1960
DOI: 10.3181/00379727-105-26093
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Effect of Intravenous Injection of Oxidized Methyl Esters of Unsaturated Fatty Acids on Chick Encephalomalacia.

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Cited by 93 publications
(3 citation statements)
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“…Because a substantial portion of the dietary LA in industrialized populations is heated prior to consumption, modern populations have substantially increased intakes of both LA and preformed LA peroxidation products. Consumption of heated oils rich in LA without adequate vitamin E [22,23], or intravenous administration of HPODEs [24], can produce cerebellar necrosis and ataxia in chicks, suggesting that dietary OXLAMs might potentially have adverse effects in CNS tissues. However, it is not yet known whether eating nonoxidized or heated vegetable oils has biochemical consequences in mammalian brain tissues.…”
Section: Discussionmentioning
confidence: 99%
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“…Because a substantial portion of the dietary LA in industrialized populations is heated prior to consumption, modern populations have substantially increased intakes of both LA and preformed LA peroxidation products. Consumption of heated oils rich in LA without adequate vitamin E [22,23], or intravenous administration of HPODEs [24], can produce cerebellar necrosis and ataxia in chicks, suggesting that dietary OXLAMs might potentially have adverse effects in CNS tissues. However, it is not yet known whether eating nonoxidized or heated vegetable oils has biochemical consequences in mammalian brain tissues.…”
Section: Discussionmentioning
confidence: 99%
“…OXLAMs and 4-HNE have been mechanistically linked to several pathological conditions including cardiovascular disease [15], steatohepatitis [16,17], neurodegenerative diseases [18], and chronic pain [6,19,20], reviewed in [3,15,21]. Consumption of heated vegetable oils rich in LA [22,23], or intravenous administration of HpODEs [24], produces cerebellar necrosis and ataxia in chicks without damaging the cerebral cortex, indicating that OXLAMs could potentially have brainregion specific neurotoxic effects in some species. Plausible mechanisms exist whereby high exposure to OXLAMs could have neurotoxic effects in humans, including endothelial cell activation [25], generalized lipid and membrane peroxidation [26,27], mitochondrial dysfunction [28], and microglial activation [2931].…”
Section: Introductionmentioning
confidence: 99%
“…Ever since it was established that lipid peroxides had mutagenic effects on cells (Wyss, Stone & Clark, 1947;Dickey, Cleland & Lotz, 1949;Ross, 1950;Loveless, 1951), there have been numerous reports on the cytotoxicity of these compounds. Fatty acid peroxides exert lethal effects when administered parenterally to mice, rabbits and chickens (Horgan, Philpot, Porter & Roodyn, 1957;Findlay, Draper & Bergan, 1970;Nishida, Tsuchiyama, Inoue & Kummerow, 1960), and to cause intense pain when injected subcutaneously into human subjects (Ferreira, 1972). At a cellular level, lipid peroxides produce lesions in the mucosal lining of the lung and small intestine (Cortesi & Privett, 1972;Olcott & Dolev, 1963) and induce aggregation of erythrocytes and blood platelets (Tsen & Collier, 1960;Mickel & Hörbar, 1974).…”
Section: Introductionmentioning
confidence: 99%