[P20] Malondialdehyde modified Human LDL (MDA - LDL), 50% glycerol20P-MD-L102
|Concentration:||1 mg/ml (OD 1.35 / 280 nm)|
|Source:||From fresh human plasma that has tested negative for Hepatitis C, HIV-I and HIV-II antibodies as well as Hepatitis surface antigens.|
|Purification:||After series of ultracentrifugations, Low Density Lipoprotein (LDL) is Isolated From human plasma and modified with MDA.|
|Purity:||≥ 98% by SDS-PAGE|
|Buffer:||In 75 mM Sodium Phosphate, 75 m M NaCl, 0.02 % NaN3, 1 mM EDTA, p H 7.4.|
|Storage:||-20ºC for long-term and short-term storage. Aliquot to avoid repeated freezing and thawing.|
*The products are for research or manufacturing use only, not for use in human therapeutic or diagnostic applications.
Oxidative damage includes oxidative modification of cellular macromolecules, induction of cell death by apoptosis or necrosis, as well as structural tissue damage. Of the many biological targets of oxidative stress, lipids are the most involved class of biomolecules. Lipid oxidation gives rise to a number of secondary products of polyunsaturated fatty acid peroxidation.
Malondialdehyde (MDA) is the principal and most studied product. Consistent evidence reveals the reaction between MDA and cellular macromolecules such as proteins, RNA and DNA (Valenzuela, 1991). Numerous experiments have shown that MDA readily modifies proteins (Nair, 1986). MDA reacts with DNA to form adducts to deoxyguanosine and deoxyadenosine which may be mutagenic and these can be quantified in several human tissues (Marnett, 1999).This aldehyde is a highly toxic molecule and should be considered as a marker of lipid peroxidation. The interaction with DNA and proteins has often been referred to as potentially mutagenic and atherogenic (Rio et al., 2005).
L.J. Marnett, Lipid peroxidation‐DNA damage by malondialdehyde, Mutat Res, 424 (1999), pp. 83–95
V. Nair, C.S. Cooper, D.E. Vietti, G.A. Turner, The chemistry of lipid peroxidation metabolites: crosslinking reactions of malondialdehyde, Lipids, 21 (1986), pp. 6–10
Rio, Daniele Del, Amanda J. Stewart, and Nicoletta Pellegrini. "A Review of Recent Studies on Malondialdehyde as Toxic Molecule and Biological Marker of Oxidative Stress." Nutrition, Metabolism and Cardiovascular Diseases 15.4 (2005): 316-28.
A. Valenzuela, The biological significance of malondialdehyde determination in the assessment of tissue oxidative stress, Life Sci, 48 (1991), pp. 301–309
|[P20]||2018||Peng, YuFeng (2018): B cell responses to apoptotic cells in MFG-E8-/- mice. In PLoS ONE 13 (10), e0205172. DOI: 10.1371/journal.pone.0205172.|
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|[P20]||2013||Li, Shijie; Kievit, Paul; Robertson, Anna-Karin; Kolumam, Ganesh; Li, Xiumin; Wachenfeldt, Karin von et al. (2013): Targeting oxidized LDL improves insulin sensitivity and immune cell function in obese Rhesus macaques. In Molecular metabolism 2 (3), pp. 256–269. DOI: 10.1016/j.molmet.2013.06.001.|
|[P20]||2011||Becker-Herman, Shirly; Meyer-Bahlburg, Almut; Schwartz, Marc A.; Jackson, Shaun W.; Hudkins, Kelly L.; Liu, Chaohong et al. (2011): WASp-deficient B cells play a critical, cell-intrinsic role in triggering autoimmunity. In J. Exp. Med. 208 (10), pp. 2033–2042. DOI: 10.1084/jem.20110200.|
|[P20]||2011||Ng, Hang Pong; Burris, Ramona L.; Nagarajan, Shanmugam (2011): Attenuated atherosclerotic lesions in apoE-Fcγ-chain-deficient hyperlipidemic mouse model is associated with inhibition of Th17 cells and promotion of regulatory T cells. In J.I. 187 (11), pp. 6082–6093. DOI: 10.4049/jimmunol.1004133.|