Chk2 deficiency alleviates irradiation-induced taste dysfunction by inhibiting p53-dependent apoptosis

Abstract

Objective

Taste dysfunction is one of the most common complications following radiotherapy, which leads to decreased appetite and life quality of patients suffering from head and neck cancer. The aim of this study was to investigate the role of Checkpoint kinase2 (Chk2) deficiency in irradiation-induced taste dysfunction.

Materials and methods

Alterations in oxidative stress, DNA damage and potential signaling pathway were compared between Chk2-deficient (Chk2^-/-) mice and their wild-type (WT) littermates pre-irradiation, and 7 and 30 days post-irradiation by biochemistry and immunohistochemistry.

Results

Chk2^-/- mice showed less loss of type II and type III taste cells, lower expression of p53, Caspase-3 and cleaved Caspase-3, and lower apoptosis levels. However, no significant differences in H₂O₂ and MDA concentrations, T-SOD and GSH-Px activities, and expression of SOD1, SOD2 and 8-OHdG were detected in the taste buds of Chk2^-/- mice as compared to that of WT mice.

Conclusion

Chk2 deficiency down-regulated the expression of p53 and inhibited cellular apoptosis, partly contributing to the radio-protective effect on taste cells, but did not alter oxidative stress levels, antioxidant ability and oxidative DNA damage in taste buds.

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