Vitamin D3 (VD3) deficiency increases DNA damage, while supplementation may exert a pro-oxidant activity, prevent viral infections and formation of tumors. The aim of this study was to investigate the mutagenicity and carcinogenicity of VD3 alone or in combination with doxorubicin (DXR) using the Somatic Mutation and Recombination Test and the Epithelial Tumor Test, both in Drosophila melanogaster. For better understanding of the molecular interactions of VD3 and receptors, in silico analysis were performed with molecular docking associated with molecular dynamics. Findings revealed that VD3 alone did not increase the frequency of mutant spots, but reduced the frequency of mutant spots when co-administered with DXR. In addition, VD3 did not alter the recombinogenic effect of DXR in both ST and HB crosses. VD3 alone did not increase the total frequency of tumor, but significantly reduced the total frequency of tumor when co-administered with DXR. Molecular modeling and molecular dynamics between calcitriol and Ecdysone Receptor (EcR) showed a stable interaction, indicating the possibility of signal transduction between VD3 and EcR. In conclusion, under these experimental conditions, VD3 has modulatory effects on the mutagenicity and carcinogenicity induced by DXR in somatic cells of D. melanogaster and exhibited satisfactory interactions with the EcR.

维生素 D3 (VD3) 缺乏会增加 DNA 损伤，而补充维生素 D3 可能会发挥促氧化活性，防止病毒感染和肿瘤形成。本研究的目的是使用体细胞突变和重组试验以及上皮肿瘤试验，在黑腹果蝇中研究单独使用 VD3 或与阿霉素 (DXR) 组合使用的 VD3 的致突变性和致癌性。为了更好地了解 VD3 和受体的分子相互作用，通过与分子动力学相关的分子对接进行了计算机分析。研究结果显示，单独使用 VD3 不会增加突变点的频率，但与 DXR 共同施用时会降低突变点的频率。此外，VD3 并没有改变 DXR 在 ST 和 HB 杂交中的重组作用。单独使用VD3并不会增加肿瘤的总频率，但与DXR联合给药时会显着降低肿瘤的总频率。骨化三醇和蜕皮激素受体（EcR）之间的分子建模和分子动力学显示出稳定的相互作用，表明VD3和EcR之间存在信号转导的可能性。总之，在这些实验条件下，VD3对DXR诱导的黑腹果蝇体细胞的致突变性和致癌性具有调节作用，并与EcR表现出令人满意的相互作用。