Stimulation of synaptosomal free radical production by fatty acids: Relation to esterification and to degree of unsaturation

Bondy, Stephen C.; Marwah, Sukhjinder

doi:10.1016/0014-5793(95)01173-c

Cited by 39 publications

(11 citation statements)

References 18 publications

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“…The production of oxygen radicals and hydroxyl radicals (Reactive Oxygen Species; ROS) can attack the unsaturation sites of PUFAs and cleave unsaturated long-chain fatty acids into saturated shortchain fatty acids and a variety of aliphatic alcohols (Benzie, 1996). The loss of unsaturated long-chain membrane fatty acids can also alter membrane fluidity (Cullis et al, 1985) and decreased levels of long-chain PUFAs were reported during necrosis and apoptosis (Bondy and Marwah, 1995;Chen et al, 1997).…”

Section: Discussionmentioning

confidence: 97%

Homocysteine-induced changes in brain membrane composition correlate with increased brain caspase-3 activities and reduced chick embryo viability

Miller¹

2003

Comparative Biochemistry and Physiology Part B: Biochemistry an

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In adult systems, high homocysteine (HoCys) levels inhibit methylation reactions and can induce apoptosis in the central nervous system. In embryos, exogenous HoCys is teratogenic and is associated with neural tube defects. Because, methylation inhibitors and inducers of apoptosis can influence membrane composition, we have studied whether or not embryonic exposure to HoCys influenced membrane phospholipid levels, membrane fatty acid composition, and Caspase-3 activities in embryonic chick brains. Embryonic exposure to HoCys caused reduced brain phosphatidylcholine levels and increased levels of brain phosphatidylethanolamine. Exogenous HoCys also promoted decreased levels of long-chain, unsaturated membrane fatty acids and increased levels of saturated short-chain membrane fatty acids. These HoCys-induced brain membrane changes correlated with HoCys-induced increases in brain Caspase-3 activities, HoCysinduced reductions in brain mass, HoCys-induced reductions in embryo mass, and HoCys-induced reductions in the percentage of embryos that survived to 11 days of development (theoretical stage 37). Thus, HoCys-induced changes in brain membrane composition correlated with HoCys-induced apoptosis and reduced embryo viability. ᮊ

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Section: Discussionmentioning

confidence: 97%

Homocysteine-induced changes in brain membrane composition correlate with increased brain caspase-3 activities and reduced chick embryo viability

Miller¹

2003

Comparative Biochemistry and Physiology Part B: Biochemistry an

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“…Second, the nonoxidative metabolism of ethanol with free fatty acids may form fatty acid ethyl adducts, cytotoxic molecules that accumulate in liver, heart, and brain tissues and that impair mitochondrial function (Beckemeier and Bora, 1998;Laposata, 1998;Zheng and Hungund, 1998;Zimakin and Deitrich, 1997). Third, free radical species may be induced by fatty acids (Bondy and Marwah, 1995). Fourth, lipid peroxide levels or lipid composition may be altered as a result of ethanol-induced free radical activity (Adachi et al, 1998b).…”

Section: Discussionmentioning

confidence: 99%

7α‐ and 7β‐Hydroperoxycholest‐5‐en‐3β‐ol in Muscle as Indices of Oxidative Stress: Response to Ethanol Dosage in Rats

Adachi

Asano

Ueno

et al. 2000

Alcoholism Clin & Exp Res

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This is the first report on 7alpha-OOH and 7beta-OOH accumulation in rat skeletal muscle, and it seems to reflect greater oxidative stress in the pathology of muscle of rats treated with acute ethanol. Together with the elevation of 18:2, these results signify perturbations in membrane lipids in response to ethanol, which may have important implications for the pathogenesis of alcohol-induced muscle disorders.

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“…⌬/⌬ Livers-LPS induces oxidant stress in the liver (37)(38)(39)(40), which promotes lipid peroxidation, particularly in the presence of polyunsaturated fatty acids (41,42). We therefore predicted that lipid peroxides would increase significantly in the livers of Mttp ⌬/⌬ mice after an LPS challenge, due to their higher basal levels of polyunsaturated fatty acids.…”

Section: Lipid Peroxidation Products In Mttpmentioning

confidence: 99%

Blocking the Secretion of Hepatic Very Low Density Lipoproteins Renders the Liver More Susceptible to Toxin-induced Injury

Björkegren¹,

Beigneux²,

Bergö³

et al. 2002

Journal of Biological Chemistry

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Recently, we generated mice lacking microsomal triglyceride transfer protein (MTP) in the liver (Mttp ⌬/⌬ ) and demonstrated that very low density lipoprotein secretion from hepatocytes was almost completely blocked. The blockade in lipoprotein production was accompanied by mild to moderate hepatic steatosis, but the mice appeared healthy. Although hepatic MTP deficiency appeared to be innocuous, we hypothesized that a blockade in very low density lipoprotein secretion and the accompanying steatosis might increase the sensitivity of Mttp ⌬/⌬ livers to additional hepatic insults. To address this issue, we compared the susceptibility of Mttp Microsomal triglyceride transfer protein (MTP)1 is critical for the assembly and secretion of apolipoprotein (apo) B-containing lipoproteins, both in the intestine and in the liver (1, 2). A genetic absence of MTP causes abetalipoproteinemia, a disease characterized by intestinal fat malabsorption, a virtual absence of chylomicrons, very low density lipoproteins (VLDL), low density lipoproteins in the plasma, and strikingly low plasma levels of triglycerides and cholesterol. The fact that a deficiency in MTP reduces the plasma levels of atherogenic lipoproteins has attracted the attention of the pharmaceutical industry. Many companies have established MTP programs, with the goal of identifying MTP inhibitors suitable for treating humans with hyperlipidemias (3, 4). Thus far, however, the efficacy and safety of these compounds in humans has not been documented.To investigate the role of MTP in lipoprotein assembly and secretion, we inactivated the MTP gene (Mttp) in mice (5). Heterozygous knockout mice (Mttp ϩ/Ϫ ) manifested slightly reduced levels of lipoprotein secretion, reduced levels of apoB100-containing lipoproteins in the plasma, and slightly increased levels of neutral lipids (triglycerides and cholesterol esters) in the liver. Homozygous knockout mice (Mttp Ϫ/Ϫ ) died during embryonic development. Subsequently, we used Cre/LoxP recombination techniques to produce mice lacking Mttp expression in the liver but not in the intestine (6). Those mice, designated Mttp ⌬/⌬ mice, exhibited strikingly reduced plasma levels of apoB100, sizable reductions in the plasma levels of cholesterol and triglycerides, and mild to moderate steatosis with increased levels of neutral lipids in the liver. The Mttp ⌬/⌬ mice were healthy and grew normally; their plasma transaminase levels were normal, and their livers were free of inflammatory infiltrates (6).The fact that it was possible to eliminate hepatic Mttp expression in a mammalian model without noticeable side effects supported the concept that it might be possible to develop MTP inhibitors to treat hyperlipidemias. Also encouraging were studies by Wetterau et al. (7) that showed that MTP inhibitors could reduce plasma lipoprotein levels in low density lipoprotein receptor-deficient rabbits without causing elevated transaminases or histologic evidence of liver inflammation.In this study, we further investigated the notion that it mig...

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Stimulation of synaptosomal free radical production by fatty acids: Relation to esterification and to degree of unsaturation

Cited by 39 publications

References 18 publications

Homocysteine-induced changes in brain membrane composition correlate with increased brain caspase-3 activities and reduced chick embryo viability

Homocysteine-induced changes in brain membrane composition correlate with increased brain caspase-3 activities and reduced chick embryo viability

7α‐ and 7β‐Hydroperoxycholest‐5‐en‐3β‐ol in Muscle as Indices of Oxidative Stress: Response to Ethanol Dosage in Rats

Blocking the Secretion of Hepatic Very Low Density Lipoproteins Renders the Liver More Susceptible to Toxin-induced Injury

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