Anticlastogenic potential of 1α,25-dihydroxyvitamin D₃ in murine lymphoma

Vitamin D₃, having gained scientific interest for so long because of its role in mineral homeostasis, has now received great importance as a possible antitumor agent. This study was undertaken in an attempt to visualize the possible anticlastogenic potential of the vitamin in an ascitic mouse lymphoma model namely, Dalton’s lymphoma. Frequencies of structural type chromosomal aberrations, sister chromatid exchanges and micronucleus assays have been chosen as the genotoxic endpoints in the proposed investigation. All these cytogenetic markers have been found to be markedly elevated during the progression of lymphoma in bone marrow cells. Vitamin D₃ effectively suppressed the frequencies of chromosomal aberrations and sister chromatid exchanges in the lymphoma-bearing mice during the entire phase of tumor growth that significantly coupled with almost two-fold increase in survival time (37 ± 2 and 68 ± 2 days in lymphoma controls and vitamin D₃- treated lymphoma-bearing mice, respectively), thus substantiating the antineoplastic efficacy of this secosteroid. The outcome of this study also is clearly reflected in the depletion of circulating (serum) vitamin D₃ levels in the lymphoma control mice compared with normal (vehicle) controls while a still higher level was maintained in the VD₃-treated lymphoma mice. This anticlastogenic property of the vitamin has so far been neglected and this is the first attempt to unravel the vitamin D₃’s effect in combating tumor development in vivo by limiting the frequencies of chromosomal aberrations, sister chromatid exchanges and micronuclei at least in transplantable murine model studied herein.