Three different
isoforms of the
enzyme nitric oxide synthase (NOS) (EC 1.14.13.39) catalyze the formation of
nitric oxide (NO) from
l-arginine, which is then converted to l-
citrulline. NO released by the constitutive
isoforms is involved in a variety of physiologic functions, whereas larger amounts of NO released from the inducible
isoform (iNOS) are mostly associated with inflammatory processes. Overproduction of NO in these processes including
sepsis and
autoimmune diseases can have deleterious consequences and pathophysiologic relevance. In this regard investigations of the regulation and function of iNOS to find specific iNOS inhibitors to block unwanted high levels of NO seem of great interest. The present article gives an overview of several methods and techniques employed to study the expression and regulation of the
inducible nitric oxide synthase in in vivo and in vitro models of
inflammation. The induction of iNOS was detected at different levels of expression and was compared to functional activity of NOS measured as
enzyme activity and
nitrite/
nitrate production, two stable end products of the NO pathway. Differences in vivo and in vitro are compared and discussed.