Hipkiss A R, Preston J E, Himswoth D T, Worthington V C, Abbot N J
Molecular Biology and Biophysics Group, King's College London, Strand, UK.
Neurosci Lett. 1997 Dec 5;238(3):135-8. doi: 10.1016/s0304-3940(97)00873-2.
Malondialdehyde (MDA) is a deleterious end-product of lipid peroxidation. The naturally-occurring dipeptide carnosine (beta-alanyl-L-histidine) is found in brain and innervated tissues at concentrations up to 20 mM. Recent studies have shown that carnosine can protect proteins against cross-linking mediated by aldehyde-containing sugars and glycolytic intermediates. Here we have investigated whether carnosine is protective against malondialdehyde-induced protein damage and cellular toxicity. The results show that carnosine can (1) protect cultured rat brain endothelial cells against MDA-induced toxicity and (2) inhibit MDA-induced protein modification (formation of cross-links and carbonyl groups).
丙二醛（MDA）是脂质过氧化的有害终产物。天然存在的二肽肌肽（β-丙氨酰-L-组氨酸）在大脑和神经支配组织中的浓度高达20 mM。最近的研究表明，肌肽可以保护蛋白质免受含醛糖和糖酵解中间体介导的交联作用。在此，我们研究了肌肽是否能保护细胞免受丙二醛诱导的蛋白质损伤和细胞毒性。结果表明，肌肽可以：（1）保护培养的大鼠脑内皮细胞免受丙二醛诱导的毒性作用；（2）抑制丙二醛诱导的蛋白质修饰（交联和羰基的形成）。
