3-nitrotyrosine and Dental-Caries

The nitric oxide (NO) receptor enzyme soluble guanylate cyclase (sGC) contains one prosthetic heme group as an αβ heterodimer, and two heterodimer isoforms (α(1)β(1), α(2)β(1)) were characterized to have enzyme activity. To test the irreversible inflammation-dependent regulation of sGC in odontoblasts, we incubated decalcified frozen sections of healthy and inflamed human third molars with antibodies against β-actin, nitrotyrosine, inducible nitric oxide synthase (iNOS), α(1)-, β(1)-, and α(2)-subunits of sGC and analyzed them at protein levels by quantitative immunohistochemistry. The irreversible inflammation induced an increase in the signal intensities for nitrotyrosine and iNOS and a decrease for the α(1)-, β(1)-, and α(2)-subunits of sGC in odontoblasts. Inflammatory mediators, reactive oxygen, and nitrogen species may impair the expression of the α(1)-, β(1)-, and α(2)-subunits in odontoblasts. The decrease of sGC at the protein level in inflamed odontoblasts is compatible with a critical role for sGC to mediate biological effects of NO in health.

Topics: Actins; Adolescent; Adult; CD11b Antigen; CD3 Complex; Dental Caries; Dental Pulp; Dentin; Guanylate Cyclase; Humans; Immunohistochemistry; Inflammation; Inflammation Mediators; Isoenzymes; Microscopy, Confocal; Nitric Oxide Synthase Type II; Odontoblasts; Pulpitis; Reactive Nitrogen Species; Reactive Oxygen Species; Receptors, Cytoplasmic and Nuclear; Soluble Guanylyl Cyclase; Tyrosine; Young Adult