Abstract
It has become apparent that endothelial and inflammatory cells can produce both superoxide (O2 −) and nitric oxide (NO). When O2 − and NO coexist, they react to yield peroxynitrite (ONOO−). ONOO− is a potent oxidant. This chapter reevaluates free radical-related injury with particular attention to the reaction of O2 −, NO, and ONOO−. Through ischemia—repefiusion study using isolated rat hearts, it is suggested that the cytotoxic molecule is ONOO−. Similarly, in the study of activated leukocyte-induced cardiac myocyte injury, ONOO− appears to be responsible for the injury. However, in activated leukocyte-induced endothelial cell injury, the hydroxyl radical plays a significant role. The evidence to infer the formation of ONOO− was obtained from a study of patients with septic shock. In conclusion, cytotoxic molecules and the mechanism underlying cell damage appear to depend not only on the effector but also on the target cells, and it is very important to identify the actual cytotoxic molecule under an individual pathological condition.
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Ishida, H., Mohammed, M.U., Su, Z., Fujishima, M., Nakazawa, H. (1998). Roles of Superoxide, Nitric Oxide, and Peroxynitrite in Various Pathological Conditions. In: Mochizuki, S., Takeda, N., Nagano, M., Dhalla, N.S. (eds) The Ischemic Heart. Progress in Experimental Cardiology, vol 1. Springer, Boston, MA. https://doi.org/10.1007/978-0-585-39844-0_5
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DOI: https://doi.org/10.1007/978-0-585-39844-0_5
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