Salim-Hanna M, Lissi E, Videla L A
Department of Chemistry, Faculty of Science, University of Santiago, Chile.
Free Radic Res Commun. 1991;14(4):263-70. doi: 10.3109/10715769109088955.
The capacity of carnosine to decrease free radical-induced damage was evaluated using the oxidation of brain homogenates, the 2,2'-azobis-2-amidino propane-induced oxidation of erythrocyte ghost membranes, the radiation induced inactivation of horseradish peroxidase and the 2,2'-azobis-2-amidino propane-induced inactivation of lysozyme. Carnosine addition up to 17 mM did not produce any significant protection in either lipid peroxidation system, as assayed by the oxygen uptake rate. Carnosine addition reduces the intensity of the visible luminescence emitted, apparently due to a dark decomposition of the luminescent intermediates. Carnosine addition protects horseradish peroxidase and lysozyme from free radical mediated inactivation. The mean carnosine concentrations required to inhibit the inactivation rates by 50% were 0.13 mM and 0.6 mM for horseradish peroxidase and lysozyme, respectively.
使用脑匀浆氧化、2,2'-偶氮二(2-脒基丙烷)诱导的红细胞鬼膜氧化、辐射诱导的辣根过氧化物酶失活以及2,2'-偶氮二(2-脒基丙烷)诱导的溶菌酶失活，评估了肌肽减少自由基诱导损伤的能力。高达17 mM的肌肽添加量在任一脂质过氧化系统中均未产生任何显著的保护作用，这通过氧气摄取率来测定。肌肽的添加降低了发出的可见发光强度，这显然是由于发光中间体的暗分解。肌肽的添加保护辣根过氧化物酶和溶菌酶免受过自由基介导的失活作用。将辣根过氧化物酶和溶菌酶的失活率抑制50%所需的平均肌肽浓度分别为0.13 mM和0.6 mM。
