Abstract
BackgroundPreviously we verified the radioprotective effect of lidocaine on the function and ultrastructure of salivary glands in rabbits. However, the underlying mechanism of lidocaine's radioprotective effect is unknown. We hypothesized that lidocaine, as a membrane stabilization agent, has a protective effect on intracellular neuroreceptor-mediated signaling and hence can help preserve the secretory function of salivary glands during radiotherapy.Methods and MaterialsRabbits were irradiated with or without pretreatment with lidocaine before receiving fractionated radiation to a total dose of 35 Gy. Sialoscintigraphy and saliva total protein assay were performed before radiation and 1 week after the last radiation fraction. Isolated salivary gland acini were stimulated with either carbachol or adrenaline. Ca2+ influx in response to the stimulation with these agonists was measured using laser scanning confocal microscopy.ResultsThe uptake of activity and the excretion fraction of the parotid glands were significantly reduced after radiation, but lidocaine had a protective effect. Saliva total protein concentration was not altered after radiation. For isolated acini, Ca2+ influx in response to stimulation with carbachol, but not adrenaline, was impaired after irradiation; lidocaine pretreatment attenuated this effect.ConclusionsLidocaine has a radioprotective effect on the capacity of muscarinic agonist-induced water secretion in irradiated salivary glands.
Highlights
Salivary gland dysfunction is one of the major side effects of radiotherapy in patients treated for head and neck cancer [1]
Lidocaine has a radioprotective effect on the capacity of muscarinic agonist-induced water secretion in irradiated salivary glands
The fluorescence alterations of the control and irradiated/lidocainepretreated groups did not significantly differ (p = 0.69). (Figure 5) Together, these results suggest that Ca2+ influx is attenuated in response to carbachol in irradiated parotid acini, which indicates impairment of intracellular muscarinic receptor-mediated signaling of the acini; pretreatment with lidocaine, has a radioprotective effect on the acini’s capacity of muscarinic agonistinduced secretion
Summary
Salivary gland dysfunction is one of the major side effects of radiotherapy in patients treated for head and neck cancer [1]. Secretory activity of salivary glands decreased to 50% of normal levels whereas less than 3% of apoptosis activity was observed 3 days after radiation [5] and that no significant cell loss was observed within 10 days after radiation [7]. This rapid radiation induced changes is not compatible with mitotic or apoptotic cell death and that an alternative hypothesis of early-stage radiation damage to the salivary glands is needed [4,7,8]. As a membrane stabilization agent, has a protective effect on intracellular neuroreceptor-mediated signaling and can help preserve the secretory function of salivary glands during radiotherapy
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