The appendix of the Sauromatum senosum inflorescence is a striking example of thermogenesis in plants. On the day of opening, the Sauromatum appendix becomes hot, reaching up to 32 °C. Aspirin, salicylic acid and 2,6-dihydroxybenzoic acid, a subclass of NSAIDs, induce a temperature rise from three mitochondrial sources: alternative oxidase, F1 FO -ATP synthase and adenine nucleotide translocator. This temperature rise is synchronized and compounded under various light/dark regimes. We studied the effect of different subgroups of NSAIDs on the temperature rise. Tissue slices of appendix of Sauromatum and Arum italicum inflorescences at a pre-mature stage were treated with the three inducers in combination with one NSAID under constant light or darkness and under different photoperiods. Temperature rise generated by the three heat sources in the presence of inducers and different non-selective NSAIDs were not compounded and occurred at three different times. Under constant light, DuP-697, ibuprofen, flurbiprofen, acetaminophen and diclofenac suppressed the temperature rise induced by the three salicylates. Desynchronization and delayed temperature rise were detected with 6/42-h light/ dark and 15/33-h light/dark regimes in the presence of celecoxib and ibuprofen. With a 24/24-h light/dark regime, temperature rise was suppressed in the presence of ibuprofen. There were differences in response to individual NSAIDs between appendix tissue of A. italicum and S. venosum. Mitochondrial energy balance is affected by NSAIDs. There is an interaction between light/dark regime and temperature rise and a relationship between timing mechanism and temperature rise.