Lipids

Mead, James F.; Alfin-Slater, Roslyn B.; Howton, David R.; Popják, G.

doi:10.1007/978-1-4613-2107-1

Cited by 77 publications

(20 citation statements)

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“…The same alteration was found for GSHPx, but no alteration was detected in the plasma MDA concentration. MDA is formed in the terminal phase of lipid peroxidation from FAs having at least three double bonds, and is strongly cytotoxic (24). In this study, the extent of lipid peroxidation as assessed from the blood plasma was maintained at a relatively low level.…”

Section: Liver Mitochondrial Phospholipidsmentioning

confidence: 93%

“…Solvents were ultrapure grade (Sigma-Aldrich, Schnelldorf, Germany) and 0.01% w:v butylated hydroxytoluene was added to prevent FA oxidation. In the frame of lipid fractionation, extracted total lipids were transferred to glass chromatographic columns, containing 300 mg silica gel (230-400 mesh) for 10 mg of lipids (24). Neutral lipids were eluted with 10 mL chloroform for the above fat amount, then 15 mL acetone:methanol (9:1, vol:vol) was added, while 10 mL pure methanol eluted the total PLs.…”

Section: Lipid Analysismentioning

confidence: 99%

“…Their statistical interaction in the multivariate model was significant (P < 0.001), suggesting a synergistic effect. In rabbit tissue membranes, margaric acid abundance is clearly dependent on two factors: odd chain FAs are exclusively synthesized by the gut microflora and odd chain saturated FAs are peripherally (position sn-1) located in PC and are primary targets of beta oxidation (being quasi-equivalent with paired chain saturated FAs in this respect), when hydrolyzed by the most abundant PLase A 2 (24). The enzymatic cleavage of an odd chain saturated FA at position sn-1 may be a part of the Lands mechanism (8,21), a means to regulate membrane fluidity via the modification of the glycerolipid FA side chain combinations.…”

Section: Liver Mitochondrial Phospholipidsmentioning

confidence: 99%

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Oral administration of fumonisin B₁and T-2 individually and in combination affects hepatic total and mitochondrial membrane lipid profile of rabbits

Szabó¹,

Szabó-Fodor²,

Fébel³

et al. 2016

Physiology International

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Weaned rabbits were fed diets contaminated with 2 mg/kg diet T-2 toxin alone, or 10 mg/kg diet fumonisin B 1 (FB 1 ) alone, and both toxins in combination (2 + 10 mg/kg, respectively) compared to a toxin-free control diet. Samplings were performed after 4 weeks (blood and liver). Bodyweight of T-2-fed group was lower after 4 weeks; the liver weight was increased dramatically (threefold of control). Liver total phospholipids (PLs) provided slight alterations in the fatty acid (FA) composition; all three toxin-treated groups showed a decrease in palmitoleic acid (C16:1 n7) proportion. In the liver mitochondrial PL FA composition, margaric acid (C17:0) proportion decreased in the separated toxin treatments compared to the combined setting. Oleic acid (C18:1 n9) proportion was increased and arachidonic acid (C20:4 n6) was decreased in the FB 1 -treated group, while docosapentaenoic acid (C22:5 n3) was decreased in the separated treatments. The total monounsaturation was significantly higher in the FB 1 group's mitochondrial PL FA profile. After 4 weeks, all toxin treatments decreased the blood plasma reduced glutathione and glutathione peroxidase activity, and FB 1 increased the plasma sphinganine/sphingosine ratio. Both mycotoxins seem to cross the hepatocellular and the hepatic mitochondrial membrane, without drastic membrane disruption, as assessed from the PL FA composition, but inducing detectable lipid peroxidation.

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Section: Liver Mitochondrial Phospholipidsmentioning

confidence: 93%

Section: Lipid Analysismentioning

confidence: 99%

Section: Liver Mitochondrial Phospholipidsmentioning

confidence: 99%

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Oral administration of fumonisin B₁and T-2 individually and in combination affects hepatic total and mitochondrial membrane lipid profile of rabbits

Szabó¹,

Szabó-Fodor²,

Fébel³

et al. 2016

Physiology International

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“…The resulting CDs absorb at 234 nm, while CTs at 268 nm. Conjugated dienes are more stable than non-conjugated dienes due to factors such as delocalisation of charge through resonance and hybridisation energy (Mead et al, 1986).…”

Section: Conjugated Dienes and Conjugated Trienesmentioning

confidence: 99%

Acute hepatic effects of low-dose fumonisin B1 in rats

Szabó

Szabó-Fodor

Fébel

et al. 2016

Acta Veterinaria Hungarica

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Adult male Wistar rats were enrolled in a study to test the acute hepatic effects of 50 mg/kg fumonisin B 1 in feed for 5 days. Fumonisin B 1 depressed growth and feed intake, and absolute and relative liver weight showed a significant increase. The proportions of C17:0, C18:3 n3, C22:5 n3 and C22:6 n3 fatty acids decreased in the hepatic phospholipid fraction. All proportional decreases modified the hepatocellular membrane lipids into a more rigid state. The fatty acid profile modifications were partly compensated for by endogenous glutathione (preventing the formation of conjugated dienes and trienes as initial phase lipid peroxidation indicators), while the enzymatic antioxidant defence system (glutathione peroxidase) was unaltered. In contrast, hepatic malondialdehyde, the cytotoxic product of end-phase lipid peroxidation showed a concentration increase even after 5 days of feeding. The results indicate a rather strong and rapid hepatic effect of FB 1 , immediately impairing membrane phospholipids, even before the enzymatic antioxidant defence is activated.Key words: Fumonisin B 1 , rat, hepatocellular membrane, fatty acids, oxidative stress, antioxidants Fumonisins are cancer-inducing metabolites of Fusarium proliferatum and Fusarium verticillioides. They have a long-chain hydrocarbon unit (mimicking to a certain extent cellular sphingosine and sphinganine), which plays a determinant role in their cell-membrane-associated toxicity. From the fumonisin group, fumonisin B 1 (FB 1 ) shows strong toxic effects and has been reported to promote hepatic tumour in rats. Fumonisin B 1 , the most abundant of the numerous fumonisin analogues, was classified by the IARC as a Group 2B carcinogen (possibly carcinogenic in humans; IARC, 2002).

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“…In addition to membranes, another PUFA-bearing domain in cells can be lipid bodies, which are lipid-rich cytoplasmic inclusions (2)(3)(4). Most cellular PUFA are derived from the essential dietary fatty acids, octadecadienoic acid (linoleic acid, 18:2n-6) and octadecatrienoic acid (␣-linoleic acid, 18:3n-3) by the process of chain elongation and desaturation (5) and are mainly degraded by ␤-oxidation (6). Apart from their important role as structural components and as a source of energy, some of these fatty acids, in particular eicosatetraenoic acid (arachidonic acid, 20:4n-6) and eicosapentaenoic acid (20:5n-3), act as precursors of physiologically active oxygenated metabolites, collectively termed eicosanoids.…”

Section: Inhibition Of Neutrophil Leukotriene Bmentioning

confidence: 99%

Inhibition of Neutrophil Leukotriene B4 Production by a Novel Synthetic N-3 Polyunsaturated Fatty Acid Analogue, β-Oxa 21:3n-3

Robinson

Rathjen

Trout

et al. 2003

The Journal of Immunology

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We recently reported the synthesis and anti-inflammatory properties of a novel long chain polyunsaturated fatty acid (PUFA) with an oxygen atom in the β-position, β-oxa-21:3 n-3 (Z,Z,Z)-(octadeca-9,12,15-trienyloxy) acetic acid). Our data, from studies aimed at elucidating the mechanism of its action, show that pretreatment of human neutrophils with the β-oxa-PUFA substantially depresses the production of leukotriene B4 (LTB4) in response to calcium ionophore, A23187, comparable to standard leukotriene inhibitors such as zileuton and nordihydroguaiaretic acid. Interestingly, the n-6 equivalent, β-oxa 21:3 n-6, is also a strong inhibitor of LTB4 production. In contrast, naturally occurring PUFA only slightly reduce, for eicosapentaenoic (20:5n-3) and docosahexaenoic (22:6n-3) acids, or increase, for arachidonic acid (20:4n-6), the formation of LTB4. The parent β-oxa-21:3n-3 molecule, rather than its derivatives (methyl ester, saturated, monohydroperoxy, or monohydroxy forms), is exclusively responsible for attenuation of LTB4 formation. β-Oxa-21:3n-3 inhibits the conversion of [3H]20:4n-6 to [3H]5-hydroxyeicosatetraenoic acid and [3H]LTB4 by neutrophils in the presence of calcium ionophore and also suppresses the activity of purified 5-lipoxygenase, but not cyclooxygenase 1 and 2. β-Oxa-21:3n-3 is taken up by neutrophils and incorporated into phospholipids and neutral lipids. In the presence of calcium ionophore, the leukocytes convert a marginal amount of β-oxa-21:3n-3 to a 16-monohydroxy-β-oxa-21:3n-3 derivative. After administration to rodents by gavage or i.p. injection, β-oxa-21:3n-3 is found to be incorporated into the lipids of various tissues. Thus, β-oxa-21:3n-3 has the potential to be used in the treatment of inflammatory diseases, which are mediated by products of the lipoxygenase pathway.

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Lipids

Cited by 77 publications

References 0 publications

Oral administration of fumonisin B₁and T-2 individually and in combination affects hepatic total and mitochondrial membrane lipid profile of rabbits

Oral administration of fumonisin B₁and T-2 individually and in combination affects hepatic total and mitochondrial membrane lipid profile of rabbits

Acute hepatic effects of low-dose fumonisin B1 in rats

Inhibition of Neutrophil Leukotriene B4 Production by a Novel Synthetic N-3 Polyunsaturated Fatty Acid Analogue, β-Oxa 21:3n-3

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Lipids

Cited by 77 publications

References 0 publications

Oral administration of fumonisin B1and T-2 individually and in combination affects hepatic total and mitochondrial membrane lipid profile of rabbits

Oral administration of fumonisin B1and T-2 individually and in combination affects hepatic total and mitochondrial membrane lipid profile of rabbits

Acute hepatic effects of low-dose fumonisin B1 in rats

Inhibition of Neutrophil Leukotriene B4 Production by a Novel Synthetic N-3 Polyunsaturated Fatty Acid Analogue, β-Oxa 21:3n-3

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Oral administration of fumonisin B₁and T-2 individually and in combination affects hepatic total and mitochondrial membrane lipid profile of rabbits

Oral administration of fumonisin B₁and T-2 individually and in combination affects hepatic total and mitochondrial membrane lipid profile of rabbits