blood pressure but significantly increased forearm blood flow (p<0.001) and plasma vitamin E level (p<0.001). However it significantly decreased lipid peroxidation status (p<0.001) and forearm vascular resistance (p<0.001). The change in plasma vitamin E concentration correlated negatively with change in lipid peroxidation status (r=-0.8; p=0.003). However, change in plasma vitamin E concentration correlated positively with change in forearm blood flow (r=0.8; p=0.006). There was an inverse correlation between change in plasma lipid peroxidation and change in forearm blood flow (r=-0.7; p=0.03). The study therefore shows that in sickle cell anaemia subjects, vitamin E supplementation increases forearm blood flow and reduces forearm vascular resistance and lipid peroxidation. The increase in forearm blood flow correlates inversely with the reduction in lipid peroxidation. This suggests that in sickle cell anaemia subjects, vitamin E supplementation could cause an increase in forearm blood flow by decreasing plasma lipid peroxidation level.

Adult↗
PubMedDate not supplied

MnSOD-plasmid liposome gene therapy decreases ionizing irradiation-induced lipid peroxidation of the esophagus.

BACKGROUND: Ionizing irradiation-induced cellular and tissue damage is mediated in part by resultant radiochemical reactions and resultant oxidative stress. Irradiation-induced reactive oxygen and nitrogen species include: superoxide, nitric oxide, hydroxyl radical and hydrogen peroxide. The biochemical combination of superoxide and nitric oxide radicals forms peroxynitrite, a potent oxidant known to induce lipid peroxidation. MATERIALS AND METHODS: The antioxidant capacity and lipid peroxidation of the esophagus were determined following irradiation. RESULTS: In the present studies, measurements of total antioxidant capacity did not change in the esophagus of control irradiated or control plasmid pNGVL3-PL intraesophageally-injected mice. In contrast, manganese superoxide dismutase-plasmid/liposome (MnSOD-PL) intraesophageally-treated mice showed a significant increase in antioxidant capacity persisting for seven days. Lipid peroxidative changes induced in the control irradiated mouse esophagus decreased over seven days after irradiation of C3H/HeNHsd mice exposed to 37 Gy in a single fraction. MnSOD-PL radioprotective gene therapy administered intraorally 24 hours prior to irradiation did not significantly reduce the kinetics of induction of total peroxidated lipids over the first seven days after irradiation but did decrease lipid peroxidation at days 14 and 21. CONCLUSION: These studies demonstrate the antioxidant function of MnSOD-PL gene therapy to the esophagus, which is detectable as a reduction in irradiation-induced lipid peroxidation.

Animals↗
PubMed2006

The utility of benzoyl peroxide in hydrophase base (Brevoxyl) in the treatment of acne vulgaris.

Available for more than 5 decades, benzoyl peroxide has been a "workhorse" of acne therapy. The benefits of this agent include reduction in Propionibacterium acnes (P. acnes) with decrease in inflammatory lesions, efficacy as both "leave on" and cleanser formulations and reduced emergence of antibiotic-resistant P. acnes strains. As the effect of benzoyl peroxide on P. acnes is a direct toxic effect rather than as a "true" antibiotic, resistance to benzoyl peroxide does not occur and has never been reported. Benzoyl peroxide in hydrophase base (Brevoxyl Creamy Washes and Gels) has shown significant efficacy in the treatment of acne, with lower irritancy than other benzoyl peroxide preparations. It is felt that the low irritancy of this product is related to a unique delivery vehicle containing dimethyl isosorbide, which dissolves benzoyl peroxide crystals on the skin. Clinical studies demonstrating the efficacy and safety of benzoyl peroxide in hydrophase base will be reviewed.

Acne Vulgaris↗
PubMed1991

In vitro phosphatidylcholine peroxidation mediated by activated human neutrophils.

Activated human polymorphonuclear leukocytes (PMNs) mediated peroxidation of dilinoleoyl phosphatidylcholine (DPLC) liposomes. Concentration-response effects were demonstrated for both PMNs and DLPC in the system studied. Chelated iron facilitated peroxidation threefold. Superoxide dismutase variably inhibited peroxidation, but never completely. Although O2-. synthesis ceased 30-40 min after PMN stimulation, lipid peroxidation continued for an additional 30-60 min, suggesting that PMNs may initiate peroxidation which subsequently becomes autocatalytic. Enhanced PMN-mediated DLPC peroxidation was noted in acidic media. Separation of DLPC reaction products by high pressure liquid chromatography demonstrated the de novo appearance of conjugated diene species. Preliminary specific ion monitoring mass spectroscopy analysis of gas chromatography fractions of reaction products (derivatized to fatty acid methyl esters/trimethylsilane hydroxyl ethers) indicated that PMN-generated oxyradicals resulted in production of conjugated 9- and 13-hydroperoxy DLPC derivatives. These results illustrate directly how activated PMNs may participate in host autoinjury by mediating phospholipid peroxidation.

Dose-Response Relationship, Drug↗
PubMed1990

On the role of lipid peroxidation and protein-bound aldehydes in the haloalkane-induced inactivation of microsomal glucose 6 phosphatase.

The inactivation of liver microsomal glucose 6 phosphatase induced either by Fe2+ or by haloalkanes (CCl4, CBrCl3) was investigated in NADPH-microsomes systems. In the case of haloalkanes, EDTA was included in the incubation mixtures, so to exclude participation of free Fe2+ in the ensuing lipid peroxidation. Microsomal glucose 6 phosphatase activity was measured along with the release of malonic dialdehyde and the appearance of carbonyl products bound to microsomal protein, taken as indices of the peroxidative process. Fe2+ was added to NADPH-microsomes at different concentrations, one (6 microM) resulting in an extent of lipid peroxidation comparable with that induced by haloalkanes, the other (60 microM) representing a situation of excess Fe2+, leading to massive lipid peroxidation. Inhibition of glucose 6 phosphatase caused by 6 microM Fe2+ was comparable to that induced by haloalkanes in EDTA-microsomes systems, which supports the view that lipid peroxidation--rather than covalent binding of free radical metabolites--represents the main event leading to the inactivation of glucose 6 phosphatase caused by haloalkanes. The production of 4-hydroxynonenal--the known toxic product of lipid peroxidation--was also studied. A remarkable accumulation of 4-hydroxynonenal was observed in the microsomal membranes after peroxidation induced by 6 microM Fe2+ or haloalkanes, as compared to the incubation medium. In addition, experiments carried out with CCl4 and CBrCl3 in vivo suggested the possible existence of a cytosolic detoxification system able to remove lipid-derived carbonyls bound to microsomal protein.

Aldehydes↗
PubMed1990

Effect of N-benzyl-D-glucamine dithiocarbamate on lipid peroxidation in testes of rats treated with cadmium.

The effect of N-benzyl-D-glucamine dithiocarbamate (BGD) on lipid peroxidation in testes, liver, and kidney of rats after cadmium injection was studied. Rats were injected subcutaneously with 5 mg CdCl2/kg and 30 min later they were injected intraperitoneally with BGD (400 mumol/kg). Cadmium treatment resulted in a significant increase in the lipid peroxidation in these organs, with a particularly remarkable increase in the testes. The increased lipid peroxidation in these organs was decreased to the control level by BGD injection after cadmium treatment. The lipid peroxidation in microsomes in testes was significantly increased compared to that of the control. BGD treatment significantly decreased the cadmium concentration in the microsomes in testes of cadmium-treated rats. The lipid peroxidation in liver and kidney microsomes was little changed. The superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities in the testes, liver, and kidney were little changed by cadmium treatment. The catalase activity in the testes was increased after cadmium injection and BGD treatment significantly decreased the increased enzyme activity. These results suggest relatively small contribution of SOD, GSH-Px, and catalase in cadmium-induced lipid peroxidation in the testes. The depressive effect of BGD on the increased lipid peroxidation in the testes of rats treated with cadmium may be in part related to the decrease in the cadmium concentration in the microsomes in testes.

Animals↗
PubMed1989

Superoxide-independent hydrogen peroxide release by activated macrophages.

The present data show that freshly explanted BCG-activated mouse peritoneal macrophages release large quantities of hydrogen peroxide upon initial contact with a foreign substratum, without the requirement for other membrane stimuli such as phorbol diesters. The hydrogen peroxide detected under these conditions does not originate from extracellularly released superoxide, since 2 x 10(5) BCG-activated macrophages spontaneously released 1.6 nmol hydrogen peroxide but only 0.2 nmol superoxide. Thus, more than 90% of the hydrogen peroxide detected was not derived from extracellular superoxide dismutation. The dissociation between hydrogen peroxide and superoxide release was further demonstrated in cytochalasin B- or lidocaine-treated cells or in the absence of glucose. Under these conditions, hydrogen peroxide release was markedly inhibited while superoxide release was unaffected. These observations provide evidence that another metabolic pathway is involved in the generation and release of hydrogen peroxide during adherence and spreading of freshly explanted activated macrophages onto a substratum.

Animals↗
PubMed1988

Polyamine lowered the hepatic lipid peroxide level in rats.

This is the first report for the hepatic lipid peroxide lowering effect of spermine in vivo. The influence of administration of polyamines on hepatic lipid peroxide level has been investigated by using normal or carbon tetrachloride (CCl4)-treated rats. Spermine was found to lower the hepatic lipid peroxide level most efficiently among polyamines used in CCl4-treated rats. In addition, the extent of liver enlargement caused by CCl4 treatment was reduced by spermine administration. Lipid peroxide lowering effect of spermine was also observed in normal rats. Hepatic spermine content was significantly increased in both normal and CCl4-treated rats after administration of spermine. Clear inverse relationship between the content of lipid peroxide and the concentration of spermine was observed. In reconstituted system containing NADPH-cytochrome P-450 reductase and extracted hepatic microsomal lipid, spermine inhibited the NADPH-dependent lipid peroxidation effectively at the concentration of 0.1 mM. From these results, we concluded that spermine exerted an inhibitory effect of lipid peroxidation in vivo as well as in vitro.

Animals↗
PubMed1987

An experimental model for hydrogen peroxide induced tissue damage: effect on cartilage and other articular tissues.

Hydrogen peroxide is a mediator of inflammation capable of damaging several cell types and biomolecules at relatively low concentrations in vitro. In order to evaluate the destructive potential of hydrogen peroxide in vivo, we devised an arthritis model in which hydrogen peroxide is initially the sole mediator of inflammation. Cationic glucose oxidase was injected intra-articularly into mouse knee joints. This enzyme produces hydrogen peroxide, using endogenous glucose as a substrate; thus a severe monoarthritis which lasts for several weeks can be induced. The contralateral joint is used as a control. Using histology and measurement of 99mTechnetium uptake we demonstrated severe oedema formation, damage to ligaments, muscles and cartilage, and infiltration of the tissue by inflammatory cells. These effects could be inhibited by the intraarticular administration of catalase. The effect of hydrogen peroxide on cartilage damage was shown to be reversible at low doses of glucose oxidase. This model shows what type of lesions can be induced by hydrogen peroxide generation in vivo. In addition we deem this model to be useful for studying chronic degenerative processes and for screening drugs that can scavenge hydrogen peroxide. The relevance of oxygen metabolites as inflammatory mediators is discussed.

Animals↗
PubMed1987

The role of phospholipase A activity in rat liver microsomal lipid peroxidation.

The involvement of phospholipase(s) A in lipid peroxidation of rat liver microsomes was investigated by: (a) determining the effects of phospholipase A inhibitors (p-bromophenylacyl bromide, chlorpromazine, mepacrine) on the accumulation of thiobarbituric acid reactivity or on levels of oxidized phospholipids in response to selected oxidative stimuli and (b) measurement of phospholipase A activities in response to these agents. Lipid peroxidation in response to various peroxidation systems was inhibited completely by exposure of microsomes to p-bromophenylacyl bromide (250 microM). The effectiveness of p-bromophenylacyl bromide was dependent on the presence of glutathione (200 microM) in preincubation mixtures. Chlorpromazine (100 microM) and mepacrine (100 microM) also effectively inhibited peroxidation, and their potency was independent of glutathione. The accumulation of oxidized phospholipids in response to the potent peroxidation stimulus alloxan/ferrous ion was similarly inhibited by p-bromophenylacyl bromide, although the level of oxidized phospholipid in response to the initiator ADP/ferrous ion was not affected. Microsomal phospholipase A1 activity, assessed using a liposomal substrate, was substantially enhanced by promoters of lipid peroxidation. Phospholipase A2 activity was not detected using a liposomal substrate but was evident using radiolabeled microsomes as endogenous substrate and was enhanced by oxidative stimuli. We conclude that phospholipase A activity may play an integral role in the microsomal lipid peroxidation mechanism. Based on this study, we hypothesize a role for phospholipases in facilitating propagation reactions.

Acetophenones↗
PubMed1984

Chemotactic activity generated in human serum from the fifth component of complement by hydrogen peroxide.

Exposure of normal human serum to various concentrations of hydrogen peroxide as low as 68.8 microM resulted in the generation of chemotactic activity for human neutrophils, which was inhibited by adding catalase prior to the exposure. Maximum chemotactic activity was obtained by hydrogen peroxide at a concentration of 1.1 mM, and the concentration greater than 1.1 mM expressed decreased activity. On the contrary, hydrogen peroxide less than 1.1 mM produced dose-dependent chemotactic activity. The generation of chemotactic activity is initiated at an incubation time of 5 minutes, and subsequently increases with up to 90 minutes. The suppression of chemotactic activity was minimum even after 180 minutes. The maximum activity was obtained by 1024-fold dilution of serum treated with 13.8 mM hydrogen peroxide. These results suggest that the disappearance of chemotactic activity at the high-dose range of hydrogen peroxide is due to neutrophil deactivation rather than inactivation of the chemotactic activity after it was generated. Similarly, purified human C5 exposed to hydrogen peroxide generated chemotactic activity. The chemotactic activity was inhibitable by antiserum to human C5. The molecular weight of chemotactically active substance was approximately 15,000. The generation of chemotactic activity was not inhibited by addition of EGTA or EDTA. These results imply that hydrogen peroxide generates C5a-like chemotactic factor through hydrolysis of C5.

Aminopeptidases↗
PubMed1983

Temporal relationship of free radical-induced lipid peroxidation and loss of latent enzyme activity in highly enriched hepatic lysosomes.

Loss of latency due to membrane lipid peroxidation induced in vitro was studied in highly purified rat liver lysosomes. Enriched fractions of lysosomes were isolated by free flow electrophoresis. Lipid peroxidation of lysosomes, assayed as malondialdehyde formation, was catalyzed by a radical generating system consisting of dihydroxyfumaric acid and Fe3+-ADP. The peroxidation reaction occurred readily at 37 degrees C and reached a plateau at 10 min; however, the loss of lysosomal latency, determined as increased percentage free beta-N-acetylglucosaminidase activity, occurred more gradually and reached a maximum after 30 min. Scavengers of superoxide, hydrogen peroxide, singlet oxygen, and hydroxyl radicals did not inhibit the peroxidation reaction nor prevent the loss of lysosomal latency. However, preincubation of the lysosomes with alpha-tocopherol effectively blocked the induction of peroxidation and substantially reduced the loss of lysosomal latency. These results indicate that the lysosomal membrane is susceptible to free radical-induced lipid peroxidation; further, this process may be the immediate cause of the subsequent disintegration of the lysosome. The nature of the protective effect of alpha-tocopherol is unclear but may be due to its interaction with the unsaturated membrane lipids and the subsequent interruption of the chain-reaction initiated by free radicals.

Aerobiosis↗
PubMedDate not supplied

Malondialdehyde formation from lipid peroxides in the thiobarbituric acid test: the role of lipid radicals, iron salts, and metal chelators.

Most of the chromogen formed when peroxidized material is heated with thiobarbituric acid (TBA) can be ascribed to a colored complex formed between malondialdehyde (MDA) and TBA. Even when little MDA is present, large amounts of MDA-TBA adduct can be formed. This is because lipid peroxides break down to release MDA during the test conditions. Iron is not essential for the breakdown of the peroxides but is essential for the formation of TBA reactivity. This can be related to the ability of iron to decompose lipid peroxides with the release of peroxy radicals, which are precursors of MDA. These peroxy radicals, when released, can initiate further peroxidation during the heating stage of the TBA test. Fatty acids in the absence of lipid peroxides do not undergo significant peroxidation during the acid-heating stage of the TBA test.

Chelating Agents↗