Glutathione and glutathione S-transferase in the rainbow trout olfactory mucosa during retrograde degeneration and regeneration of the olfactory nerve.

In the peripheral olfactory organ, continual olfactory receptor neuron (ORN) turnover exposes neighboring cells to potentially damaging cellular 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 investigated GSH and GST during retrograde degeneration and regeneration of the olfactory nerve in rainbow trout. In these fish, prolonged ORN physiological activity and structural integrity following transection of the olfactory nerve may be mediated by GSH and GST. In the olfactory mucosa, early changes following nerve lesion and prior to ORN degeneration included a shift of intense GSH labeling from the dendrites and perikarya of a subpopulation of ORN, and from melanophores, to olfactory nerve 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, GSH labeling was confined to melanophores, and GST-IR was absent. As ORN repopulated the olfactory mucosa, GST-IR was widespread. The combination of increased GST activity (92% of preoperative values) and low GSH levels suggests GSH utilization for GST conjugation reactions. These changes imply that GSH provides protection from cellular debris associated with ORN degeneration. Recovery of GST activity and widespread GST-IR during regeneration indicates modulation of neuroprotective, developmental, and/or physiological processes by GST.