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While the importance of endothelial dysfunction in cardiovascular disease is well accepted, most evidence suggests that the primary mechanism by which this occurs is via oxidative stress in which superoxide either directly inactivates NO (by forming peroxynitrite), uncouples the endothelial NO synthase, or passively increases an inhibitory substrate (asymmetric dimethylarginine) by inhibiting the enzyme, dimethylarginine dimethylaminohydrolase.[18] In this regard, UA has been shown to help preserve endothelial NO levels via its role as an antioxidant, either by blocking the uncoupling of endothelial NO synthase by reacting with peroxynitrite,[18] or by preventing the oxidant-induced inactivation of extracellular superoxide dismutase.[19] A paradox then develops, for how can UA, which is the most abundant (about six times as ascorbate) antioxidant in plasma,[6] induce endothelial dysfunction in vivo

Research Approach 2.2

Heterogeneity in the molecular composition of excitatory postsynaptic sites during development of hippocampal neurons in culture

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