Radiotherapy for head and neck cancer typically leads to loss of taste among cancer patients. We proposed that loss of taste after irradiation may be due to continued natural taste cell death, paired with temporary interruption of cell replacement. One possible strategy for averting taste loss may be to reduce epithelial cell death, so that cell proliferation is not interrupted. Protein kinase C delta (PKCδ) has been shown to positively regulate apoptosis and/or cell cycle arrest. The aim of this study was to test whether the effects of radiation on taste epithelium are mitigated in PKCδ null mice. The heads of wild type and PKCδ null adult mice were irradiated with a single 8Gy dose, and the lingual epithelia were examined for proliferative activity (Ki67 - ir) at progressive days post-irradiation (dpi). Our initial results showed that the dramatic reduction in the proliferative index typically observed in the taste epithelia of irradiated wild type mice 1 - 3 days after irradiation was mitigated significantly by loss of PKCδ in the PKCδ null mice. Our data suggest that PKCδ may be required for apoptotic cell death and/or cell cycle arrest in irradiated taste epithelium. | Mitigation of irradiation effects on taste epithelium in the protein Kinase C Delta Null Mouse
