Disease relevance of Lipid Peroxidation

• Adriamycin: the role of lipid peroxidation in cardiac toxicity and tumor response [1].
• Control studies (no ischemia) showed no change in parameters of lipid peroxidation during 1 h of perfusion and ventilation with 20% or 95% O2 [2].
• These findings indicate that glucose enhances LDL lipid peroxidation by an oxidative pathway involving superoxide and raise the possibility that the chronic hyperglycemia of diabetes accelerates lipoprotein oxidation, thereby promoting diabetic vascular disease [3].
• Aldose reductase functions as a detoxification system for lipid peroxidation products in vasculitis [4].
• In vivo externalization of phosphatidylserine and phosphatidylethanolamine in the membrane bilayer and hypercoagulability by the lipid peroxidation of erythrocytes in rats [5].

Psychiatry related information on Lipid Peroxidation

• These results suggest that the activation of this enzyme occurs early in the course of AD, before the onset of overt dementia, thereby implicating 12/15LOX-mediated lipid peroxidation in the pathogenesis of AD [6].
• The brains of patients with Alzheimer's disease contain increased levels of lipid-peroxidation products such as 4-hydroxy-2-nonenal or acrolein, and enhanced lipid peroxidation can also be detected in cerebrospinal fluid and plasma from such patients [7].
• Thus Se supplementation of healthy New Zealand subjects increased GSHPx activities but did not produce any adaptive changes in other components of the lipid peroxidation defense mechanisms [8].
• That alcohol abuse may lead to testicular lipid peroxidation is suggested by the fact that ethanol is a known testicular toxin and its chronic use leads to both endocrine and reproductive failure [9].
• Ethanol-induced oxygen radical formation and lipid peroxidation in rat brain: effect of chronic alcohol consumption [10].

High impact information on Lipid Peroxidation

• Overexpression of Bcl-2 functioned to suppress lipid peroxidation completely [11].
• Isoprostanes are products of arachidonic acid catalyzed by free radicals, which reflect oxidative stress and lipid peroxidation in vivo [12].
• Recent studies suggest that glucose may be an incidental substrate of AR, which appears to be more adept in catalyzing the reduction of a wide range of aldehydes generated from lipid peroxidation [13].
• One potential source of endogenous DNA adducts is lipid peroxidation, which generates mutagenic carbonyl compounds such as malondialdehyde [14].
• Furthermore, under 2% oxygen, in liposomes, bilirubin suppresses the oxidation more than alpha-tocopherol, which is regarded as the best antioxidant of lipid peroxidation [15].

Chemical compound and disease context of Lipid Peroxidation

• These results suggest that adriamycin has at least two mechanisms of tissue damage: one, which involves lipid peroxidation, is blocked by tocopherol and results in cardiac toxicity; the other, which involves binding to DNA, is not antagonized by tocopherol and is responsible for tumor response [1].
• Cystic fibrosis, breath pentane, and lipid peroxidation [16].
• Rats were then pretreated with parenteral alpha-tocopherol, and its effect on i.v. TCDC toxicity was evaluated by liver blood tests and by assessing mitochondrial lipid peroxidation [17].
• Although lipid peroxidation in the subendothelial space has been hypothesized to play a central role in atherogenesis, the role of vitamin E in preventing lipid peroxidation and lesion development remains uncertain [18].
• When salicylate trapping of hydroxyl radicals and measurement of levels of malondialdehyde were used, there was no evidence throughout disease progression in mice for enhanced production of hydroxyl radicals or lipid peroxidation, respectively [19].

Biological context of Lipid Peroxidation

• Resulting disruptions of intracellular signaling cascades through interference with the synthesis of phosphatidic acid, decreases in phosphorylation potential and lipid peroxidation are mechanisms by which solvent alcohols can affect the rate of cell proliferation and, consequently, cell number [20].
• Cell death was thus postulated to occur due to lipid peroxidation via a sequence involving lipid hydroperoxide-induced, iron-mediated formation of alkoxyl, lipid, and peroxyl radicals [21].
• RESULTS: Two hours after ethanol administration, ethane exhalation (an index of lipid peroxidation) increased by 133%, although hepatic lipids were unchanged [22].
• In 2 inducible expression systems, core protein also increased lipid peroxidation products and induced antioxidant gene expression as well [23].
• Treatment with parenteral alpha-tocopherol was associated with a 60%-70% reduction in AST and ALT levels, improved histology, and a 60% reduction in mitochondrial lipid peroxidation in rats receiving TCDC [17].

Anatomical context of Lipid Peroxidation

• Iron liberated from pigment could account for the lipid peroxidation and increased production of malondialdehyde observed in monocytes fed with pigment or in RBC ghosts and liposomes incubated at pH 6.5 in presence of pigment and low amounts of H2O2 [24].
• Erythrocyte membrane lipid peroxidation was induced in rats by administering phenylhydrazine, an oxidant drug [5].
• Experiments were carried out using rat liver microsomes to examine the effect of O2 tensions found in the liver and of GSH on CCl4-induced covalent binding and lipid peroxidation [25].
• Doxorubicin (Adr), daunorubicin (Dnr), and analogs of Adr modified in daunosamine (4'-epi-Adr and 3'-N-acetyl-Adr) were investigated with respect to their reaction with Fe(III) and analyzed for the ability of the corresponding iron complexes to sustain lipid peroxidation of isolated human platelet membranes [26].
• This protection was associated with markedly diminished alveolar-capillary protein leak, endothelial and epithelial membrane injury, lipid peroxidation, and pulmonary neutrophil recruitment [27].

Associations of Lipid Peroxidation with chemical compounds

• The mechanism of lipid peroxidation and the manner in which antioxidants function is reviewed. beta-Carotene is a purported anticancer agent, which is believed by some to have antioxidant action of a radical-trapping type [28].
• Other alkenals such as trans-4-hydroxy-2-nonenal have previously been isolated from microsomal systems when treated with halogenated hydrocarbons or subjected to lipid peroxidation [29].
• The toxic activity in the active filtrates was not due to continuing oxidation of NADPH nor to continuing liver microsomal lipid peroxidation [30].
• With carbon tetrachloride, lipid peroxidation and covalent binding to hepatic constituents have been dominant themes over the years [31].
• Effects of vitamin E on lipid peroxidation in healthy persons [32].

Gene context of Lipid Peroxidation

• With age, serum lipid peroxidation and lesion size increased, whereas serum PON activity decreased [33].
• Lipid peroxidation and oxidative damage occurred in right ventricular cardiomyocytes in HO-1(-/-), but not wild-type, mice [34].
• In carbonyl iron-treated rats, hepatic superoxide dismutase activity was significantly decreased, whereas hepatocyte lipid peroxidation, as measured by malondialdehyde levels, was significantly increased when compared with control rats at or above iron concentrations of 100 and 185 mumol/g dry wt, respectively [35].
• BACKGROUND & AIMS: Inflammatory stimuli and lipid peroxidation up-regulate cyclooxygenase (COX)-2 [36].
• Pathological analyses and measurements of lipid peroxidation, tumor necrosis factor (TNF)-alpha, COX-1 and COX-2 messenger RNA (mRNA), endotoxin, and liver and plasma thromboxane were performed [36].

Analytical, diagnostic and therapeutic context of Lipid Peroxidation

• Increased degradation of myocardial adenine nucleotides and concomitant lipid peroxidation may play a specific role in the development of reperfusion injury [37].
• Iron chelation by deferoxamine inhibits lipid peroxidation during cardiopulmonary bypass in humans [38].
• (a) The level of lipid peroxidation judged by malondialdehyde (MDA) measurement by HPLC, was higher in the transformed cells than in the nontransformed cells [39].
• Immunoprecipitation and Western blot analyses showed that exposure of cultures to A beta induced conjugation of 4-hydroxynonenal (HNE), an aldehydic product of lipid peroxidation, to the neuronal glucose transport protein GLUT3 [40].
• We therefore assessed circulating levels of the antioxidants vitamin A, vitamin E, beta-carotene and lycopene, indices of lipid peroxidation and hemodynamic changes during elective orthotopic liver transplantation in 12 patients [41].

References