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Lipid peroxidation as a mechanism of alcoholic liver injury: role of iron mobilization and microsomal induction.

Lipid peroxidation has been invoked as a mechanism of alcoholic liver injury but its role has been controversial and the mechanism by which it occurs is unclear. Catalytic iron is known to play an important role in cellular injury and is produced during mobilization of ferritin iron. In vivo administration of a large acute dose of ethanol (5 g/kg) which produces hepatic lipid peroxidation in chow-fed rats resulted in mobilization of non-heme iron. The generation of NADH from alcohol metabolism via ADH or superoxide from acetaldehyde-xanthine oxidase mobilized iron from horse spleen ferritin in vitro. Chronic feeding of alcohol as 36% of energy for 6 weeks does not itself produce peroxidation in the rat but potentiates acute effects of ethanol. It produced microsomal induction which enhanced iron-stimulated lipid peroxidation and increased hepatic non-heme iron. Carbon monoxide increased rather than decreased accumulation of microsomal peroxidation products in vitro suggesting that cytochrome P-450 reductase mediates peroxidation but cytochrome P-450 may metabolize products. Incubation at lowered oxygen tensions equivalent to those observed in the perivenular zone (pO2 = 24 mmHg) enhanced in vitro iron mobilization but decreased peroxidation. Lipid peroxidation and its stimulation by iron mobilization and microsomal induction may be an important contributory mechanism of alcohol-induced liver injury.

Animals↗
PubMed1989

Lipid peroxidation: a mechanism for alcohol-induced testicular injury.

That alcohol abuse may lead to testicular lipid peroxidation is suggested by the fact that ethanol is a known testicular toxin and its chronic use leads to both endocrine and reproductive failure. Because testicular membranes are rich in polyenoic fatty acids that are prone to undergo peroxidative decomposition, it is reasonable to consider that lipid peroxidation may contribute to the membrane injury and gonadal dysfunction that occurs as a result of alcohol abuse and/or chronic use. The present report reviews the studies supporting the concept that testicular lipid peroxidation is a metabolic consequence of chronic alcohol administration to animals and that its presence correlates with the gonadal injury present in animals ingesting ethanol for prolonged periods. Consistent with such a mechanism for putative alcohol-associated testicular toxicity are the observed reductions in the testicular content of polyenoic fatty acids and glutathione (GSH) content of the testes of alcohol-fed animals as compared to isocalorically fed controls. The later finding demonstrates that ethanol modifies the precarious antioxidant balance of testicular tissue such that enhanced peroxidation can occur. It is well known that peroxidation injury can be attenuated when it occurs in association with dietary vitamin A supplementation. Thus, it is of interest to note that vitamin A, acting as an antioxidant, stabilizes testicular membranes by reducing lipid peroxidation and prevents the alcohol-induced atrophy that occurs in animals not receiving vitamin-A-enriched diets. Taken together, these observations suggest that the enhanced peroxidation of testicular lipids that occurs following ethanol exposure may be an important factor in the pathogenesis of alcohol-associated gonadal injury.

Animals↗
PubMed1989

Peroxidation induced changes in synaptosomal transport of dopamine and gamma-aminobutyric acid.

The effects of iron-dependent peroxidation on respiration and neurotransmitter transport of brain nerve endings has been studied. Rat brain synaptosomes were peroxidized by exposure to an ADP-Fe/ascorbate system and the protective effect of added Se, Cd, or Zn was investigated with regard to dopamine and gamma-aminobutyric acid (GABA) transport. Peroxidation impaired the respiration of synaptosomes by about 20% and caused a marked increase in dopamine uptake; but in contrast, peroxidation induced a large decrease in synaptosomal uptake of GABA. The increased dopamine transport into synaptosomes was partially prevented by the presence of Zn, Se, or Cd. The presence of Zn, Cd, or Se, in order of decreasing effectiveness, also slowed down ADP-Fe/ascorbate mediated peroxidation of synaptosomes. Peroxidation caused a significant inhibition of veratridine-dependent release of both dopamine and GABA from synaptosomes, but the KCl-dependent release of these neurotransmitters was not effected by peroxidation. These results implicate that peroxidation damage of nerve endings may lead to large changes in neurotransmitter transport thus resulting in an alteration in the function of the central nervous system.

Animals↗
PubMed1989

Effect of hyperlipidemic serum on lipid peroxidation, synthesis of prostacyclin and thromboxane by cultured endothelial cells: protective effect of antioxidants.

An increased lipid peroxides and a decreased production of prostacyclin have been shown in advanced atherosclerotic lesions and plasma. Our purpose was to determine whether the similar findings could be observed in cultured endothelial cells, and whether antioxidants could protect the cell against peroxide injury. In these experiments we have used bovine aortic endothelial cells in culture to address the issue of hyperlipidemia-induced arterial damage. Results of the present study showed that different concentration of hyperlipidemic sera from atherogenic rabbits induced a time- and dose-dependent alteration in the production of prostacyclin and levels of lipid peroxides in endothelial cells. Endothelial cells incubated with hyperlipidemic serum increased prostacyclin generation significantly during the initial stages and then continuously decreased. When endothelial cells were incubated for 36 h, TXA2 generation was also impaired and at the same time the cellular lipid peroxides content increased. There was a positive correlation between the concentration of hyperlipidemic serum and lipid peroxides and an inverse correlation with prostacyclin synthesis. The medium supplemented with antioxidant selenium or vitamin E showed a significant decrease in lipid peroxides and an increase in prostacyclin synthesis. These results suggest that both hyperlipidemic serum and lipid peroxides injury endothelial cells and inactivate prostacyclin synthetase, resulting in a decrease of prostacyclin production, while antioxidants have a protective effect. We conclude that the increase in lipid peroxides in association with hyperlipidemia results in alteration of prostacyclin synthesis that may play an important role in the pathogenesis of atherosclerosis.

Animals↗
PubMed1994

Mutagenesis resulting from DNA damage by lipid peroxidation in the supF gene of Escherichia coli.

In vitro incubation of rat microsomal lipids with NADPH and Fe3+ in the presence of cytochrome P450 reductase produces lesions in double-stranded pZ189 plasmid DNA, the mutagenic potential of which was analyzed after transfection into Escherichia coli host cells that had been induced for SOS functions by ultraviolet irradiation. The extent of lipid peroxidation, when monitored by the formation of thiobarbituric acid reaction substances, was increased with increased addition of lipids in the reaction mixture. Mutagenesis was determined with the forward mutation assay using the supF gene of pZ189 as a target. When treated pZ189 DNA was used to transfect host cells, a seven-fold increase in mutation frequency for SOS uninduced hosts and a 12-fold increase in mutation frequency for SOS induced hosts was observed at 50% survival compared to that observed with untreated DNA. Sequence analysis shows that incubation of pZ189 DNA in the lipid peroxidation reaction mixture results mostly in single base substitutions, the most frequent base change being G:C-->C:G transversion, followed by G:C-->T:A transversion. The fact that, in the SOS induced hosts, the spectrum obtained by lipid peroxidation is similar to that of hydrogen peroxide suggests the possible involvement for mutagenesis of superoxide produced during lipid peroxidation, but not lipid peroxidation end products such as aldehyde or alkane. Treatment of pZ189 DNA with increasing extents of lipid peroxidation did not yield increasing formation of 8-hydroxyguanine. The results suggest that the origins of G:C-->C:G and G:C-->T:A transversions may be (an) as yet unidentified lesion(s) generated by lipid peroxidation.

Animals↗
PubMed2005

Antioxidant effect of bovine serum albumin on membrane lipid peroxidation induced by iron chelate and superoxide.

Albumin is supposed to be the major antioxidant circulating in blood. This study examined the prevention of membrane lipid peroxidation by bovine serum albumin (BSA). Lipid peroxidation was induced by the exposing of enzymatically generated superoxide radicals to egg yolk phosphatidylcholine liposomes incorporating lipids with different charges in the presence of chelated iron catalysts. We used three kinds of Fe3+-chelates, which initiated reactions that were dependent on membrane charge: Fe3+-EDTA and Fe3+-EGTA catalyzed peroxidation in positively and negatively charged liposomes, respectively, and Fe3+-NTA, a renal carcinogen, catalyzed the reaction in liposomes of either charge. Fe3+-chelates initiated more lipid peroxidation in liposomes with increased zeta potentials, followed by an increase of their availability for the initiation of the reaction at the membrane surface. BSA inhibits lipid peroxidation by preventing the interaction of iron chelate with membranes, followed by a decrease of its availability in a charge-dependent manner depending on the iron-chelate concentration: one is accompanied and the other is unaccompanied by a change in the membrane charge. The inhibitory effect of BSA in the former at high concentrations of iron chelate would be attributed to its electrostatic binding with oppositely charged membranes. The inhibitory effect in the latter at low concentrations of iron chelate would be caused by BSA binding with iron chelates and keeping them away from membrane surface where lipid peroxidation is initiated. Although these results warrant further in vivo investigation, it was concluded that BSA inhibits membrane lipid peroxidation by decreasing the availability of iron for the initiation of membrane lipid peroxidation, in addition to trapping active oxygens and free radicals.

Animals↗
PubMed2005

Effect of scutellarin on nitric oxide production in early stages of neuron damage induced by hydrogen peroxide.

The aims of the present study were to investigate the regulatory function of scutellarin on production of nitric oxide (NO) as well as activities of constitutive NO synthase (cNOS) and inducible NO synthase (iNOS) in early stages of neuron damage induced by hydrogen peroxide. Direct detection of NO production was performed on primary cultures of living rat neuronal cells with an electrochemical sensor. Hydrogen peroxide significantly increased culture supernatant levels of NO, the total integral value of the defined areas (500-6500 sxpA) reached 3.68 x 10(6). Pre-treatment with scutellarin, caused the total integral value to decrease in a dose-dependent fashion (3.24 x 10(6), 2.15 x 10(6), 1.84 x 10(6) for groups 10, 50, and 100 uM scutellarin, respectively). After exposure to 2.0mM hydrogen peroxide for 2h, malondialdehyde (MDA) level, a marker of lipid peroxidation, was remarkably increased. The elevation can be suppressed by scutellarin. Hydrogen peroxide also caused significant loss of neuron viability. In comparison with the control group, scutellarin significant attenuated the loss. Results also showed that hydrogen peroxide increased activity of cNOS, which was markedly inhibited by scutellarin. However, exposure of neuronal cells to hydrogen peroxide did not lead to an increase in iNOS activity. In conclusion, our results suggest that NO production, which increased in early stages of neuron damage induced by hydrogen peroxide can be effectively inhibited by scutellarin. Moreover, our results indicate that increase in NO production is mediated by cNOS.

Animals↗
PubMed2006

The effect of alpha-tocopherol on lipid peroxidation of microsomes and mitochondria from rat testis.

The testis is a remarkably active metabolic organ; hence it is suitable not only for studies of lipid metabolism in the organ itself but also for the study of lipid peroxidation processes in general. The content of fatty acids in testis is high with a prevalence of polyunsaturated fatty acids (PUFA) which renders this tissue very susceptible to lipid peroxidation. Studies were carried out to evaluate the effect of alpha-tocopherol in vitro on ascorbate-Fe(++) lipid peroxidation of rat testis microsomes and mitochondria. Chemiluminescence and fatty acid composition were used as an index of the oxidative destruction of lipids. Special attention was paid to the changes produced on the highly PUFA [C20:4 n6] and [C22:5 n6]. Lipid peroxidation of testis microsomes or mitochondria induced a significant decrease of both fatty acids. Total chemiluminescence was similar in both kinds of organelles when the peroxidized without (control) and with ascorbate-Fe(++) (peroxidized) groups were compared. Arachidonic acid was protected more efficiently than docosapentaenoic acid at all alpha-tocopherol concentrations tested when rat testis microsomes or mitochondria were incubated with ascorbate-Fe(++). The maximal percentage of inhibition in both organelles was approximately 70%; corresponding to an alpha-tocopherol concentration between 1 and 0.25 mM. IC50 values from the inhibition of alpha-tocopherol on the chemiluminescence were higher in microsomes (0.144 mM) than mitochondria (0.078 mM). The protective effect observed by alpha-tocopherol in rat testis mitochondria was higher compared with microsomes, associated with the higher amount of [C20:4 n6]+[C22:5 n6] in microsomes that in mitochondria. It is proposed that the vulnerability to lipid peroxidation of rat testis microsomes and mitochondria is different because of the different proportion of PUFA in these organelles The peroxidizability index (PI) was positively correlated with the level of long chain fatty acids. The results demonstrated the protective effect of alpha-tocopherol on lipid peroxidation in microsomes and mitochondria from rat testis.

Animals↗
PubMed2006

Role of endogenous hydrogen peroxide in the development of nitrate tolerance.

The present study was designed to test the hypothesis that hydrogen peroxide plays a role in the development of nitrate tolerance. Isolated rat aortic rings were suspended in organ chambers for isometric tension recording. The rings were incubated with (tolerant) and without (control) nitroglycerin (10(-4) M) for 90 min, followed by repeated rinsing for 1 h. Hydrogen peroxide release in control and tolerant tissues was measured fluorimetrically using amplex red. Nitroglycerin (10(-9)-10(-4) M) caused concentration-dependent relaxations in control (-logEC50=7.15+/-0.1) and tolerant rings (-logEC50=5.83+/-0.1) contracted with norepinephrine. Nitrate tolerance was evident by a >20-fold rightward shift in the nitroglycerin concentration-response curve in tissues exposed previously to nitroglycerin for 90 min. Incubation of the rings with the superoxide dismutase (SOD)-mimetic, tempol (10(-4) M), during the 90-min exposure period to nitroglycerin caused a leftward shift in the nitroglycerin concentration-response curve in tolerant rings (-logEC50=6.84+/-0.2), but had no effect on the response to nitroglycerin in control rings. Treatment of the rings with catalase (1200 U/ml) or ebselen (1.5x10(-5) M), a glutathione peroxidase-mimetic, during the 90-min exposure period to nitroglycerin resulted in a further rightward shift in the nitroglycerin concentration-response curve in tolerant rings (-logEC50=5.41+/-0.1 and 4.98+/-0.1; catalase and ebselen respectively), without altering the response to nitroglycerin in control rings. In the presence of catalase, the effect of tempol on nitrate tolerance was abolished (-logEC50=5.46+/-0.1). Hydrogen peroxide release was reduced by approximately 64% in nitrate tolerant tissues when compared to control. The decrease in hydrogen peroxide release was completely reversed by treatment with tempol, whereas treatment with ebselen caused a further decrease in hydrogen peroxide release in nitrate tolerant tissues. Addition of hydrogen peroxide (3x10(-5) M) to nitrate tolerant rings caused a leftward shift in the nitroglycerin concentration-response curve in tolerant rings (-logEC50=7.18+/-0.3), but had no effect on the response to nitroglycerin in control rings. These results suggest that nitrate tolerance is associated with decreased endogenous formation of hydrogen peroxide, which attenuates nitrate tolerance development. SOD-mimetics may reduce nitrate tolerance, in part, by increasing the formation of hydrogen peroxide.

Animals↗
PubMed2006

Measurement of hydrogen peroxide in an advanced oxidation process using an automated biosensor.

A hydrogen peroxide biosensor was used to monitor hydrogen peroxide concentrations in a UV/hydrogen peroxide immobilised Fenton advanced oxidation process (AOP). The biosensor is based on gas phase monitoring and thus is more resistant to fouling from the liquid phase constituents of industrial processes. The biosensor is supplied with catalase continually, therefore overcoming any problems with enzyme degradation, which would occur in an immobilised enzyme biosensor. The biosensors response was linear within the experimental range 30-400mg H(2)O(2)l(-1) with a R(2) correlation of 0.99. The hydrogen peroxide monitor was used to monitor residual peroxide in an AOP, operated with a step overload of hydrogen peroxide, with correlation factors of 0.96-0.99 compared to offline hydrogen peroxide determinations by UV spectroscopy. Sparging the sample with nitrogen was found to be effective in reducing the interference from dissolved gases produced with the AOP itself. It is proposed that this biosensor could be used to improve the effectiveness of AOPs via hydrogen peroxide control.

Automation↗
PubMed1992

Low-dose aspirin inhibits lipid peroxides and thromboxane but not prostacyclin in pregnant women.

OBJECTIVE: Preeclampsia is associated with an imbalance of increased thromboxane and decreased prostacyclin and an abnormal increase of lipid peroxides. Lipid peroxides are toxic compounds that damage cells and inhibit prostacyclin synthesis. Low-dose aspirin therapy reduces the incidence of preeclampsia, presumably by selective inhibition of thromboxane to restore a balance between thromboxane and prostacyclin. However, the effectiveness of low-dose aspirin might also relate to inhibition of lipid peroxides. STUDY DESIGN: To test this hypothesis, 10 women at risk of preeclampsia were placed on low-dose aspirin therapy (81 mg/day) between 9 and 34 weeks of gestation. Plasma samples were collected before and after 3 to 4 days and 3 to 4 weeks of aspirin therapy. Samples were analyzed for thromboxane and prostacyclin by radioimmunoassay of their stable metabolites, thromboxane B2 and 6-keto-prostaglandin F1 alpha, and for lipid peroxides by hydrogen peroxide equivalents. RESULTS: Low-dose aspirin significantly decreased (p < 0.05) both lipid peroxides (130 +/- 18 vs 92 +/- 11 and 68 +/- 9 nmol/ml, mean +/- SE) and thromboxane (502 +/- 67 vs 138 +/- 67 and 8 +/- 5 pg/ml), but it did not affect prostacyclin (55 +/- 10 vs 41 +/- 8 and 40 +/- 11 pg/ml, p > 0.1). CONCLUSION: Low-dose aspirin selectively inhibits both lipid peroxides and thromboxane without affecting prostacyclin. Inhibition of both lipid peroxides and thromboxane by low-dose aspirin reveals a new mechanism of action and may account for its effectiveness in the prevention of preeclampsia.

Aspirin↗
PubMed1999

Validation of the peroxidative indicators, cis-parinaric acid and parinaroyl-phospholipids, in a model system and cultured cardiac myocytes.

cis-Parinaric acid is increasingly being used in eukaryotic cells as a very sensitive marker for the initial stages of lipid peroxidation. Despite the increased application of this probe, no extensive validation, especially in cellular systems, has been performed. cis-Parinaric acid can either be inserted freely into biomembranes or incorporated (bio)synthetically into lipids (parinaroyl-lipid). Therefore, a direct comparison was made between the peroxidative behaviour of the two parinaroyl probes and the endogenous polyunsaturated fatty acids arachidonic and linoleic acid, in both an artificial lipidic system and in cultured neonatal rat heart cells. Three different radical generating systems were used, i.e., hydrogen peroxide, cumene hydroperoxide and the thermo-labile 2,2'-azobis(2-amidinopropane hydrochloride) (AAPH). The data demonstrate that the peroxidation rate of cis-parinaric acid is higher than that of the parinaroyl, arachidonoyl and linoleoyl lipids. The latter three displayed comparable peroxidation rates, showing that the peroxidative decay of parinaroyl-lipid is a good marker for the degradation of endogenous polyunsaturated fatty acids. Experimental results using the freely inserted cis-parinaric acid could potentially lead to an overestimation of the inflicted damage and should be interpreted with care. In addition, a comparison was made with the measurement of conjugated dienes and malon dialdehyde as thiobarbituric acid reactive substances. The results demonstrate that measurement of conjugated dienes and malon dialdehyde only provide information on peroxidative processes in vitro, but are not suitable for in-depth studies in cultured cells. In contrast, the use of the parinaroyl probes is a suitable, straightforward, sensitive and reproducible method for detecting the initial stages of lipid peroxidation in living cells.

Animals↗
PubMed1987

Crocidolite-induced lipid peroxidation in rat lung microsomes. I. Role of different ions.

Lipid peroxidation is increased by ferrous or ferric ions in rat lung microsomes both from rats pretreated with 3-methylcholanthrene and from untreated controls. This increase was dependent on the concentration of these ions in the reaction mixture. Crocidolite alone increased peroxidation in microsomal fractions. However, addition of ferric or ferrous ions with the crocidolite did not give a greater increase in the amount of peroxidation in microsomes. Chelation with EDTA of iron, whether originally present as free ions in the solution or attached to crocidolite, prevented lipid peroxidation. NADPH alone, when added to the microsomal fractions, did not produce any significant effect. However, when added concomitantly with crocidolite fibers, NADPH reduced the effect of crocidolite on lipid peroxidation. Magnesium, manganese, and calcium ions did not produce any significant effect on lipid peroxidation in the presence or absence of crocidolite. A reduced pH enhanced the rate of lipid peroxidation in line with increased solubility of iron salts at these pH values. All the above observations, taken together, lead to the conclusion that it is the iron in the crocidolite that is responsible for the latter's ability to enhance lipid peroxidation.

Animals↗
PubMed1987

Crocidolite-induced lipid peroxidation. II. Role of antioxidants.

Asbestos fibers in vitro produce lipid peroxidation in rat lung microsomes. Butylated hydroxytoluene prevented this peroxidation. Ascorbate in low concentrations enhanced peroxidation of lipids but inhibited it at concentrations above 4 mmole/liter so that it partially protected membrane lipids from peroxidation produced by asbestos fibers. Reduced glutathione added to microsomes gave increased peroxidation at increased concentrations up to 20 mmol/liter. At 40 mmol/liter peroxidation was prevented. Glutathione had no obvious effect on the level of peroxidation produced by asbestos fibers. The 105,000g supernatant cell fraction added either with or without glutathione gave a decrease in the amount of lipid peroxidation produced by asbestos fibers. The protective action of these reducing agents suggests a possible use as prophylactic agents against the harmful effects of inhaled asbestos.

Animals↗
PubMed2001

Mechanisms of hydrogen peroxide-induced relaxation in rabbit mesenteric small artery.

The effects of hydrogen peroxide were studied on isolated rabbit mesenteric small artery; rabbit superior mesenteric artery and mouse aorta were also studied as reference tissues. For mesenteric small artery, hydrogen peroxide (1 to 100 microM) relaxed a norepinephrine-stimulated artery in a concentration-dependent manner. The relaxation was not significantly affected by removal of the endothelium and was less pronounced in arteries contracted with high-KCl solution plus norepinephrine than in those contracted with norepinephrine alone. The relaxation response to hydrogen peroxide was increased by isobutylmethylxanthine and zaprinast, inhibited by diclofenac, methylene blue and dithiothreitol and unaffected by atropine, tetraethylammonium, superoxide dismutase, deferoxamine, dimethyl sulfoxide or the Rp stereoisomer of adenosine cyclic monophosphothioate. Hydrogen peroxide shifted concentration-contractile response curves for norepinephrine to the right and downwards. Norepinephrine and caffeine elicited a transient, phasic contraction of the mesenteric small artery exposed for 0.5, 1 and 2 min to a Ca2+-free solution. Hydrogen peroxide inhibited the norepinephrine-induced contraction, and to a lesser extent the caffeine-induced contraction, and verapamil did not alter the contraction to norepinephrine. These pharmacological properties of hydrogen peroxide were similar to those of 8-bromo cGMP; 8-bromo cGMP inhibited more potently the norepinephrine-induced than the KCl-induced contraction and the contraction elicited by norepinephrine in Ca2+-free solution. The present results suggest that hydrogen peroxide induces endothelium-independent relaxation of the rabbit mesenteric small artery precontracted with norepinephrine. The effects of hydrogen peroxide may be at least in part mediated by cGMP and cyclooxygenase products in the vascular smooth muscles now used.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed2003

Catalase induction protects Haemonchus contortus against hydrogen peroxide in vitro.

The response of Haemonchus contortus to oxidative stress in vitro was examined by measuring catalase activities in adult and L4 stage worms exposed to hydrogen peroxide generated by a glucose/glucose oxidase system. Adult nematodes showed increases of up to 2.3-fold in catalase activity after 42 h exposure to the peroxide. L4 nematodes showed up to 4.6-fold induction. A two-stage dose-response was apparent, with catalase activities increasing as the peroxide levels increased, before a return to control levels at higher peroxide concentrations, most likely reflecting a balance between induction and toxicity of the inducing agent itself. Adult nematodes exposed to low levels of peroxide for 24h (hence, having enhanced catalase activities) showed an ability to tolerate subsequent exposure to toxic levels of the peroxide compared to worms with no pre-exposure. An increase of up to approximately threefold in the LC(50) of the hydrogen peroxide generating system was observed after hydrogen peroxide pre-exposure. This indicates that exposure to low oxidant levels lead to an increase in defensive enzyme activities, which allows the nematode to survive subsequent oxidant threats more effectively. The ability of H contortus to increase its catalase activity may be crucial in allowing it to respond to the production of reactive oxygen species by host phagocytes in vivo.

Animals↗
PubMed2001

Enhanced level of n-3 fatty acid in membrane phospholipids induces lipid peroxidation in rats fed dietary docosahexaenoic acid oil.

The effect of dietary docosahexaenoic acid (DHA, 22:6n-3) oil with different lipid types on lipid peroxidation was studied in rats. Each group of male Sprague-Dawley rats was pair fed 15% (w/w) of either DHA-triglycerides (DHA-TG), DHA-ethyl esters (DHA-EE) or DHA-phospholipids (DHA-PL) for up to 3 weeks. The palm oil (supplemented with 20% soybean oil) diet without DHA was fed as the control. Dietary DHA oils lowered plasma triglyceride concentrations in rats fed DHA-TG (by 30%), DHA-EE (by 45%) and DHA-PL (by 27%), compared to control. The incorporation of dietary DHA into plasma and liver phospholipids was more pronounced in the DHA-TG and DHA-EE group than in the DHA-PL group. However, DHA oil intake negatively influenced lipid peroxidation in both plasma and liver. Phospholipid peroxidation in plasma and liver was significantly higher than control in rats fed DHA-TG or DHA-EE, but not DHA-PL. These results are consistent with increased thiobarbituric acid reactive substances (TBARS) and decreased alpha-tocopherol levels in plasma and liver. In addition, liver microsomes from rats of each group were exposed to a mixture of chelated iron (Fe(3+)/ADP) and NADPH to determine the rate of peroxidative damage. During NADPH-dependent peroxidation of microsomes, the accumulation of phospholipid hydroperoxides, as well as TBARS, were elevated and alpha-tocopherol levels were significantly exhausted in DHA-TG and DHA-EE groups. During microsomal lipid peroxidation, there was a greater loss of n-3 fatty acids (mainly DHA) than of n-6 fatty acids, including arachidonic acid (20:4n-6). These results indicate that polyunsaturation of n-3 fatty acids is the most important target for lipid peroxidation. This suggests that the ingestion of large amounts of DHA oil enhances lipid peroxidation in the target membranes where greater amounts of n-3 fatty acids are incorporated, thereby increasing the peroxidizability and possibly accelerating the atherosclerotic process.

Animals↗
PubMed1997

Mutagenic activity and specificity of hydrogen peroxide in the ad-3 forward-mutation test in two-component heterokaryons of Neurospora crassa.

In the ad-3 forward-mutation test, hydrogen peroxide was at best a weak mutagen in nongrowing conidia from a DNA repair-proficient heterokaryon (H-12, uvs-2+/uvs-2+) but was a moderate mutagen in nongrowing conidia from a DNA-repair-deficient heterokaryon (H-59, uvs-2/uvs-2) over a narrow range of high concentrations. H-59 also was more sensitive than H-12 to the killing activity of hydrogen peroxide at high concentrations. Thus, a DNA-repair pathway, of which the gene product of the uvs-2+ allele is a part, appears to be involved in the repair of hydrogen peroxide-induced DNA lesions at low survival in these strains. There was slightly, but significantly, more killing by hydrogen peroxide of nongrowing conidia from H-12 and H-59 in the presence of O2 than in the absence of O2 (presence of N2). Thus, the killing activity of hydrogen peroxide was enhanced by O2. The Mutational Spectra of hydrogen peroxide-induced ad-3 mutants shows that hydrogen peroxide induced mainly gene/point mutations but also some multilocus deletion mutations in H-12 and H-59. Multiple-locus mutations occurred only in H-59, but the frequency was very low. The frequencies of the 3 kinds of intracistronic complementation pattern among ad-3BR mutants (gene/point mutations) suggest that hydrogen peroxide induced both base-pair substitutions and frameshift mutations in both strains.

DNA Damage↗