SEARCH · Search PubMed

Results for “PEROXIDES”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

SourceResearch connectionFrom yearThrough year

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 757 records · Page 42Linked to original sources

PubMed1997

Dietary selenium increases cellular glutathione peroxidase activity and reduces the enhanced susceptibility to lipid peroxidation of plasma and low-density lipoprotein in kidney transplant recipients.

The glutathione system plays a major role in the protection of cells against oxidative stress in humans. The aim of the present study was to find out the relationship between the glutathione system and plasma lipid peroxidation in six renal transplant recipients (who are under oxidative stress and thus at high risk for atherosclerosis), by using dietary selenium to activate the glutathione system. 2,2'-Azobis-2-amidinopropane hydrochloride (AAPH)-induced plasma lipid peroxidation was increased (by 60%) in all six patients in comparison to normal subjects. A similar pattern of increased plasma lipid peroxidation was found even in the basal state (in the absence of added AAPH). CuSO4-induced low-density lipoprotein (LDL) oxidation measured by peroxide formation was also significantly increased by 2.3-fold in the patients' LDL in comparison to normal LDL. Even in the absence of CuSO4, the LDL oxidation state was also increased in the patients' LDL in comparison to normal LDL. We thus analyzed the effect of dietary selenium (0.2 mg/day for a period of 3 months, followed by an additional 3 months on placebo) on plasma and on LDL lipid peroxidation. Selenium treatment resulted in a 50% reduction in AAPH-induced plasma lipid peroxidation. The susceptibility of the patients' plasma to lipid peroxidation returned toward baseline values 3 months after termination of the selenium treatment. Similar results, although less pronounced (only 15% reduction), were obtained for CuSO4-induced LDL oxidation. Analyses of the patients' red blood cell (RBC) glutathione system revealed low levels of reduced glutathione and decreased activities of RBC glutathione peroxidase and glutathione reductase by 23%, 18%, and 20%, respectively, in comparison to normal RBC. Selenium treatment resulted in a significant elevation of RBC glutathione peroxidase and glutathione reductase activities and in reduced glutathione content by 64%, 57%, and 11%, respectively; this effect was also paralleled by a 39% reduction in the RBC oxidized glutathione content. On termination of the selenium treatment, and after 3 months on placebo, all of these values of the glutathione system elements returned toward baseline levels. We thus conclude that dietary selenium, which activates the glutathione system, is a potent antioxidant against plasma and LDL lipid peroxidation in renal transplant recipients, and may thus be considered antiatherogenic.

Adult↗

PubMed1991

Lipid peroxidation of rat erythrocyte membrane induced by adriamycin-Fe3+.

Adriamycin-Fe3+ caused lipid peroxidation of erythrocyte membrane in relation to its concentration. Adriamycin-Fe3+ had a high affinity for membrane and the adriamycin-Fe(3+)-binding membranes membranes was also found to cause lipid peroxidation. Under aerobic conditions, adriamycin-Fe3+ caused a reduction of cytochrome c and ferrous iron formed spontaneously. Superoxide dismutase (EC 1.15.1.1) (SOD) strongly inhibited the reduction of cytochrome c; however, the enzyme promoted formation of ferrous iron independent of enzymatic action. These results suggest that cytochrome c was reduced by superoxide radical (O2-) or an adriamycin-iron-O2 complex such as adriamycin-Fe(3+)-O2-, but not by adriamycin-Fe2+. The ferrous iron chelator bathophenanthroline sulfonate (BPS) completely inhibited oxygen consumption caused by adriamycin-Fe3+, indicating that ferrous iron is absolutely required for the lipid peroxidation. SOD and hydroxyl radical scavengers did not inhibit the lipid peroxidation, indicating that O2- and hydroxyl radical were not involved in membrane peroxidation. The peroxidation reaction was dramatically inhibited by Tris buffer (2-amino-2-hydroxymethyl-1,3-propanediol). However, hydroxyl radical generation and lipid peroxidation in Tris buffer were not related obviously, indicating that Tris did not act as a hydroxyl radical scavenger. The initial rate of TBARS (thiobarbituric acid reactive substances) formation induced by a mixture of adriamycin-Fe3+ and adriamycin-Fe2+ was much faster than that induced by adriamycin-Fe2+ or adriamycin-Fe3+ alone. These results made it became possible to speculate that the lipid peroxidation might be initiated by an adriamycin-Fe(3+)-oxygen-adriamycin-Fe2+ complex.

Animals↗

PubMed1994

Leukotriene B4 formation upon halothane-induced lipid peroxidation in liver membrane fractions under low O2 concentrations in vitro.

Lipid peroxidation was induced in rat liver membrane fractions in vitro upon NADPH-dependent metabolic activation of the anesthetic agent halothane at low O2 concentrations. Halothane-induced lipid peroxidation was dependent on time, concentration of halothane, and the calculated O2 concentrations present in the system. Lipid peroxidation was inducible at increasing O2 concentrations up to 12 microM, decreased at higher O2 concentrations up to 48 microM, and was not detectable at normoxic conditions. Leukotriene B4 (LTB4) was identified as a product arising upon lipid peroxidation by reverse-phase high-pressure liquid chromatography combined with a radioimmunoassay. LTB4 formation was maximal under conditions of maximal lipid peroxidation at a calculated O2 concentration of 12 microM. Even at high concentrations, the 5-lipoxygenase inhibitors MK886 (10 microM), ZD2138 (20 microM), and ZM230487 (20 microM) were not inhibitory in halothane-induced lipid peroxidation nor in the associated formation of LTB4. Synthetic LTB4 was transformed into its 20-hydroxy derivative by omega-oxidation in an O2-concentration-dependent manner, being considerably reduced at the low O2 concentrations that maximally promoted lipid peroxidation. The collective evidence of these data raises the possibility that exposure to halothane might lead to peroxidation-associated net synthesis of LTB4 through 5-lipoxygenase-independent escape routes in liver tissue under physiologically or pathophysiologically low O2 concentrations.

Aerobiosis↗

PubMed1993

Lipid peroxidation in human milk and infant formula: effect of storage, tube feeding and exposure to phototherapy.

Preformed lipid peroxidation products present in the feed may contribute to the total reactive oxygen radical load infants have to deal with and may play a role in the pathogenesis of necrotizing enterocolitis and bronchopulmonary dysplasia. In this study, the occurrence of lipid peroxidation in human milk and feeding formulas for preterm babies was evaluated in vitro. Free linoleic acid (18:2) and its hydroperoxide (18:2OOH) were measured by gas chromatography-mass spectrometry and the concentration of 18:2OOH and the 18:2OOH/18:2 ratio were used as indices of peroxidation. In all feeds peroxidation products were present, but the proportion of peroxidized 18:2 was greater in infant formula. Storage of human milk (+4 degrees C for four days) increased lipid peroxidation. Exposure to light during tube feeding increased peroxidation in infant formula but not in human milk. Different procedures for preparation, storage and feeding may decrease the concentration of these potentially toxic peroxidized lipids in human milk and infant formula.

Enteral Nutrition↗

PubMed1980

Vitamin E and selenium protection from in vivo lipid peroxidation.

Some of the vitamins and many of the metals that are being considered at this symposium interact in lipid peroxidation. Some of these interactions have been studied in vivo. Measurement of in vivo lipid peroxidation in the rat is accomplished by gas chromatographic analysis of pentane, a minor peroxidation product that is exhaled in the breath. In the rat, lipid peroxidation is proportional to dietary polyunsaturated lipids when the animal is deficient in antioxygenic agents. The chain-breaking antioxidant vitamin E is the main protector against in vivo lipid peroxidation. Dietary selenium, through its involvement in the biosynthesis of glutathione peroxidase, functions in a secondary antioxygenic role as a hydroperoxide reducer. In rats fed a vitamin E-deficient diet, injection of some hydroperoxides, iron, or vitamin C leads to initiation of in vivo lipid peroxidation, apparently by decomposing hydroperoxides to free radicals. Carbon tetrachloride, a toxic halogenated hydrocarbon, is metabolized by liver microsomes and initiates in vivo lipid peroxidation in the liver. These examples show that practical information on interactions involving in vivo lipid peroxidation can be obtained by studies that use the pentane method.

Animals↗

PubMed2000

Effects of atypical antioxidative agents, S-nitrosoglutathione and manganese, on brain lipid peroxidation induced by iron leaking from tissue disruption.

A fluorescent assay of brain lipid peroxidation was used for screening new antioxidants for the prevention of neurodegeneration caused by free radicals. Incubation of rat brain homogenates led to a temperature-dependent increase in production of fluorescent adducts of peroxidized polyunsaturated fatty acids; it was inhibited completely by lowering the incubation temperature to 4 degrees C. This tissue disruption-induced brain lipid peroxidation at 37 degrees C was blocked by deferoxamine (IC50 = 0.3 microM) and EDTA; it was augmented by adding submicromolar iron and hemoglobin. Ferrous ion's pro-oxidative activities were five times more potent than ferric ion. Micromolar manganese completely inhibited lipid peroxidation, confirming earlier unexpected in vivo reports. Trolox and vitamin C suppressed brain lipid peroxidation with IC50 values of 20 and 500 microM, respectively. U-78517F was approximately 20 times more potent than Trolox. 17 beta-Estradiol, hydralazine, S-nitrosoglutathione and 3-hydroxybenzylhydrazine were as potent as Trolox. Melatonin, glutathione, alpha-lipoic acid and l-deprenyl were about 20 times less potent than Trolox. Surprisingly, N-tert-butyl-alpha-phenylnitrone was a weak antioxidant. Furthermore, this procedure can also detect pro-oxidative side effects of vitamin C, oxidized glutathione, penicillamine and Angeli's salt. The present results obtained from this selective fluorescent assay are consistent with earlier reports that iron complexes promote while manganese inhibits brain lipid peroxidation caused by cell disruption. S-Nitrosoglutathione, melatonin, 17 beta-estradiol, and manganese have been successfully tested in cell/animal models for their potential neuroprotective effects. In conclusion, monitoring fluorescent adducts of peroxidizing polyunsaturated fatty acids in brain homogenates is a simple, quantitative method for studying iron-dependent brain lipid peroxidation and for screening of potential neuroprotective antioxidants in both in vitro and in vivo preparations.

Animals↗

PubMed1983

Production of superoxide and hydrogen peroxide in medium used to culture Legionella pneumophila: catalytic decomposition by charcoal.

The difficulties associated with the growth of Legionella species in common laboratory media may be due to the sensitivity of these organisms to low levels of hydrogen peroxide and superoxide radicals. Exposure of yeast extract (YE) broth to fluorescent light generated superoxide radicals (3 microM/h) and hydrogen peroxide (16 microM/h). Autoclaved YE medium was more prone to photochemical oxidation than YE medium sterilized by filtration. Activated charcoals and, to a lesser extent, graphite, but not starch, prevented photochemical oxidation of YE medium, decomposed hydrogen peroxide and superoxide radicals, and prevented light-accelerated autooxidation of cysteine. Also, suspensions of charcoal in phosphate buffer and in charcoal yeast extract medium readily decomposed exogenous peroxide (17 and 23 nmol/ml per min, respectively). Combinations of bovine superoxide dismutase and catalase also decreased the rate of photooxidation of YE medium. Medium protected from light did not accumulate appreciable levels of hydrogen peroxide, and autoclaved YE medium protected from light supported good growth of Legionella micdadei. Various species of Legionella (10(4) cells per ml) exhibited sensitivity to relatively low levels of hydrogen peroxide (26.5 microM) in challenge experiments. The level of hydrogen peroxide that accumulated in YE medium over a period of several hours (greater than 50 microM) was in excess of the level tolerated by Legionella pneumophila, which contained no measurable catalase activity. Strains of L. micdadei, Legionella dumoffi, and Legionella bozmanii contained this enzyme, but the presence of catalase did not appear to confer appreciable tolerance to exogenously generated hydrogen peroxide.

Bacteriological Techniques↗

PubMed1993

Binding of small, acid-soluble spore proteins to DNA plays a significant role in the resistance of Bacillus subtilis spores to hydrogen peroxide.

Dormant spores of Bacillus subtilis which lack the majority of the alpha/beta-type small, acid-soluble proteins (SASP) (termed alpha- beta- spores) that coat the DNA in wild-type spores are significantly more sensitive to hydrogen peroxide than are wild-type spores. Hydrogen peroxide treatment of alpha- beta- spores causes DNA strand breaks more readily than does comparable treatment of wild-type spores, and alpha- beta- spores, but not wild-type spores, which survive hydrogen peroxide treatment have acquired a significant number of mutations. The hydrogen peroxide resistance of wild-type spores appears to be acquired in at least two incremental steps during sporulation. The first increment is acquired at about the time of alpha/beta-type SASP synthesis, and the second increment is acquired approximately 2 h later, at about the time of dipicolinic acid accumulation. During sporulation of the alpha- beta- strain, only the second increment of hydrogen peroxide resistance is acquired. In contrast, sporulation mutants which accumulate alpha/beta-type SASP but progress no further in sporulation acquire only the first increment of hydrogen peroxide resistance. These findings strongly suggest that binding of alpha/beta-type SASP to DNA provides one increment of spore hydrogen peroxide resistance. Indeed, binding of alpha/beta-type SASP to DNA in vitro provides strong protection against cleavage of DNA by hydrogen peroxide.

Bacillus subtilis↗

PubMed1984

Bactericidal and cytotoxic effects of hypothiocyanite-hydrogen peroxide mixtures.

Lactoperoxidase catalyzes the oxidation of thiocyanate by hydrogen peroxide into hypothiocyanite, a reaction which can protect bacterial and mammalian cells from killing by hydrogen peroxide. The present study demonstrates, however, that lactoperoxidase in the presence of thiocyanate can actually potentiate the bactericidal and cytotoxic effects of hydrogen peroxide under specific conditions, such as when hydrogen peroxide is present in the reaction mixtures in excess of thiocyanate. The toxic agent was also formed in the absence of lactoperoxidase in a reaction between hypothiocyanite and hydrogen peroxide. Sulfate, sulfite, cyanate, carbonate, and ammonia, which have been postulated to be formed in the chemical oxidation of hypothiocyanite by hydrogen peroxide, were not bactericidal and did not potentiate the bactericidal effect of hydrogen peroxide. Cyanosulfurous acid, the only other postulated product of the chemical oxidation of hypothiocyanite by hydrogen peroxide, may be the killing agent.

Anti-Bacterial Agents↗

PubMed1985

Lack of antibacterial activity after intravenous hydrogen peroxide infusion in experimental Escherichia coli sepsis.

The intravenous administration of hydrogen peroxide has been reported to benefit patients with pneumonia and to reduce Plasmodium parasitemia in experimentally infected mice. We assessed the antibacterial activity of intravenously infused hydrogen peroxide against hydrogen peroxide-susceptible Escherichia coli (MBC of hydrogen peroxide, 0.23 mM) in experimentally infected rabbits. No decrease in the level of bacteremia was detected at the maximum intravenous infusion rate of hydrogen peroxide physiologically tolerated by the rabbits (2.0 mumol/h). Moreover, the addition ex vivo of greater amounts of hydrogen peroxide to human or murine blood containing E. coli resulted in no detectable antibacterial action. In contrast, ethyl hydrogen peroxide, which is not affected by catalase, was bactericidal when added ex vivo to human blood containing E. coli. These results suggest that extracellular hydrogen peroxide, whether of exogenous or endogenous origin, does not have antibacterial activity in the blood of animals having even low levels of catalase.

Animals↗

PubMed2004

Cytotoxicity of hydrogen peroxide produced by Enterococcus faecium.

Although the opportunistic bacterial pathogen Enterococcus faecium is a leading source of nosocomial infections, it appears to lack many of the overt virulence factors produced by other bacterial pathogens, and the underlying mechanism of pathogenesis is not clear. Using E. faecium-mediated killing of the nematode worm Caenorhabditis elegans as an indicator of toxicity, we determined that E. faecium produces hydrogen peroxide at levels that cause cellular damage. We identified E. faecium transposon insertion mutants with altered C. elegans killing activity, and these mutants were altered in hydrogen peroxide production. Mutation of an NADH oxidase-encoding gene eliminated nearly all NADH oxidase activity and reduced hydrogen peroxide production. Mutation of an NADH peroxidase-encoding gene resulted in the enhanced accumulation of hydrogen peroxide. E. faecium is able to produce hydrogen peroxide by using glycerol-3-phosphate oxidase, and addition of glycerol to the culture medium enhanced the killing of C. elegans. Conversely, addition of glucose, which leads to the down-regulation of glycerol metabolism, prevented both C. elegans killing and hydrogen peroxide production. Lastly, detoxification of hydrogen peroxide either by exogenously added catalase or by a C. elegans transgenic strain overproducing catalase prevented E. faecium-mediated killing. These results suggest that hydrogen peroxide produced by E. faecium has cytotoxic effects and highlight the utility of C. elegans pathogenicity models for identifying bacterial virulence factors.

Animals↗

PubMed2004

Differential gene expression in response to hydrogen peroxide and the putative PerR regulon of Synechocystis sp. strain PCC 6803.

We utilized a full genome cDNA microarray to identify the genes that comprise the peroxide stimulon in the cyanobacterium Synechocystis sp. strain PCC 6803. We determined that a gene (slr1738) encoding a protein similar to PerR in Bacillus subtilis was induced by peroxide. We constructed a PerR knockout strain and used it to help identify components of the PerR regulon, and we found that the regulatory properties were consistent with the hypothesis that PerR functions as a repressor. This effort was guided by finding putative PerR boxes in positions upstream of specific genes and by careful statistical analysis. PerR and sll1621 (ahpC), which codes for a peroxiredoxin, share a divergent promoter that is regulated by PerR. We found that isiA, encoding a Chl protein that is induced under low-iron conditions, was strongly induced by a short-term peroxide stress. Other genes that were strongly induced by peroxide included sigD, sigB, and genes encoding peroxiredoxins and Dsb-like proteins that have not been studied yet in this strain. A gene (slr1894) that encoded a protein similar to MrgA in B. subtilis was upregulated by peroxide, and a strain containing an mrgA knockout mutation was highly sensitive to peroxide. A number of genes were downregulated, including key genes in the chlorophyll biosynthesis pathway and numerous regulatory genes, including those encoding histidine kinases. We used PerR mutants and a thioredoxin mutant (TrxA1) to study differential expression in response to peroxide and determined that neither PerR nor TrxA1 is essential for the peroxide protective response.

Bacterial Proteins↗

PubMed1991

Effect of hydrogen peroxide on growth of Candida, Cryptococcus, and other yeasts in simulated blood culture bottles.

The addition of hydrogen peroxide to blood contained in liquid culture medium increased the dissolved-O2 partial pressure in direct proportion to the volume injected. The effect of hydrogen peroxide on the growth of subcultured clinical isolates of Candida albicans, Cryptococcus neoformans, Torulopsis glabrata, and other yeasts and on the growth of blood culture isolates of representative pathogenic bacteria was compared with its effect on their growth in vented and unvented stationary bottles. C. albicans and C. neoformans grew significantly better in bottles to which hydrogen peroxide had been added than in vented or unvented bottles. The advantage of hydrogen peroxide over venting was most marked with several slowly growing strains. Similar results were obtained in shaker cultures with strains of C. albicans which were inoculated directly from positive blood cultures. The effect of hydrogen peroxide tended to diminish during serial passage. T. glabrata grew less well when hydrogen peroxide was added, perhaps because of the absence of oxidase. The growth of Staphylococcus aureus, Pseudomonas aeruginosa, and Enterococcus faecalis was not significantly inhibited or augmented by the addition of hydrogen peroxide. The growth of Escherichia coli was inhibited slightly. The value of the addition of hydrogen peroxide to blood cultures to improve the isolation of yeasts needs to be established by a clinical trial which would compare this method with established methods.

Blood↗

PubMed1993

Intensity of inflammatory damage and serum lipid peroxide concentrations in liver disease.

AIMS: To investigate variations in serum lipid peroxide activities in relation to various clinical entities of liver disease. METHODS: Serum lipid peroxides were measured fluorometrically in eight patients with acute hepatitis, six with liver steatofibrosis, five with chronic persistent hepatitis, 15 with chronic active hepatitis, 28 with liver cirrhosis, 22 with hepatocellular carcinoma; 19 patients with extrahepatic disease (six malignant, 13 benign) were used as controls. RESULTS: Higher serum lipid peroxide concentrations were found in patients with acute hepatitis (4.52 (SEM 0.56)) nmol/ml than in all other groups of patients (p < 0.01). No significant difference was found among the mean values detected in the groups of patients affected by chronic liver disease and extrahepatic diseases. A history of chronic alcohol consumption was not associated with higher lipid peroxide concentrations. A significant correlation (R2 = 0.4538, R = 0.6737, F = 7.617, p = 0.0000) was found between serum lipid peroxides and a set of indices of inflammation (ESR, total leucocyte count, C-reactive protein) and of hepatic function (aspartate aminotransferase (AST) or alkaline phosphatase (ALP) or bilirubin). Of these, bilirubin was the most significant indicator of inflammation. Analysis of covariance showed a significant difference in lipid peroxide values among groups, even when bilirubin was chosen as an independent variable. CONCLUSIONS: Raised serum lipid peroxide concentrations can be found during acute inflammatory liver disease. Acute change in liver function, reflected by high bilirubin concentrations, seems to be more important for intravascular liberation of lipid peroxides than existence of specific aetiological factors or of severe longstanding global liver damage.

Acute Disease↗

PubMed1993

Sporocidal properties of peracetic acid and hydrogen peroxide, alone and in combination, in comparison with chlorine and formaldehyde for ultrafiltration membrane disinfection.

The sporocidal properties of peracetic acid, hydrogen peroxide, chlorine, and formaldehyde were compared in vitro using a dilution-neutralization micromethod. A combination of peracetic acid and hydrogen peroxide was also tested to assess their interactions. The activities of these agents, which are widely used as disinfectants, were evaluated against Bacillus spore isolates found on stored membranes and collection cultures. Peracetic acid and chlorine exhibited an excellent antimicrobial activity, with a destruction of 10(5) spores/mL after 5 min of contact. Generally the effects of the biocides tested were time dependent. The sporocidal activities of hydrogen peroxide and formaldehyde were the lowest. The combination of peracetic acid and hydrogen peroxide, tested by a checkerboard micromethod, was found to be synergistic. The minimal sporocidal concentration (MSC) was established in terms of time for each biocide. The lowest MSC values for peracetic acid, hydrogen peroxide, chlorine, and formaldehyde were 168-336 ppm (1-2 h of contact), 5625-11250 ppm (5-7 h), 168-336 ppm (2-3 h), and 1875-3750 ppm (5-30 min), respectively. The MSC of a biocide combination of peracetic acid and hydrogen peroxide showed that synergy was maintained with increasing contact time and that the MSC could be reduced by two to eight times when compared with those of the biocides alone. Optimal concentrations and contact times of those chemicals that were promising in vitro were then tested for their ability to disinfect ultrafiltration membranes. The sporocidal activities of peroxide compounds and chlorine were confirmed and the synergism between peracetic acid and hydrogen peroxide was also maintained.(ABSTRACT TRUNCATED AT 250 WORDS)

Bacillus↗

PubMed1997

Peroxide resistance of ER Ca2+ pump in endothelium: implications to coronary artery function.

We examined the effects of peroxide on the sarco(endo)plasmic reticulum Ca2+ (SERCA) pump in pig coronary artery endothelium and smooth muscle at three organizational levels: Ca2+ transport in permeabilized cells, cytosolic Ca2+ concentration in intact cells, and contractile function of artery rings. We monitored the ATP-dependent, azide-insensitive, oxalate-stimulated 45Ca2+ uptake by saponin-permeabilized cultured cells. Low concentrations of peroxide inhibited the uptake less effectively in endothelium than in smooth muscle whether we added the peroxide directly to the Ca2+ uptake solution or treated intact cells with peroxide and washed them before the permeabilization. An acylphosphate formation assay confirmed the greater resistance of the SERCA pump in endothelial cells than in smooth muscle cells. Pretreating smooth muscle cells with 300 microM peroxide inhibited (by 77 +/- 2%) the cyclopiazonic acid (CPA)-induced increase in cytosolic Ca2+ concentration in a Ca2+-free solution, but it did not affect the endothelial cells. Peroxide pretreatment inhibited the CPA-induced contraction in deendothelialized arteries with a 50% inhibitory concentration of 97 +/- 13 microM, but up to 500 microM peroxide did not affect the endothelium-dependent, CPA-induced relaxation. Similarly, 500 microM peroxide inhibited the angiotensin-induced contractions in deendothelialized arteries by 93 +/- 2%, but it inhibited the bradykinin-induced, endothelium-dependent relaxation by only 40 +/- 13%. The greater resistance of the endothelium to reactive oxygen may be important during ischemia-reperfusion or in the postinfection immune response.

Animals↗

PubMed1987

Role of lipid peroxidation in gastric mucosal lesions induced by HCl, NaOH, or ischemia.

We investigated whether lipid peroxidation is an important biochemical mechanism in acute gastric mucosal injury induced by acid, base, or postischemic reperfusion. Lipid peroxidation products, i.e., the concentration of conjugated dienes (absorbance at 242 nm), products absorbing at 270 nm, and malondialdehyde were measured in the gastric mucosa of rats killed 30 s or 1, 3, or 6 min after intragastric (ig) administration of 0.6 N HCl or 0.2 N NaOH. No increase in any of the lipid peroxidation products was detected at any of the time intervals. Mucosal lesions, however, were already visible at 30 s. Cumene hydroperoxide (1 ml, 100 mM ig) induced neither mucosal lesions nor lipid peroxidation. In vitro incubation of mucosal homogenates with cumene hydroperoxide (1 or 10 mM) however, rapidly induced elevation of the three parameters of lipid peroxidation. Ischemia induced by clamping the blood vessels of the stomach for 20, 30, and 40 min followed by reperfusion for 10, 30, and 40 min did not induce lipid peroxidation, despite the development of hemorrhagic mucosal lesions. Similarly, in gastric mucosal lesions induced by hemorrhagic shock no lipid peroxidation products were detected. In the small intestine, however, prolonged ischemia (2 h) followed by reperfusion (30 min) resulted in mucosal necrosis and elevation of malondialdehyde levels. These results suggest that lipid peroxidation is not a major pathogenetic mechanism in rapidly developing acute gastric mucosal injury caused by 0.6 N HCl or 0.2 N NaOH, or in the more slowly developing mucosal injury caused by postischemic reperfusion.

Animals↗

PubMed1986

Ethane production as a measure of lipid peroxidation after renal ischemia.

After renal ischemia, oxygen free radicals are formed and produce tissue injury, in large part, through peroxidation of polyunsaturated fatty acids. We used an in vivo method to monitor lipid peroxidation after renal ischemia, the measurement of ethane in expired gas, to determine the time course of lipid peroxidation and the effect of several agents to limit lipid peroxidation after renal ischemia. In anesthetized rats there was no significant increase in ethane production during 60 min of renal ischemia. During the first 10 min of renal reperfusion, there was a prompt increase in ethane production from 2.9 +/- 1.3 to 6.3 +/- 1.9 pmol/min (P less than 0.05). Ethane production was significantly increased during the first 50 min of reperfusion and then rapidly tapered to base-line levels. Preischemic administration of allopurinol to prevent superoxide radical generation or the superoxide radical scavenger superoxide dismutase prevented the increase in ethane production during postischemic reperfusion. These studies confirm that there is increase lipid peroxidation following renal ischemia that can be prevented by agents which limit the formation or accumulation of oxygen free radicals. This in vivo method for measuring lipid peroxidation could also be employed to study the effects of ischemia on lipid peroxidation in other organs, as well as to monitor lipid peroxidation in other forms of injury.

Allopurinol↗