[P20] Malondialdehyde modified Human LDL (MDA - LDL), 50% glycerol, Academy Bio-medical Company, Inc.

[P20] Malondialdehyde modified Human LDL (MDA - LDL), 50% glycerol

20P-MD-L102

Academy Bio-Medical Company, Inc.

  • $169.00


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.

 

Importance

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

 

Citations

[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.
[P20] 2018 Wray-Dutra, Michelle N.; Al Qureshah, Fahd; Metzler, Genita; Oukka, Mohamed; James, Richard G.; Rawlings, David J. (2018): Activated PIK3CD drives innate B cell expansion yet limits B cell–intrinsic immune responses. In J. Exp. Med. 215 (10), pp. 2485–2496. DOI: 10.1084/jem.20180617.
[P20] 2017 Grönwall, Caroline; Amara, Khaled; Hardt, Uta; Krishnamurthy, Akilan; Steen, Johanna; Engström, Marianne et al. (2017): Autoreactivity to malondialdehyde-modifications in rheumatoid arthritis is linked to disease activity and synovial pathogenesis. In Journal of autoimmunity 84, pp. 29–45. DOI: 10.1016/j.jaut.2017.06.004.
[P20] 2016 Jackson, Shaun W.; Scharping, Nicole E.; Jacobs, Holly M.; Wang, Shari; Chait, Alan; Rawlings, David J. (2016): Cutting Edge: BAFF Overexpression Reduces Atherosclerosis via TACI-Dependent B Cell Activation. In J.I. 197 (12), pp. 4529–4534. DOI: 10.4049/jimmunol.1601198.
[P20] 2015 Kolhatkar, Nikita S.; Brahmandam, Archana; Thouvenel, Christopher D.; Becker-Herman, Shirly; Jacobs, Holly M.; Schwartz, Marc A. et al. (2015): Altered BCR and TLR signals promote enhanced positive selection of autoreactive transitional B cells in Wiskott-Aldrich syndrome. In J. Exp. Med. 212 (10), pp. 1663–1677. DOI: 10.1084/jem.20150585.
[P20] 2014 Jackson, S. W.; Scharping, N. E.; Kolhatkar, N. S.; Khim, S.; Schwartz, M. A.; Li, Q.-Z. et al. (2014): Opposing Impact of B Cell-Intrinsic TLR7 and TLR9 Signals on Autoantibody Repertoire and Systemic Inflammation. In J.I. 192 (10), pp. 4525–4532. DOI: 10.4049/jimmunol.1400098.
[P20] 2014 Schwartz, Marc A.; Kolhatkar, Nikita S.; Thouvenel, Chris; Khim, Socheath; Rawlings, David J. (2014): CD4+ T cells and CD40 participate in selection and homeostasis of peripheral B cells. In J.I. 193 (7), pp. 3492–3502. DOI: 10.4049/jimmunol.1400798.
[P20] 2014 Zhu, Xinmei; Ng, Hang Pong; Lai, Yen-Chun; Craigo, Jodi K.; Nagilla, Pruthvi S.; Raghani, Pooja; Nagarajan, Shanmugam (2014): Scavenger Receptor Function of Mouse Fcγ Receptor III Contributes to Progression of Atherosclerosis in Apolipoprotein E Hyperlipidemic Mice. In J.I. 193 (5), pp. 2483–2495. DOI: 10.4049/jimmunol.1303075.
[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.

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