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At least 55 records · Page 3Linked to original sources
PubMed1991

Plasma lipoprotein peroxidation potential: a test to evaluate individual susceptibility to peroxidation.

Peroxidation of lipids is believed to play a key role in various degenerative diseases. However, few simple tests are able to detect individual susceptibility or resistance to peroxidation. Measurement of the basal concentrations of lipid peroxides in plasma is not satisfactory because they are so low. Therefore, we developed a test to determine susceptibility of whole plasma to metal/H2O2-catalyzed peroxidation. Incubation of 300-500 microL of plasma with H2O2/cupric acetate resulted in the formation of products from fatty acids (malonaldehyde, measured by thiobarbituric acid assay) and cholesterol (predominantly cholest-3,5-dien-7-one, measured by gas-liquid chromatography). In the presence of Cu2+, formation of malonaldehyde and cholest-3,5-dien-7-one increased at least 10-fold over basal values. Lipid peroxide (malonaldehyde) and cholesterol oxide concentrations after peroxidation were significantly higher (P less than 0.01) in diabetic plasma than in normal plasma. Because susceptibility to plasma peroxidation represents a balance between pro-oxidant factors and antioxidant protection, this test may be useful in determining individual susceptibility to peroxidation as influenced by nutritional and clinical status.

Adult↗
PubMed1990

Intestinal motility disorder induced by peroxides: possible role of lipid peroxidation.

The effect of oxidative stress on the rat small intestine was investigated by pretreatment of isolated segments from the jejunum with hydrogen peroxide or cumene hydroperoxide. Both peroxides induced responses in the small intestine, viz. a contraction followed by a slow relaxation. The contraction could be blocked by the cyclooxygenase inhibitor indomethacin and the phospholipase A2 inhibitor quinacrine, suggesting a role for prostaglandins in the response. Pretreatment of intestinal segments with the peroxides diminished the muscarinic cholinergic response to methacholine. The lipoxygenase inhibitor nordihydroguaiaretic acid (NDGA) and the antioxidant butylated hydroxytoluene (BHT) both protected against the damage induced by cumene hydroperoxide, but did not influence the effect of hydrogen peroxide on the muscarinic response. In contrast to hydrogen peroxide, cumene hydroperoxide induced lipid peroxidation in intestinal membranes, which could also be blocked by NDGA or BHT. We conclude that cumene hydroperoxide alters the muscarinic response in the rat jejunum by the induction of lipid peroxidation, whereas the damage by hydrogen peroxide is probably induced intracellularly.

Animals↗
PubMed1994

Inhibition of S-(1,2-dichlorovinyl)-L-cysteine-induced lipid peroxidation by antioxidants in rabbit renal cortical slices: dissociation of lipid peroxidation and toxicity.

Precision-cut, rabbit renal slices were used to examine the effects of three novel antioxidants (U-74006, U-74500, and U-78517) on S-(1,2-dichlorovinyl)-L-cysteine (DCVC)-induced lipid peroxidation and toxicity. Slices exposed to DCVC showed a dose- and time-dependent increase in lipid peroxidation (TBARS) and a decrease in cellular viability, as evidenced by the loss of intracellular potassium, during the course of a 3 hour incubation. Subsequent studies employed DCVC concentrations of 100 microM. Microemulsion formulations of U-78517, U-74500, and U-74006 (100 microM) inhibited DCVC-induced lipid peroxidation by 100 +/-, 50 +/-, and < 5% (not significant), respectively. However, none of these antioxidants had a significant effect on DCVC-dependent cytotoxicity, as indicated by intracellular potassium release. The effects of U-78517, the most potent of the three antioxidants, were similar to those observed with two model antioxidants, diphenyl-p-phenylenediamine (DPPD) and the iron chelator, deferoxamine. Aminooxyacetic (AOAA), an inhibitor of renal cysteine conjugate beta-lyase, had only a minimal effect on DCVC-induced lipid peroxidation, and no effect on toxicity. These data represent the first report of DCVC-induced lipid peroxidation in rabbit renal cortical slices, a system which has been widely used to investigate mechanisms of nephrotoxicity, including that induced by DCVC. Our results demonstrate that DCVC-induced lipid peroxidation in renal slices can be inhibited by a variety of antioxidant compounds operating by different mechanisms. Because inhibition of lipid peroxidation had minimal effect on DCVC-dependent cytotoxicity, the data suggest that DCVC-induced lipid peroxidation is not a major mechanism in the cytotoxicity induced by this compound.

Aminooxyacetic Acid↗
PubMed1999

Peroxide-inducible catalase in Aeromonas salmonicida subsp. salmonicida protects against exogenous hydrogen peroxide and killing by activated rainbow trout, Oncorhynchus mykiss L., macrophages.

Aeromonas salmonicida subsp. salmonicida expresses a single cytoplasmically located catalase which was found to be inducible by exposure to 20 microM hydrogen peroxide in mid-exponential phase resulting in a 4 fold increase in activity. Subsequent exposure to 2 mM peroxide in late-exponential/early-stationary phase resulted in further induction of catalase activity which increased to 20 fold higher levels than those found in uninduced cultures. Exponentially induced cultures were protected against subsequent exposure to 10 mM peroxide which was lethal to non-induced cultures. Bacteria subjected to induction in mid-exponential and early-stationary phase were resistant to 100 mM peroxide, although viability was greatly reduced. Growth of the bacterium under iron-restricted conditions had no effect on the peroxide induction of catalase. As current evidence indicates, the latter is an iron-co-factored heme catalase, this result suggests that catalase induction has a high priority in the metabolism of iron. Furthermore, exposure to peroxide also induces expression of periplasmic MnSOD. A. salmonicida MT423 was resistant to normal rainbow trout macrophages, but was susceptible to killing by activated macrophages. However, if catalase was induced by prior exposure to 20 microM peroxide during mid-exponential phase, A. salmonicida was resistant to killing by activated macrophages. The ability of A. salmonicida to upregulate periplasmic MnSOD and cytoplasmic catalase production under iron restricted conditions and low level peroxide (conditions expected to exist during the early stages of an infection) may be vital for its ability to withstand attack by phagocytic cells in vivo.

Aeromonas↗
PubMed1998

Autoxidation of rat brain homogenate: evidence for spontaneous lipid peroxidation. Comparison with the characteristics of Fe2+- and ascorbic acid-stimulated lipid peroxidation.

Aerobically-incubated brain homogenates are known to undergo autoxidation characterized by spontaneous TBARS production, presumably as a result of lipid peroxidation. However, TBARS measurement alone, because of its lack of specificity, is not sufficient to demonstrate the occurrence of lipid peroxidation in complex biological systems. This study, undertaken to determine whether or not spontaneous oxidation of rat brain homogenate is due to lipid peroxidation, measured different specific markers of this process (fatty acids, lipid aldehydes and the formation of fluorescence products) and studied changes in alpha-tocopherol. Incubation of rat brain homogenates at 37 degrees C under air led to spontaneous TBARS formation, which was accompanied by lipid aldehydes and lipid fluorescence products as well as polyunsaturated fatty acid (PUFA) degradation. Alpha-tocopherol was also consumed. On the whole, these results demonstrate that autoxidation of brain homogenate is a spontaneous lipid peroxidation process. When homogenates were exposed to Fe2+ and ascorbic acid-induced oxidative stress, lipid peroxidation was enhanced. However, spontaneous and stimulated peroxidation showed similar patterns not characteristic of classical lipid peroxidation, i.e. without the lag and accelerating phases typical of a propagating chain reaction. PUFA degradation was limited despite stimulation of peroxidation.

Animals↗
PubMedDate not supplied

Comparison of clindamycin/benzoyl peroxide, tretinoin plus clindamycin, and the combination of clindamycin/benzoyl peroxide and tretinoin plus clindamycin in the treatment of acne vulgaris: a randomized, blinded study.

In the treatment of mild to moderate acne vulgaris, the combination of an antibiotic and benzoyl peroxide provides enhanced efficacy over the individual agents, with the potential to decrease the emergence of resistant strains of P. acnes. To evaluate treatment regimens combining the daily use of a clindamycin/benzoyl peroxide gel, a tretinoin gel, and a clindamycin gel, the current randomized, evaluator-blind study was conducted. Results demonstrate that once-daily administration of clindamycin/benzoyl peroxide gel (combination formulation) was as effective as clindamycin/benzoyl peroxide gel + tretinoin gel + clindamycin gel. Both of these regimens provided greater efficacy than tretinoin + clindamycin. Treatment with clindamycin/benzoyl peroxide demonstrated a significant benefit over other treatments at Week 2, highlighting its rapid onset of action. All regimens were safe and generally well tolerated, with less severe peeling seen in patients who received clindamycin/benzoyl peroxide. In conclusion, the regimens that included clindamycin/benzoyl peroxide were more effective than tretinoin + clindamycin in the treatment of acne vulgaris, with no clinical advantage of adding tretinoin + clindamycin to once-daily clindamycin/benzoyl peroxide treatment.

Acne Vulgaris↗
PubMed2000

Comparison of hydrogen peroxide generation and the content of lipid peroxidation products in lung cancer tissue and pulmonary parenchyma.

Lipid peroxidation, as a well-known index of reactive oxygen species activity, not only in lung biochemistry, is an oxidative process associated with membrane lipid destruction. Also, the oxidative modification of nucleic acids by reactive oxygen species is of remarkable biological importance as it may contribute to malignant conversion, but its exact role in lung cancer biology is still not clear. Our study aimed to investigate the level of lipid peroxidation ex vivo in tumour tissue and lung parenchyma obtained from patients with lung cancer. Forty-two patients with lung cancer were enrolled into the study. During a surgical resection, tumour tissue and lung parenchyma were obtained and concentration of lipid peroxidation products, thiobarbituric acid-reactive substances and Schiff bases, and spontaneous generation of hydrogen peroxide, were measured. The concentration of thiobarbituric acid-reactive substances (P<0.001) in the tumour tissue was higher than that in lung parenchyma. In small cell lung cancer as well as in squamous cell carcinoma patients, a positive correlation between spontaneous generation of hydrogen peroxide in tumour tissue and clinical stage (r = 0.43; r = 0.46; respectively) was found. Our results prove enhanced lipid peroxidation in cancer tissue as compared with matched-lung parenchyma. In small cell lung cancer and squamous cell carcinoma patients, the high level of oxidative stress, expressed as a spontaneous generation of hydrogen peroxide in tumour tissue, was associated with clinical progression of tumour's stage.

Aged↗
PubMed2003

Effectiveness of treatment with carbamide peroxide and hydrogen peroxide in subjects affected by dental fluorosis: a clinical trial.

Dental fluorosis is an endemic dental health problem around the world; so, it is important to develop clinical alternatives that are non-invasive and inexpensive. In this study, nightguard vital bleaching technique (NVBT), using carbamide and hydrogen peroxide as active agents, has shown itself to be effective in whitening teeth affected by dental fluorosis. Carbamide peroxide at 10 and 20% and hydrogen peroxide at 7.5% showed good clinical effectiveness in improving clinical appearence, but it is important to point out that clinical success is only in cases of class 1 to 3 of the Tooth Surface Index of Fluorosis. When comparing 10 and 20% concentrations of carbamide peroxide, there was no difference in the clinical effectiveness (p > 0.05); but when comparing both concentrations of carbamide peroxide against hydrogen peroxide, results showed that carbamide peroxide was more effective in whitening in cases of dental fluorosis, the difference being statistically significant (p < 0.05). NVBT has two advantages: it is a non-invasive technique and the relationship cost/benefit is excellent; only a few patients reported tenderness or mild tooth sensitivity.

Adolescent↗
PubMed1981

A study of the peroxidation of fatty acid micelles promoted by ionizing radiation, hydrogen peroxide and ascorbate.

the kinetics of peroxidation of fatty acid micelles promoted by ionizing radiation, hydrogen peroxide and ascorbate were compared. At the dose-rate range of ionizing radiation studied, the higher the dose-rate, the greater the total dose required to produce the same effect. With ascorbate, the rate of lipid peroxidation was dependent on the concentration of the promoter only up to 1 X 10(-4) M, beyond which a decreasing rate of peroxidation induction was observed. Higher concentration of ascorbate also suppressed the promoting effect of ionizing radiation. Formate, a hydroxyl radical scavenger, inhibited the peroxidation process promoted by these three agents. Caesium was found to be slightly inhibitory. EDTA and deoxycholate were also inhibitory, which may be attributed to iron-chelating and micelle-disrupting capacity, respectively. Addition of iron (Fe2+ or Fe3+) to EDTA-chelated fatty acid micelles re-initiated the peroxidation process. The ease of fatty acid oxidation at pH 7.5 was arochidonic (20:4) greater than linolenic (18:3) greater than linoleic (18:2). This order was reversed at pH 11.5. Similarities in the kinetics of peroxidation obtained suggest that certain biological sequelae encountered in cells treated with these seemingly dissimilar agents might arise through some common mechanism(s).

Ascorbic Acid↗
PubMed2000

Melatonin suppresses autoxidation and hydrogen peroxide-induced lipid peroxidation in monkey brain homogenate.

OBJECTIVES: Melatonin, the major secretory product of the pineal gland, is known as an effective antioxidant and neuroprotector. Its neuroprotective actions and mechanisms have been documented in a variety of rodent brain models. However, little is known of melatonin's antioxidative capacity in the brain of primates. Herein, we investigated whether melatonin would suppress autoxidation and exogenous hydrogen peroxide-induced lipid peroxidation in monkey cerebral cortical homogenates. MATERIALS AND METHODS: The monkey brain was dissected during routine autopsy and immediately frozen at -80 degrees C until the experiment. A sample of cerebral cortex (50 mg) was homogenized in 1 ml ice cold phosphate buffer (20 mM, pH 7.4) at 0-4 degrees C. Four different treatments of cerebral cortical homogenates were performed: 1) homogenates incubated in a water bath at different temperatures (4 degrees C, 25 degrees C or 37 degrees C, respectively) for two hours to induce autoxidation; 2) homogenates co-incubated with different concentrations of melatonin at 37 degrees C for 2 hours; 3) homogenates co-incubated with 1 mM vitamin C and different concentrations of hydrogen peroxide at 37 degrees C for 1 hour to induce membrane lipid peroxidation; 4) homogenates incubated with different concentrations of melatonin and 1 mM H2O2 plus 1 mM vitamin C. After incubation, homogenates were analyzed for products of lipid peroxidation (malondialdehyde and 4-hydroxy-alkenals). RESULTS: The levels of lipid peroxidation products significantly increased in monkey cerebral cortical homogenates as a consequence of autoxidation or after the addition of H2O2 plus vitamin C. Melatonin not only suppressed the increase in lipid peroxidation induced by H2O2 plus vitamin C but also inhibited lipid breakdown resulting from autoxidation. The concentrations of melatonin required to suppress lipid peroxidation resulting from autoxidation or induced by exogenous oxidants in monkey cerebral cortical homogenates were in the same dose range. CONCLUSION: The results show for the first time that melatonin functions as an antioxidant and neuroprotector in primate brain tissue as was observed previously in rodent brain. The data provide information supporting the use of melatonin in the treatment of neurodegenerative disorders that involve oxidative damage to brain lipids.

Journal Article↗
PubMed1991

Cytochrome c-catalyzed membrane lipid peroxidation by hydrogen peroxide.

Cytochrome c(3+)-catalyzed peroxidation of phosphatidylcholine liposomes by hydrogen peroxide (H2O2) was indicated by the production of thiobarbituric acid reactive substances, oxygen consumption, and emission of spontaneous chemiluminescence. The iron chelator diethylenetriaminepentaacetic acid (DTPA) only partially inhibited peroxidation when H2O2 concentrations were 200 microM or greater. In contrast, iron compounds such as ferric chloride, potassium ferricyanide, and hemin induced H2O2-dependent lipid peroxidation which was totally inhibitable by DTPA. Cyanide and urate, which react at or near the cytochrome-heme, completely prevented lipid peroxidation, while hydroxyl radical scavengers and superoxide dismutase had very little or no inhibitory effect. Changes in liposome surface charge did not influence cytochrome c3+ plus H2O2-dependent peroxidation, but a net negative charge was critical in favoring cytochrome c(3+)-dependent, H2O2-independent lipid auto-oxidative processes. These results show that reaction of cytochrome c with H2O2 promotes membrane oxidation by more than one chemical mechanism, including formation of high oxidation states of iron at the cytochrome-heme and also by heme iron release at higher H2O2 concentrations. Cytochrome c3+ could react with mitochondrial H2O2 to yield "site-specific" mitochondrial membrane lipid peroxidation during tissue oxidant stress.

Cytochrome c Group↗
PubMed1993

Relationship between peroxisome-proliferating sulfur-substituted fatty acid analogs, hepatic lipid peroxidation and hydrogen peroxide metabolism.

The effect of the administration of three peroxisome-proliferating sulfur-substituted fatty acid analogs on hepatic antioxidant status and lipid peroxidation was studied in rats. After 14 days of treatment, the ratio of induction of peroxisomal fatty acyl-CoA oxidase to catalase was 4.2 and 3.5 in rats treated with 1,10 bis-(carboxymethylthio)decane (BCMTD) and 1-mono (carboxymethylthio)tetradecane (CMTTD), respectively, while the corresponding ratio was 1.3 in 1-mono (carboxyethylthio)tetradecane (CETTD)-treated rats. As compared to the controls an increase in hepatic hydrogen peroxide content was noted in BCMTD- and CMTTD-treated rats, but not CETTD-treated rats. Hepatic lipid peroxidation was increased in all the three treatment groups in a manner not related to the potency of the compounds to induce the peroxisomal hydrogen peroxide metabolizing enzymes. Hepatic glutathione content increased while the activities of its associated enzymes such as glutathione transferase, glutathione peroxidase and glutathione reductase decreased in all the treated rats. Taken together, our data show a relationship between the levels of hydrogen peroxide and lipid peroxidation in rat livers treated with BCMTD and CMTTD. However, increased hepatic lipid peroxidation in CETTD-treated rats cannot be accounted for by the changes in the peroxisomal enzymes.

Acyl-CoA Oxidase↗
PubMed2004

Involvement of lipid peroxidation and organic peroxides in UVA-induced matrix metalloproteinase-1 expression.

Ultraviolet A (UVA) irradiation causes human skin aging and skin cancer at least partially through the activation of matrix metalloproteinases (MMPs). MMP-1, the interstitial collagenase, is responsible for the degradation of collagen and is involved in tumor progression in human skin. The present study uses human skin fibroblast cells (FEK4) to investigate the involvement of lipid peroxidation and the role of peroxides as possible mediators in MMP-1 activation by UVA. Preincubation with the antioxidants butylated hydroxytoluene and Trolox reduced UVA-dependent MMP-1 upregulation, suggesting that peroxidation of membrane lipids is involved. Blocking the iron-driven generation of lipid peroxides and hydroxyl radicals by different iron chelators led to a decrease in UVA-induced MMP-1 mRNA accumulation. Moreover, modulation of glutathione peroxidase activity by use of the specific inhibitor mercaptosuccinate (MS) or by the depletion of glutathione (using buthionine-S, R-sulfoximine, BSO), enhanced the UVA-dependent MMP-1 response. Finally, UVA irradiation generated a significant increase in intracellular peroxide levels which is augmented by pretreatment of the cells with BSO or MS. Our results demonstrate that lipid peroxidation and the production of peroxides are important events in the signalling pathway of MMP-1 activation by UVA.

Antioxidants↗
PubMed1999

Demonstration of the presence of lipid peroxide-modified proteins in human atherosclerotic lesions using a novel lipid peroxide-modified anti-peptide antibody.

Immunohistochemical demonstration of oxidation-specific epitopes using antibodies developed against oxidized low density lipoprotein (Ox-LDL), LDL modified by products of lipid peroxidation (e.g. malondialdehyde-modified LDL), and lipid peroxide-modified albumin has been considered as strong evidence for the presence of oxidatively modified proteins in atherosclerotic lesions. However, the antigens used in the development of these antibodies were derived from lipoproteins and other proteins that are constituents of both normal and atherosclerotic arteries. In order to demonstrate the unequivocal presence of oxidatively modified proteins, we have used a 15 amino acid synthetic peptide derived from the sequence of human glycodelin. Using an antibody developed against this peptide and the second antibody developed against the lipid peroxide-modified peptide, we immunostained progressive human atherosclerotic lesions. Antibody to the unmodified peptide did not react with antigenic epitopes present in mild, moderate, or severe human atherosclerotic lesions. In contrast, the antibody developed against lipid peroxide-modified peptide highly reacted with tissue samples and provided strong evidence for the presence of lipid peroxide-modified proteins. This study suggests the presence of lipid peroxide-modified proteins in the lesion and that these epitopes are derived by direct interaction of lysine residues with lipid peroxides.

Antibodies, Monoclonal↗
PubMed1988

Influence of lipid peroxidation and hydrogen peroxide on muscarinic cholinergic receptors and ATP level in rat myocytes and lymphocytes.

Isolated rat neonatal cardiac myocytes and rat lymph-node lymphocytes were treated with Fe2+ cumene hydroperoxide or hydrogen peroxide. The intensity of lipid peroxidation was estimated by measuring production of malondialdehyde (MDA). The level of muscarinic cholinergic receptors was determined by [3H]-QNB binding. Cumene hydroperoxide treatment was found to induce lipid peroxidation in both myocytes and lymphocytes, the process being more pronounced in myocytes. An important decrease of muscarinic cholinergic receptor level and a significant drop of intracellular ATP level in these cells were simultaneously observed. In both cell types, hydrogen peroxide treatment decreased the ATP level while lipid peroxidation and muscarinic cholinergic receptors were unaffected. The different effect of hydrogen peroxide on lipid peroxidation and the level of muscarinic cholinergic receptors on the one hand and the ATP level on the other suggests that this substance acts mainly in the intracellular space.

Adenosine Triphosphate↗
PubMed1994

[Alteration of lipid peroxidation and the activity of peroxide metabolism enzymes in the liver, kidney and lung following the administration of paraquat in mice].

The sequential changes of the activity of peroxide metabolism enzymes and thiobarbituric acid reaction substance (TBARS) as an indicator of lipid peroxide concentration were observed to analyze the mechanisms of tissue injury due to the administration of paraquat in DDY mice. Each six mice were decapitated at 3, 6, 9, 12, 15, 18, 21 or 24 hours following the intraperitoneal administration of paraquat 60 mg.kg-1, and the liver, kidney and lung were removed and homogenized to quantify lipid peroxide concentration and the activity of peroxide metabolism enzymes. In the liver and kidney, TBARS increased gradually and reached the maximum level at 9 hours after the administration of paraquat in the liver and at 12 hours in the kidney. Significant increases in superoxide dismutase (SOD), glutathione peroxidase and catalase (CAT) activities were observed at 15 or 18 hours after the injection of paraquat. In the lung, lipid peroxide concentration decreased significantly and the activities of SOD and CAT increased at 15 hours after injection of paraquat. TBARS in serum started to increase at 9 hours after the administration of paraquat and reached the maximum level at 15 hours. These findings indicate that the induction of peroxide metabolism enzymes followed the increase of TBARS which was induced by paraquat in the liver and kidney. However, the enzyme induction was produced by paraquat without the increase of TBARS in the lung. Active oxygen radicals play an important role in the toxic action of paraquat and might produce the induction of peroxide metabolism enzymes following the administration of paraquat.

Animals↗
PubMed1988

Lipid peroxidation and cell viability in isolated hepatocytes in a redesigned oxystat system: evaluation of the hypothesis that lipid peroxidation, preferentially induced at low oxygen partial pressures, is decisive for CCl4 liver cell injury.

An oxystat system is described which is capable of maintaining steady-state oxygen partial pressures (PO2) at levels between 0.1 and 300 mm Hg for hours or even days in incubations of respiring cells. The system was used to study effects of the hepatotoxin carbon tetrachloride (CCl4) on lipid peroxidation and cell viability in isolated hepatocytes from phenobarbital-pretreated rats at various steady-state PO2. At PO2 below 35 mm Hg, with a maximum effect at 7 mm Hg, CCl4 induced an immediate lipid peroxidation, the rate of which slowed down during further incubation. AT PO2 between 35 and 70 mm Hg, CCl4 initially induced only slight lipid peroxidation, while there was a significant increase in lipid peroxidation after approximately 30 min. At PO2 above 100 mm Hg, no lipid peroxidation was induced by CCl4. At PO2 of 70 mm Hg and below, with the maximum effect at 3 mm Hg, CCl4 also induced marked losses of cell viability. Under anaerobic conditions and at PO2 greater than 70 mm Hg, CCl4 was without effect on the viability of the liver cells. Cells isolated from the pericentral area of the liver lobule showed more lipid peroxidation and loss of cell viability than cells from the periportal area of the lobule. These results provide further evidence for the decisive role of lipid peroxidation, preferentially induced at low PO2, in CCl4 liver injury.

Animals↗
PubMed1982

Rabbit liver microsomal lipid peroxidation. The effect of lipid on the rate of peroxidation.

Rat and rabbit liver microsomes catalyze an NADPH-cytochrome P-450 reductase-dependent peroxidation of endogenous lipid in the presence of the chelate, ADP-Fe3+. Although liver microsomes from both species contain comparable levels of NADPH-cytochrome P-450 reductase and cytochrome P-450, the rate of lipid peroxidation (assayed by malondialdehyde and lipid hydroperoxide formation) catalyzed by rabbit liver microsomes is only about 40% of that catalyzed by rat liver microsomes. Microsomal lipid peroxidation was reconstituted with liposomes made from extracted microsomal lipid and purified protease-solubilized NADPH-cytochrome P-450 reductase from both rat and rabbit liver microsomes. The results demonstrated that the lower rates of lipid peroxidation catalyzed by rabbit liver microsomes could not be attributed to the specific activity of the reductase. Microsomal lipid from rabbit liver was found to be much less susceptible to lipid peroxidation. This was due to the lower polyunsaturated fatty acid content rather than the presence of antioxidants in rabbit liver microsomal lipid. Gas-liquid chromatographic analysis of fatty acids lost during microsomal lipid peroxidation revealed that the degree of fatty acid unsaturation correlated well with rates of lipid peroxidation.

Adenosine Diphosphate↗