The involvement of jasmonic acid (JA) signaling in LED-delayed senescence remains poorly understood. Here, we applied blue-white combined (B + W) LED irradiation, methyl jasmonate (MeJA), and B + W LED combined with JA biosynthesis inhibitor diethyldithiocarbamic acid (B + W - DIECA) to investigate the role of JA in mediating mitochondrial function in Pleurotus eryngii . Both B + W LED irradiation and MeJA treatments alleviated browning and decay of P. eryngii , and stimulated mitochondrial antioxidant enzymes, facilitating efficient scavenging of reactive oxygen species, and helping reduce mitochondrial malondialdehyde accumulation and mitochondrial oxidative damage. Moreover, B + W LED irradiation and MeJA treatments increased energy metabolism-related enzyme activities, thereby increasing ATP levels by 17.86–81.14% and 22.94–132.90% after day 2, respectively, comparing with controls. These combined effects helped maintain the mitochondrial membrane potential. Crucially, DIECA counteracted the benefits of B + W LED irradiation by inhibiting JA accumulation. In contrast, B + W LED treatment alone significantly increased the levels of intracellular JA (21.14–99.20%), mitochondrial JA (21.18–100.46%), and JA-Ile (35.63–117.04%) relative to controls during storage. These increases were attributed to the upregulation of JA biosynthetic enzymes, including LOX, AOS, AOC and OPR. Our results indicate that B + W LED irradiation may sustain mitochondrial function in P . eryngii by inducing JA biosynthesis. • Blue-white LED irradiation delayed mitochondrial oxidative damage in Pleurotus eryngii. • Blue-white LED irradiation induced jasmonic acid (JA) biosynthesis in Pleurotus eryngii . • JA biosynthesis inhibitor counteracted the benefit effects of blue-white LED irradiation. • JA was a key signaling molecule in blue-white LED-delayed senescence of Pleurotus eryngii .
Luo et al. (2026) studied this question.