作者: Gerald M. Rosen , Howard J. Halpern
DOI: 10.1016/0076-6879(90)86156-P
关键词: Hydrogenase 、 Glutathione 、 Nicotinamide adenine dinucleotide phosphate 、 Superoxide 、 Radical 、 Menadione 、 Metabolism 、 Chemistry 、 Spin trapping 、 Biochemistry
摘要: Publisher Summary Severe limitations confronting the field of free radical biology are inability to correlate formation specific radicals with cellular injury. Despite importance these data, surprisingly little has been published on this topic. This chapter discusses approaches overcome problem. It four studies,several indicators membrane injury, including trypan blue exclusion, leakage lactate dehydrogenase (LDH), and release 15 Cr. also presents subtle measures cell toxicity, such as inhibition glucose metabolism by measuring 14 CO 2 release, diminition in [ C] leucine incorporation into proteins, alterations glutathione nicotinamide adenine dinucleotide phosphate hydrogenase (NADPH) levels. One reasons study menadione-mediated injury is presented because menadione semiquinone via one-electron reduction reductases oxygen independent, whereas generation superoxide during quinone dependent. allows separation effects associated from those generation.