Delayed chemiluminescence of luminol/ascorbic acid system triggered by ultrasound.

Sonochemiluminescence (SCL) of luminol is typically characterized by the immediate emission of light driven by acoustic cavitation. Here, we report a novel "memory effect" phenomenon termed Delayed Chemiluminescence Induced by Ultrasound (DCLIU), observed in the luminol/ascorbic acid (H2A)/Co2+/CO32- system. Contrary to the conventional role of H2A as a simple radical scavenger, we demonstrate that trace H2A induces a distinct secondary emission peak after ultrasonic irradiation has stopped. Mechanistic investigations reveal that this delay corresponds to an ultrasound-triggered redox cycle in which H2A initially suppresses emission by scavenging cavitation-generated reactive oxygen species (ROS). However, the resulting ascorbyl radical intermediates (A•-) subsequently act as pro-oxidants, reducing dissolved oxygen in the presence of Co2+ to regenerate superoxide radical anion (O2•-) and accumulate hydroperoxide anions (HO2-). Once H2A is depleted, the accumulated oxidants produce intense chemiluminescence from the luminol/HO2-/Co2+/CO32- system. This delayed emission is absent in N2-saturated solutions, confirming the critical role of dissolved oxygen. From an analytical chemistry perspective, both the delay duration and the integrated emission intensity exhibit a linear response to H2A concentration in the nanomolar range (LOD = 1.2 nM). The method demonstrates high selectivity against common interferents and was successfully applied to quantify ascorbic acid in commercial beverages and vitamin supplements.