Effects of diets enriched in linoleic acid and its peroxidation products on brain fatty acids,oxylipins, and aldehydes in mice

Background

Linoleic acid (LA) is abundant in modern industrialized diets. Oxidized LA metabolites (OXLAMs) and reactive aldehydes, such as 4-hydroxy-2-nonenal (4-HNE), are present in heated vegetable oils and can be endogenously synthesized following consumption of dietary LA. OXLAMs have been implicated in cerebellar degeneration in chicks; 4-HNE is linked to neurodegenerative conditions in mammals. It unknown whether increasing dietary LA or OXLAMs alters the levels of oxidized fatty acids (oxylipins), precursor fatty acids, or 4-HNE in mammalian brain.

The isoprostanes: Novel prostaglandin-like products of the free radical-catalyzed peroxidation of arachidonic acid

The isoprostanes (IsoPs) are a unique series of prostaglandin-like compounds formed in vivo from the free radical-catalyzed peroxidation of arachidonic acid. This review summarizes our current knowledge regarding these compounds. Novel aspects of the biochemistry and bioactivity of IsoPs are detailed and methods by which these compounds are analyzed are discussed. A considerable portion of this review deals with the utility of measuring IsoPs as markers of oxidant injury in human diseases particularly in association with risk factors that predispose to atherosclerosis, a condition in which excessive oxidative stress has been causally implicated.     

Atrazine-induced alterations in rat erythrocyte membranes: ameliorating effect of vitamin E

Erythrocytes are a convenient model to understand oxidative damage to the membranes induced by various xenobiotics. The objective of the present study was to investigate the propensity of atrazine to induce oxidative stress and its possible attenuation by vitamin E. Experimental animals were orally administered atrazine (300 mg kg(-1) body weight, daily) and vitamin E (100 mg kg(-1) body weight, daily) for a period of 7, 14, and 21 days. Erythrocyte membranes were prepared and analyzed for acetylcholinesterase (AChE) activity, lipid peroxidation (LPO), and lipid composition. Susceptibility of erythrocytes to atrazine exposure was further investigated in terms of morphological alterations by scanning electron microscopy (SEM). Results indicate that atrazine exposure caused a significant inhibition of AChE activity and induction of oxidative stress in terms of increased malondialdehyde (MDA) levels. Atrazine treatment significantly decreased total lipid, cholesterol, and phospholipid content of erythrocyte membranes. SEM revealed varying degrees of distortion depending on duration of atrazine exposure. However, administration of vitamin E ameliorated the oxidative stress and changes in the erythrocyte membranes induced by atrazine.     

Dichloroacetate- and trichloroacetate-induced phagocytic activation and production of oxidative stress in the hepatic tissues of mice after acute exposure

Dichoroacetate (DCA) and trichloroacetate (TCA) are by-products formed during chlorination of the drinking water and were found to be hepatotoxic and hepatocarcinogenic in rodents. In this study, the abilities of the compounds to induce oxidative stress and phagocytic activation have been studied in B6C3F1 mice. Groups of mice were administered 300 mg/kg of either DCA or TCA, p.o, and were sacrificed after 6 or 12 h. Peritoneal lavage cells (PLCs) were isolated and assayed for superoxide anion (SA) production, and hepatic tissues were assayed for the production of SA, lipid peroxidation (LP), and DNA-single strand breaks (SSBs). TCA resulted in significant production of SA in the PLCs, and in the production of SA, LP, and DNA-SSBs in the hepatic tissues, 12 h after dosing, as compared with the control. DCA administration, on the other hand, resulted in significant increases in the productions of LP and DNA-SSBs in the hepatic tissues at both time points, and in SA production in PLCs and hepatic tissues, 6 h after dosing. However, DCA-induced increases in SA production in PLC and hepatic tissues declined at the 12-h time point, reaching control level in the hepatic tissues. These results may implicate the contribution of phagocytic activation to the induction of oxidative stress in the hepatic tissues and also the role of SA production in the induction of LP and/or DNA damage in those tissues, in response to the compounds. The results also suggest studying the involvement of these mechanisms in the long-term hepatotoxicity/hepatocarcinogencity of the compounds.     

Glucose promotes membrane cholesterol crystalline domain formation by lipid peroxidation

Oxidative damage to vascular cell membrane phospholipids causes physicochemical changes in membrane structure and lipid organization, contributing to atherogenesis. Oxidative stress combined with hyperglycemia has been shown to further increase the risk of vascular and metabolic diseases. In this study, the effects of glucose on oxidative stress-induced cholesterol domain formation were tested in model membranes containing polyunsaturated fatty acids and physiologic levels of cholesterol. Membrane structural changes, including cholesterol domain formation, were characterized by small angle X-ray scattering (SAXS) analysis and correlated with spectrophotometrically-determined lipid hydroperoxide levels. Glucose treatment resulted in a concentration-dependent increase in lipid hydroperoxide formation, which correlated with the formation of highly-ordered cholesterol crystalline domains (unit cell periodicity of 34 Å) as well as a decrease in overall membrane bilayer width. The effect of glucose on lipid peroxidation was further enhanced by increased levels of cholesterol. Treatment with free radical-scavenging agents inhibited the biochemical and structural effects of glucose, even at elevated cholesterol levels. These data demonstrate that glucose promotes changes in membrane organization, including cholesterol crystal formation, through lipid peroxidation.     

Recent developments in vitamin E nutrition of turkeys

Research and field observations have shown that vitamin E status of poults is often inadequate during the 5 to 21-day posthatching period. Although overt consequences of this inadequacy may not be evident and clear-cut, subtle adverse effects on health and metabolic efficiency are probable. These latter effects can result in uneconomical performance of turkeys. It therefore seems advisable to supplement the first diet (starter or prestarter) of poults with 100 to 150 IU of vitamin E. The cost of doing so will contribute little to the total cost of production and may facilitate more efficient turkey production. In the meantime, other alternatives that may be effective and economical need to be evaluated.     

Lead-catalyzed peroxidation of essential unsaturated fatty acid

In the present study, the reaction mixtures (lead compounds with essential unsaturated fatty acids) were preincubated at 37°C for 24 h prior to the measurement of malondialdehyde (MDA) by HPLC. The metal-catalyzed reactions were also compared in the presence of butylated hydroxytoluene (BHT), a free radical scavenger. Our results showed that according to the difference in the number of double bonds of essential unsaturated fatty acids, the kinds of lead compounds, and the concentrations of lead compounds, the extent of lipid peroxidation was different. The addition of BHT to the reaction mixtures significantly reduced the production of MDA (P<0.01). These in vitro studies support prior in vivo reports that the important mechanism of the acute toxic effects of the lead compounds is owing at least in part, to metal-catalyzed peroxidation of polyun-saturated fatty acids.     

In Vivo Lipid Peroxidation in Rat Brain Following Intracortical Fe2+ Injection

Cerebral contusion, cortical laceration, intracerebral hematoma formation, and hemorrhagic cortical infarction cause extravasation of red blood cells, followed by hemolysis, decompartmentalization of iron, formation and deposition of hemosiderin, and an increased incidence of epilepsy. In this experiment, 10 microliter of an aqueous solution containing 100 mmol/L FeCl2, 100 mmol/L CoCl2, or 0.9% (wt/vol) NaCl were injected at a depth of 1.8 mm into rat isocortex. The rate of formation of fluorescent compounds was measured in chloroform-methanol extracts of isocortical homogenates. Significant increases in the quantity of fluorescent products of lipid peroxidation were found 120 min after the injection of 100 mmol/L FeCl2. Cobaltous chloride and saline injection had no effect on the levels of fluorescent products found in the cortical homogenates. Although the intracortical deposition of aqueous solutions containing CoCl2 or FeCl2 in rodent cortex causes acute epileptiform discharges, the epileptogenic effect of CoCl2 is transient, while the injection of iron salts causes persistent seizures. Since CoCl2 injection failed to cause formation of lipid peroxidation products while the isocortical injection of iron caused significant increase in fluorescence within the injected hemisphere, we suggest that the occurrence of iron-induced lipid peroxidation may be of importance in initiation of recurrent seizures in the rat.     

Quantification of 5- and 15-HPETE''s by direct chemical ionization mass spectrometry

This report describes the application of direct chemical ionization mass spectrometry (DCIMS) to the identification and quantification of 5- and 15-HPETEs. A unique feature of the method is use of a polyimide-coated fused silica fiber that allows vaporization of the hydroperoxides, with very low excess energy, into the plume of the chemical ionization reagent gas plasma. Mass spectra are obtained that allow identification of the nonreduced and nonderivatized free acid forms of 5- and 15-HPETE as well as their quantification from 1 microgram to 100 picograms.     

Formate oxidation by Wolinella recta ATCC 33238 with oxygen as electron acceptor

Abstract The formate oxidizing capacity of Wolinella recta ATCC 33238 was studied in relation to growth under anaerobic and microaerobic conditions. Three distinct activities could be recognized: (a) cyanide-insensitive H₂O₂-producing oxidation of formate; (b) peroxidation of formate (H₂O₂-consuming); (c) oxidation of formate via an electron transport chain with oxygen as the electron acceptor. The contribution of these different formate oxidizing components during the growth of W. recta was dependent on the extent of aeration. It is suggested that due to the relative increase in overall H₂O₂ formation at higher oxygen tensions growth of W. recta appears possible only under anaerobic and microaerobic conditions.