By J. F. Parkinson (auth.), Jack R. Lancaster Jr., John F. Parkinson (eds.)
The invention of mammalian nitric oxide (NO) synthesis from L-arginine has ended in a profound elevate in our knowing of easy physiological and pathophysiological procedures. The NO-dependent rules of steroidogenic cytochromes P450, equivalent to aromotase, and native, tissue-specific legislation of NOS isoform expression by way of sexual steroid hormones, resembling estrogen and progesterone, delivers to supply new insights into the law of endocrinological strategies. examine at the interplay among the NO and sexual steroid platforms tend to result in novel healing ideas to be used in ailments linked to perturbations of the endocrine approach.
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Extra resources for Nitric Oxide, Cytochromes P450, and Sexual Steroid Hormones
1996). 2 NOS-3 Targeting via Lipid Modification NOS-3 is a membrane associated protein in endothelial cells (Pollock et al. 1991). The cDNA cloning of bovine and human NOS-3 reveals the presence of a myristoylation consensus sequence at the immediate NHzterminal (Sessa et al. 1992; Lamas et al. 1992) and native NOS-3 can be biosynthetically labelled with myristate (Pollock et al. 1992). The NHzterminal sequence of human NOS-3 is: I-MGNLKSVAQEPGPPCGLGLGLGLGLCGKQGPATPAPEPSR-40 Mutation of the proposed myristoylation site Gly2~Ala results in almost complete expression of NOS-3 as a cytosolic protein and blocks incorporation of [3H]myristate into the protein (Sessa et al.
This may mean that, in addition to inducing increased vascular oxygen delivery by vasodilation, increased NO may also reversibly inhibit oxygen consumption in tissue surrounding the vessel thus extending the diffusion distance of 02 into the tissue. This would not be a permanent effect because: (1) the effect of NO on mitochondrial cytochrome oxidase is reversible and (2) inhibited mitochondria will produce 02- which will remove the NO and restore respiration. These effects are distinct from those of high-level chronic NO production at sites of inflammation, where the effects of NO on mitochondria are irreversible and probably involve destruction of cellular iron containing proteins, including mitochondrial electron transfer components.
1980; Hibbs, Jr. et al. 1984, 1987, 1988, 1990; Drapier and Hibbs, Jr. 1986). , complexes I and II (Granger and Lehninger 1982), and that reagent NO added to cells (anaerobically) results in this same pattern of inhibition (Hibbs, Jr. et al. 1988; Stuehr and Nathan 1989; Stadler et al. 1991). 04 EPR signals in NO producing AMs (Lancaster, Jr. and Hibbs, Jr. 1990) and their tumor cell targets (Pellat et al. 1990). This signal corresponds to the dithioldinitrosyl (DTDN) iron species which can also be observed in purified iron-sulfur containing enzymes treated with NO (anaerobically) (Dervartanian et al.