Blue fluorescent hexagonal boron nitride quantum dots (h-BNQDs) of ∼10 nm size as an effective enhancer for DNA cleavage activity of anticancer drug doxorubicin (DOX) were synthesized using simple one-step hydrothermal disintegration of exfoliated hexagonal boron nitride at very low temperature ∼ 120 °C. Boron nitride quantum dots (BNQDs) at a concentration of 25 μg/ml enhanced DNA cleavage activity of DOX up to 70% as checked by converting supercoiled fragment into nicked circular PBR322 DNA. The interaction of BNQDs with DOX is proportional to the concentration of BNQDs, with binding constant K_b ∼0.07338 μg/ml. In addition, ab initio theoretical results indicate that DOX is absorbed on BNQDs at the N-terminated edge with binding energy −1.075 eV and prevented the normal replication mechanisms in DNA. BNQDs have been shown to kill the breast cancer cell MCF-7 extensively as compared with the normal human keratinocyte cell HaCaT. The cytotoxicity of BNQDs may be correlated with reduced reactive oxygen species level and increased apoptosis in MCF-7 cells, which may be liable to enhance the anticancerous activity of DOX. The results provide a base to develop BNQD-DOX as a more effective anticancer drug.

通过在非常低的温度下简单地一步分解脱落的六角形氮化硼，合成了约10 nm大小的蓝色荧光六角形氮化硼量子点（h -BNQDs）作为抗癌药物阿霉素（DOX）DNA裂解活性的有效增强剂约120°C。浓度为25μg/ ml的氮化硼量子点（BNQDs）将超螺旋片段转化为带切口的圆形PBR322 DNA，从而将DOX的DNA裂解活性提高了70％。BNQD与DOX的相互作用与BNQD的浓度成正比，结合常数K _b约0.07338μg/ ml。此外，从头开始的理论结果表明，DOX以结合能-1.075 eV吸附在N末端的BNQD上，并阻止了DNA中正常的复制机制。与正常人角质形成细胞HaCaT相比，BNQD已显示出可广泛杀死乳腺癌MCF-7细胞。BNQDs的细胞毒性可能与降低的活性氧水平和MCF-7细胞凋亡增加有关，这可能会增强DOX的抗癌活性。该结果为开发BNQD-DOX作为更有效的抗癌药物提供了基础。