Concentration:	1 mg/ml (OD 1.35 / 280 nm)
Source:	Malondialdehyde modification from Human Albumin.
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

[P19]

2007

Odhiambo, Adam; Perlman, David H.; Huang, Hua; Costello, Catherine E.; Farber, Harrison W.; Steinberg, Martin H. et al. (2007): Identification of oxidative post-translational modification of serum albumin in patients with idiopathic pulmonary arterial hypertension and pulmonary hypertension of sickle cell anemia. In Rapid communications in mass spectrometry : RCM 21 (14), pp. 2195–2203. DOI: 10.1002/rcm.3074.

 

academy biomed[A05]绵羊抗人类载脂蛋白AII多克隆抗体12A-S1a学院生物医学公司$ 155.00$ 155.00目录号数量1寄主物种： 羊浓度： 1毫克/毫升（OD 1.35 / 280 nm）抗原： 人类载脂蛋白AII纯化： 亲和纯化缓冲： 75 mM磷酸钠，75 mM NaCl，0.5 mM EDTA，0.02％NaN3，pH 7.2特异性 与人载脂蛋白AII特异性结合。免疫印迹和ELISA的稀释范围：1,000至80,000。用： 该抗体可用于检测血浆和脂蛋白中的载脂蛋白AII，免疫测定，免疫印迹，酶结合或生物素化。存储： -20°C长期保存，4°C短期保存。等分试样，以避免反复冻结和解冻。 *这些产品仅用于研究或制造用途，不能用于人体治疗或诊断应用。 重要性Apo AII占HDL的25％。它在人血浆中以77条氨基酸残基的2条相同链的二聚体形式存在，并通过二硫键连接。据报道，单链的分子量为8.7kDa（Brewer等，1972）。对小鼠的研究报道，apoAII可能具有促动脉粥样硬化作用（Warden等，1993）。然而，一项大型的欧洲前瞻性研究中的病例对照研究表明，血浆Apo AII浓度与冠心病事件密切相关（Birjmohun等，2007）。Birjmohun，RS，GM Dallinga-Thie，JA Kuivenhoven，ESg Stroes，JD Otvos，NJ Wareham，R.Luben，JJp Kastelein，K.-T. Khaw和SM Boekholdt。“载脂蛋白A-II与未来冠状动脉疾病的风险成反比。” 循环116（2007）：2029-035。Brewer，HB，SE Lux，R.Ronan和KM John。“人ApoLp-Gln-II（apoA-II），一种从高密度脂蛋白复合物中分离的载脂蛋白的氨基酸序列。” 美国国家科学院院刊69.5（1972）：1304-308。Warden，C.，C.Hedrick，J.Qiao，L.Castellani和A.Lusis。“过表达载脂蛋白A-II的转基因小鼠中的动脉粥样硬化。” 科学261（1993）：469-72。