3-Hydroxy-1 -nonene: 1-Nonen

Hydroxy-1-nonene 1-Nonen-3-ol (21964-44-3), 68, 210 (2S, 3S )-3-HYDROXY-3-PHENYL-2-METHYLPROPANOIC ACID, 68, 83 (1-Hydroxy-2-propenyl)trimethylsilane, 66, 14,15... 

Aldini, G., Carini, M., Beretta, G., Bradamante, S., and Fadno, R. B. (2002). Carnosine is a quencher of 4-hydroxy-nonenal Though what is the mechanism of reaction Biochem. Biophys. Res. Commun. 298, 699-706. 

Benedetti, A., M. Comporti, and H. Esterbauer. 1980. Identification of 4-hydroxy-nonenal as a cytotoxic product originating from the peroxidation of liver microsomal lipids. Biochim. Bionhv.c. Acta 620 281-296. 

Endothelial-derived relaxing factor Glutathione 4 hydroxy-nonenal Hemoxygenase 1 Hydrogen peroxide Intercellular adhesion molecule 1 Linoleic acid... 

Several oxysterol classes present in oxLDL appear to be cytotoxic toward fibroblasts, ECs, and vascular smooth muscle cells, especially 7-hydroperoxycholes-terol (7-OOH-chol), 7P- and 7a-hydroxycholesterol (7-OH-chol), 7-ketocholesterol (7-keto-chol), and cholesterol epoxides (epoxy-chol). 7p-OOH-chol, a precursor of hydroxyl- and keto-oxysterols, was reported to be the most toxic. During LDL oxidation 7P-OOH-chol was produced in three to five times higher quantities than 7a-OOH-chol, other oxysterols and even hydroxy-nonenal, which is one of the most abundant lipid oxidation products. Cytotoxicity of oxysterols was connected to increased cellular oxidative stress. Some studies suggest that oxysterols are even involved in oxidative stress induction. Animal models indicate that dietary oxysterols can significantly decrease glutathione levels and increase expression of glutathione peroxidase and superoxide dismutase. In apolipoprotein-deficient mice, the NADPH-oxidase activity was induced by 7-keto-chol, 7p-OH-chol, and Sp,6P-epoxy-chol. The increased activity of NADPH oxidase yields more superoxide anions that amplify oxidative stress. 

To determine whether 4-hydroxynonenal could account for the acute effects of ozone on human alveolar macrophages, Hamilton jr. et al. (1998) exposed healthy, non-smoking volunteers to 0.4 ppm ozone or air for 1 h with exercise (each subject served as his/her own control). Six hours after ozone exposure, cells obtained by airway lavage were examined for apoptotic cell injury, presence of 4-hydroxynonenal adducts, and expression of stress proteins. Significant apoptosis was evident in airway lung cells after ozone exposure. Western analysis demonstrated an increase in a 32-kDa 4-hydroxynonenal protein adduct and a number of stress proteins, viz., 72-kDa heat shock protein and ferritin, in alveolar macrophages after ozone exposure. All these effects could be replicated by in vitro exposure of alveolar macrophages to 4-hydroxy-nonenal. 

Wawra, E., 2 11ner, H., Schaur, R.J., Tillian, H.M. and Schauenstein, E. (1986) The inhibitory effect of 4-hydroxy-nonenal on DNA-polymerase alpha and beta from rat liver and rapidly dividing Yoshida ascites hepatoma. Cell Biochem. Fund. 4, 31-36. 

In WHHL rabbits, aortic accumulation of hydroxide of CE and TG is not required nor is a-tocopherol depleted during atherosclerosis (385). It was suggested that the atherogenecity of oxLDL in cultured humans aortic SMC is a result of LDL aggregation and not oxidation (386). PC hydroxyalkenals, a class of oxidized PC, are present in vivo and possess multiple functions characteristic of oxLDL and 4-hydroxy nonenal (387). 

Both adds are highly ichthyotoxic for Eupomacentrus leucostictus as well as a fourth derivative, 4-hydroxy-nonen-2-al but the 1-glyceride of the first acid, also present in the alga, has no toxicity. 

One well studied system is that of the serum low density lipoprotein (LDL sections 5.3.5(e) and 5.5.3). When the lipids of this lipoprotein are peroxidized, the apoprotein becomes fragmented and there is cross-linking and residue modification. Two products of lipid oxidation, malonaldehyde and 4-hydroxy nonenal, are responsible, the latter reacting with lysines of apoprotein-B by an addition reaction. As a result LDL no longer binds to the fibroblast receptor (section 5.5.3) and has an extended half-life in blood. 

The identification and quantification of potentially cytotoxic carbonyl compounds (e.g. aldehydes such as pentanal, hexanal, traw-2-octenal and 4-hydroxy-/mAW-2-nonenal, and ketones such as propan- and hexan-2-ones) also serves as a useful marker of the oxidative deterioration of PUFAs in isolated biological samples and chemical model systems. One method developed utilizes HPLC coupled with spectrophotometric detection and involves precolumn derivatization of peroxidized PUFA-derived aldehydes and alternative carbonyl compounds with 2,4-DNPH followed by separation of the resulting chromophoric 2,4-dinitrophenylhydrazones on a reversed-phase column and spectrophotometric detection at a wavelength of378 nm. This method has a relatively high level of sensitivity, and has been successfully applied to the analysis of such products in rat hepatocytes and rat liver microsomal suspensions stimulated with carbon tetrachloride or ADP-iron complexes (Poli etui., 1985). 

Selley et al. (1992) have recently employed gas chromatography combined with mass spectrometric detection to determine levels of the cytotoxic monounsaturated aldehyde 4-hydroxy-/7 t-2-nonenal in the blood plasma of healthy human subjects, and patients with rheumatoid and osteoarthritis. Intriguingly, this lipid peroxidation end-product is present at a concentration ofc. lx 10 mol/dm in healthy and osteoarthritic human plasma samples (but significantly elevated in those collected from rheumatoid arthritis patients). Although at least some of this could originate from the oxidative degradation of PUFAs invm, there may be a relationship existing between these levels and the frequency of thermally/... 

Dick et al. [88] studied the antioxidant effects of NADPH-dependent alkenal/one oxidor-eductase (AO), also known as leukotriene B4 12-hydroxydehydrogenase, 15-oxoprostaglan-din 13-reductase, and dithiolethione-inducible gene-1. It was found that AO catalyzed the hydrogenation of many a,(3-unsaturated aldehydes and ketones and protected against cytotoxic action of 4-hydroxy-2-nonenal. 

The importance of superoxide-mediated damage to cancer cells was also demonstrated in the experiments with overexpressed mitochondrial MnSOD. Hirose et al. [186] showed that the overexpression of mitochondrial MnSOD enhanced the survival of human melanoma cells exposed to cytokines IL-1 and TNF-a, anticancer antibiotics doxorubicin and mitomycin C, and y-irradiation. Similarly, Motoori et al. [187] found that overexpression of MnSOD reduced the levels of reactive oxygen species in mitochondria, the intracellular production of 4-hydroxy-2-nonenal, and prevented radiation-induced cell death in human hepatocellular... 

Van der Vtiet, A., Van der Aar, E.M., and Bast, A., 1991, The Upid peroxidation product 4-hydroxy-2,3-trans-l nonenal decreases rat intestinal smooth muscle function in-vitro by alkylation of sulphydryl groups, J. Pharm. Pharmacol. 43 515-517. 

Hydroxy-1-nonene was prepared by the following procedure 0.219 mol (25.0 g) of heptaldehyde (Eastman Kodak Co.), distilled prior to use, was stirred in 450 mL of anhydrous ether (Note 2) under a nitrogen atmosphere. The solution was cooled to 0 C with an ice bath and 0.260 mol (260.4 mL) of vinylmagnesium bromide (1.0 M solution in tetrahydrofuran, Aldrich Chemical Company, Inc., 1.2 equiv) was then added dropwise over a 0.5-hr period. The... 

Liu, Y., Xu, G., and Sayre, L. M. (2003). Carnosine inhibits (E)-4-hydroxy-2-nonenal-induced protein cross-linking Structural characterization of the carnosine-HNE adducts. Chem. Res. Toxicol. 16,1589-1597. 

Orioli, M., Aldini, G., Beretta, G., Mattei Facino, R., and Carini, M. (2005). LC-ESI-MS/MS determination of 4-hydroxy-trans-2-nonenal Michael adducts with cysteine and histidine-containing peptides as early markers of oxidative stress inexcitable tissues. ]. Chromatogr. B Arnlyt. Technol. Biomed. Life Sci. 827,109-118. 

In relation to cancer, there is some evidence that highly oxidized and heated fats may have carcinogenic characteristics. HNE (4-hydroxy-2-frans-nonenal), a secondary lipid peroxidation product derived from linoleic acid oxidation, has assumed particular interest because it has shown cytotoxic and mutagenic properties. Its toxicity, as well other secondary lipid peroxidation products (HHE 4-hydroxy-2-frans-hexenal and HOE 4-h yd roxy-2-trans-oc ten al), is explained through the high reactivity with proteins, nucleic acids, DNA, and RNA. Research links them to different diseases such as atherosclerosis, Alzheimer s, and liver diseases (Seppanen and Csallany, 2006). Research is rapidly progressing, but results are still not conclusive. 

Seppanen, C. M. and Csallany, A. (2006). The effect of Intermittent and continuous heating of soybean oil at frying temperature on the formation of 4-hydroxy-2-(rans-nonenal and other a-, p-unsaturated hydroxyaldehydes. J. Am. Oils Chem. Soc. 83,121-127. 

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