Vitamin D Resists Cyclophosphamide-Induced Genomic and DNA Damage in CHL Cells In Vitro and in Mice In Vivo

Abstract

Vitamin D as an adjuvant therapy for cancer patients is hoped to have a beneficial outcome based on its physiological activity, but clinical trials so far by addition of vitamin D show unremarkable curative improvement, mechanism for explain this phenomena is not well-understood. The aim of this study was to determine whether vitamin D resists cyclophosphamide (CP)-induced genomic and DNA damage. In CHL cells in vitro, 1α,25-(OH)₂D₃ at 10, 50, and 100 nM was found to alleviate the frequency of chromosomal aberration with an alleviation range of 40.7–44.0%. There was a dose-dependent decrease for a proportion of γ-H2AX foci positive cells in response to an increase in 1α,25-(OH)₂D₃ concentration. Two vitamin D₃ injections of 1,000, 5,000, or 10,000 IU suppressed CP-induced micronucleus formation in mice BMCs with an alleviation range of 36.7–44.5%, mitigated lymphocytes DNA damage reflected by lower tail DNA, tail length and olive tail moment parameter in comet assay. Vitamin D showed an antagonistic effect on CP-induced genomic and DNA damage. Our data suggest that vitamin D as an adjuvant combine antineoplastic drug with genotoxicity administer to tumor patients is contraindicant.

Disclosure Statement

No potential conflict of interest was reported by the authors.

Additional information

Funding

This work was financially supported by the National Natural Science Foundation of China.