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⁺/CO₃^2- 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⁺/CO₃^2- 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.