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Chk2 deficiency alleviates irradiation‐induced taste dysfunction by inhibiting p53‐dependent apoptosis
Author(s) -
Yuan Zhiyao,
Ma Junchi,
Meng Xin,
Chen Ning,
Shen Ming
Publication year - 2018
Publication title -
oral diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.953
H-Index - 87
eISSN - 1601-0825
pISSN - 1354-523X
DOI - 10.1111/odi.12822
Subject(s) - oxidative stress , apoptosis , dna damage , taste , antioxidant , caspase 3 , chemistry , medicine , endocrinology , cancer research , pharmacology , biochemistry , programmed cell death , dna
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 kinase 2 (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 postirradiation 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 H 2 O 2 and MDA concentrations, T‐ SOD and GSH ‐Px activities, and expression of SOD 1, SOD 2, and 8‐ OH dG were detected in the taste buds of Chk2 −/− mice as compared to those of WT mice. Conclusion Chk2 deficiency downregulated the expression of p53 and inhibited cellular apoptosis, partly contributing to the radioprotective effect on taste cells, but did not alter oxidative stress levels, antioxidant ability, and oxidative DNA damage in taste buds.