GLUTATHIONE AND GLUTATHIONE-S-TRANSFERASE IN THE RAINBOW-TROUT OLFACTORY MUCOSA DURING RETROGRADE DEGENERATION AND REGENERATION OF THE OLFACTORY NERVE

Citation
Sl. Starcevic et Bs. Zielinski, GLUTATHIONE AND GLUTATHIONE-S-TRANSFERASE IN THE RAINBOW-TROUT OLFACTORY MUCOSA DURING RETROGRADE DEGENERATION AND REGENERATION OF THE OLFACTORY NERVE, Experimental neurology, 146(2), 1997, pp. 331-340
Citations number
43
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
00144886
Volume
146
Issue
2
Year of publication
1997
Pages
331 - 340
Database
ISI
SICI code
0014-4886(1997)146:2<331:GAGITR>2.0.ZU;2-X
Abstract
In the peripheral olfactory organ, continual olfactory receptor neuron (ORN) turnover exposes neighboring cells to potentially damaging cell ular debris such as free radicals. These, in turn, may be inactivated by binding directly onto glutathione (GSH) or by enzymatic conjugation with glutathione S-transferase (GST). In this study, we have investig ated GSH and GST during retrograde degeneration and regeneration of th e olfactory nerve in rainbow trout. In these fish, prolonged ORN physi ological activity and structural integrity following transection of th e olfactory nerve may be mediated by GSH and GST. In the olfactory muc osa, early changes following nerve lesion and prior to ORN degeneratio n included a shift of intense GSH labeling from the dendrites and peri karya of a subpopulation of ORN, and from melanophores, to olfactory n erve fascicles. GSH levels were unchanged, but GST activity decreased by 33% and GST-immunoreactivity (GST-IR) in nerve fascicles diminished slightly. When the process of massive degeneration terminated and ORN were largely absent, GSH levels and GST activity decreased further, G SH labeling was confined to melanophores, and GST-IR was absent. As OR N repopulated the olfactory mucosa, GST-IR was widespread. The combina tion of increased GST activity (92% of preoperative values) and low GS H levels suggests GSH utilization for GST conjugation reactions. These changes imply that GSH provides protection from cellular debris assoc iated with ORN degeneration. Recovery of GST activity and widespread G ST-IR during regeneration indicates modulation of neuroprotective, dev elopmental, and/or physiological processes by GST. (C) 1997 Academic P ress.