Inoculation with endophytic fungus Gilmaniella sp. induced multiple responses in host plantlets of Atractylodes lancea, including the burst of NO, SA, H(2)O(2), and the accumulation of volatile oil. To investigate the pathways that the three signal molecules affect the volatile oil production, the plantlets were treated with NO specific scavenger 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide potassium salt (cPTIO), SA synthesis inhibitor trans-cinnamic acid (trans-CA), membrane NADPH oxidase inhibitor diphenylene iodonium (DPI) and catalase (CAT). The results showed pretreatment of plantlets with cPTIO, DPI/CAT and trans-CA inhibited the burst of signal molecules and volatile oil accumulation induced by the fungus. Exogenous NO donor SNP could promote SA and H(2)O(2) production as well as volatile oil accumulation. Combined application of trans-CA and DPI/CAT could inhibit the promotion effects of exogenous NO. Exogenous SA and H(2)O(2) had no effects on NO production, but they could reverse the total inhibitory effects of cPTIO, CAT/DPI and trans-CA toward volatile oil accumulation. Exogenous H(2)O(2) had promotion effect on SA production, yet CAT/DPI could not significantly prevent SA synthesis. These data indicated NO mediates violate oil accumulation induced by the fungus through SA and H(2)O(2) dependent pathways. H(2)O(2) can regulate SA production, but does not act as upstream signal molecule. (C) 2010 Elsevier Ltd. All rights reserved.