Date Pit Carbon Dots Induce Acidic Inhibition of Peroxidase and Disrupt DNA Repair in Antibacteria Resistance

Carbon nanodots (C‐dots) are emerging as a new type of promising agent in anticancer, imaging, and new energy. Reports as well as the previous research indicate that certain C‐dots can enhance targeted cancer therapy. However, in‐depth mechanisms for such anticancer effect remain unclear. In this work, treatment provided by the date pit‐derived C‐dots, exhibits significant DNA damage; Annexin V/7‐AAD‐mediated apoptosis, and G2/M cell cycle arrest in prostate cancer cells. The application of C‐dots to the cell generally leads to acidulation of the cell medium, cooperated with membrane compact. The date pit‐derived C‐dots are observed inhibiting the horseradish peroxidase. Moreover, the C‐dots disrupt likely through nucleotide excision DNA repair at low dose during DNA ligation step suggesting the antimicrobial effect and targeting Pim‐1, EGFR, mTOR, and DNA damage pathways in cancer cells. For the first time the detailed and novel mechanisms underlying the C‐dots, derived from the date‐pit, as an efficient, low‐cost, and green nanomaterial are reveled for cancer therapy and anti‐infection. Date‐pit‐derived C‐dots can induce cell death, cell cycle arrest in cancer, and mediate acidic inhibition of peroxidase stimulated by UV as a potential intrinsic nanozyme. The C‐dots disrupt DNA repair in antibacteria drug resistance. The provided low‐cost, agricultural‐waste‐derived green materials of C‐dots are new avenues in cancer therapy and anti‐infection.