Effect of Corn Oil Feeding on Lipid Peroxidation in Rats

Iritani, Nobuko; Fukuda, Eiko; Kitamura, Yohko

doi:10.1093/jn/110.5.924

Cited by 39 publications

(8 citation statements)

References 31 publications

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“…Recent studies have suggested that oxidant stress may play an important role in the pathogenesis of hepatic injury during cholestasis (6,(12)(13)(14)(15)(16). Supporting this proposed mechanism is the observation that ␣-tocopherol, the major membraneassociated, lipid-soluble antioxidant, reduces both the generation of ROS and injury to hepatocytes exposed to hydrophobic bile acids (17,18) and in the intact rat infused with bile acids (6).…”

mentioning

confidence: 99%

Role of Oxidant Stress in the Permeability Transition Induced in Rat Hepatic Mitochondria by Hydrophobic Bile Acids

et al. 2001

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Hydrophobic bile acids may cause hepatocellular necrosis and apoptosis during cholestatic liver diseases. The mechanism for this injury may involve mitochondrial dysfunction and the generation of oxidant stress. The purpose of this study was to determine the relationship of oxidant stress and the mitochondrial membrane permeability transition (MMPT) in hepatocyte necrosis induced by bile acids. The MMPT was measured spectrophotometrically and morphologically in rat liver mitochondria exposed to glycochenodeoxycholic acid (GCDC). Freshly isolated rat hepatocytes were exposed to GCDC and hepatocellular necrosis was assessed by lactate dehydrogenase release, hydroperoxide generation by dichlorofluorescein fluorescence, and the MMPT in cells by JC1 and tetramethylrhodamine methylester fluorescence on flow cytometry. GCDC induced the MMPT in a dose-and Ca 2ϩ -dependent manner. Antioxidants significantly inhibited the GCDC-induced MMPT and the generation of hydroperoxides in isolated mitochondria. Other detergents failed to induce the MMPT and a calpain-like protease inhibitor had no effect on the GCDC-induced MMPT. In isolated rat hepatocytes, GCDC induced the MMPT, which was inhibited by antioxidants. Blocking the MMPT in hepatocytes reduced hepatocyte necrosis and oxidant stress caused by GCDC. Oxidant stress, and not detergent effects or the stimulation of calpain-like proteases, mediates the GCDC-induced MMPT in hepatocytes. We propose that reducing mitochondrial generation of reactive oxygen species or preventing increases in mitochondrial Ca 2ϩ may protect the hepatocyte against bile acid-induced necrosis. 1-3). Although hydrophobic bile acids cause injury to isolated hepatocytes (4), cultured hepatocytes (5), and the intact liver (6), the mechanisms of this toxicity are not fully understood. Both hepatocellular necrosis at higher bile acid concentrations (4) and apoptosis at lower concentrations (7) have been demonstrated and are proposed as playing a role in cholestatic liver injury. Hepatocyte necrosis is characterized by cellular swelling, loss of mitochondrial respiratory function, depleted cellular ATP levels, and formation of plasma membrane blebs that rupture and release cellular contents (8, 9). In cholestatic liver ABSTRACT519

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confidence: 99%

Role of Oxidant Stress in the Permeability Transition Induced in Rat Hepatic Mitochondria by Hydrophobic Bile Acids

et al. 2001

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“…It has been shown that the fatty acid composition of various tissues, including the erythrocytes, can be altered by dietary fats in particular,results in increases in membrane linoleic and arachidonic acids. Since linoleic acid can undergo lipid peroxidation in vivo [21], this raises the question whether the difference in the amount of corn oil added to the two diets resulted in a difference in the amount of linoleic acid incorporated into the membrane and consequently accounts for the difference in erythrocyte oxidant stress. Data from studies on the effect of dietary corn oil on the erythrocyte membrane fatty acid profile indicate that, in general, amounts of corn oil greater than the 5% used here are necessary to produce significant changes in erythrocyte fatty acids.…”

Section: Erythrocyte Malonyldialdehyde Formation Before and During Inmentioning

confidence: 99%

Effect of dietary cholesterol on erythrocyte peroxidant stress in vitro and in vivo

Bereza

Brewer

Hill

1985

Biochimica et Biophysica Acta (BBA) - Lipids and Lipid Metaboli

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The effect of dietary variation of plasma cholesterol concentrations on the susceptibility of erythrocytes to in vitro and in vivo peroxidant stress was studied in rats. Malonyldialdehyde, produced in vivo (endogenous malonyldialdehyde) or following in vitro exposure of cells to 10 mM H2O2 (H2O2 malonyldialdehyde), was used as a measure of peroxidant stress. After 5 weeks, the plasma cholesterol concentrations in rats receiving 1.2% cholesterol + 0.6% cholic acid in their diet rose to 6-times that of control rats receiving a diet without added cholesterol; at the same time, erythrocyte H2O2 malonyldialdehyde in the cholesterol-fed rats decreased significantly relative to the control rats. During subsequent exposure of both groups to in vivo peroxidant stress with phenylhydrazine in two separate dose trials, erythrocyte peroxidant stress remained significantly lower in the cholesterol-fed rats: at a dose of 100 mumol/100 g body weight, H2O2 malonyldialdehyde was lower; at a dose of 25 mumol/100 g body weight, both endogenous and H2O2 malonyldialdehyde were lower. Erythrocyte membrane cholesterol concentrations were 12% higher in the cholesterol-fed rats than in controls. The effects of in vivo peroxidant stress on plasma cholesterol were also studied. In vivo peroxidant stress at the higher dose of phenylhydrazine produced a decrease in plasma cholesterol concentrations of control rats. The lower dose had no effect on this group and the plasma cholesterol concentrations were unchanged in the cholesterol-fed rats during both treatments. The data suggest that elevated plasma cholesterol concentrations are protective against erythrocyte peroxidant stress. The mechanism of cholesterol's protective effect is probably mediated through elevated membrane cholesterol concentrations.

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“…Hydroperoxides may convert to other radical species that can damage cell membrane [4]. A high concentration of PUFA's in the cell membrane make them very susceptible to peroxidative damage [5,6] and ultimately the damage can be of such an extent that it may result in cell death due to the interaction of peroxidation products with biomolecules of important and/or regulatory functions [7]. The peroxidation of membrane lipids may result in inactivation of membrane bound enzymes, cross-linking of membrane lipids and proteins, damage to membrane receptors and ultimately cell death [8][9][10].…”

Section: Introductionmentioning

confidence: 99%

Lipid Peroxidation Serum Levels in Breast Cancer Patients

2016

IJCRT

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This prevalence study was conducted to compare lipid peroxide serum levels of breast cancer patients to a control group. Sixteen cases and 12 controls were interviewed for socio-demographic characteristics, medical, cancer and lifestyle history anthropometrical measurements and dietary assessment. A blood sample was collected for quantitative determination of serum lipid peroxides using a colorimetric endpoint assay. The prevalence odds ratio showed a strong and statistically significant inverse association (OR= 6.60; p= 0.02) between breast cancer and lipid peroxide levels. Lipid peroxide levels in serum were different between cases and controls although a level of statistical significance was not attained. The confounding effect of vitamin C, total fat intake, saturated and monounsaturated fatty acid intake was evaluated using a stratified analysis. It revealed that the association between breast cancer and lower lipid peroxidation levels remained strong even after controlling for the variables. Vitamin supplementation and polyunsaturated fatty acid intake appear to modify the levels of serum lipid peroxides. These findings are consistent with previous studies that showed possible inhibitory role of lipid peroxidation products on breast cancer growth.

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Effect of Corn Oil Feeding on Lipid Peroxidation in Rats

Cited by 39 publications

References 31 publications

Role of Oxidant Stress in the Permeability Transition Induced in Rat Hepatic Mitochondria by Hydrophobic Bile Acids

Role of Oxidant Stress in the Permeability Transition Induced in Rat Hepatic Mitochondria by Hydrophobic Bile Acids

Effect of dietary cholesterol on erythrocyte peroxidant stress in vitro and in vivo

Lipid Peroxidation Serum Levels in Breast Cancer Patients

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