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Screening for microorganisms that inhibit aflatoxin production from environments showed that <i>Penicillium citrinum</i> inhibited aflatoxin production by <i>Aspergillus parasiticus</i>. The inhibitory substance in the culture medium of <i>P. citrinum</i> was confirmed to be citrinin (CTN). RT-PCR analyses showed that CTN did not inhibit expressions of aflatoxin biosynthetic genes (<i>aflR</i>, <i>pksL1</i>, and <i>fas-1</i>) of <i>A. parasiticus</i>, whereas feeding experiments using <i>A. parasiticus</i> showed that CTN inhibited the in vivo conversion of dihydrosterigmatocystin to AFB₂·AFG₂. These results suggest that CTN inhibits a certain post-transcriptional step in aflatoxin biosynthesis. CTN in the culture medium of <i>A. parasiticus</i> was found to be decreased or lost with time, suggesting that a certain metabolite produced by <i>A. parasiticus</i> is the cause of the CTN decrease; we then purified, characterized, and then analyzed the substance. Physico-chemical analyses confirmed that the metabolite causing a decrease in CTN fluorescence was kojic acid (KA) and the resulting product was identified as a novel substance: (1<i>R</i>,3<i>S</i>,4<i>R</i>)-3,4-dihydro-6,8-dihydroxy-1-(3-hydroxy-6-(hydroxymethyl)-4-oxo-4<i>H</i>-pyran-2-yl)-3,4,5-trimethyl-1<i>H</i>-isochromene-7-carboxylic acid, which was named “CTN-KA adduct”. Our examination of the metabolites’ toxicities revealed that unlike CTN, the CTN-KA adduct did not inhibit aflatoxin production by <i>A. parasiticus</i>. These results indicate that CTN’s toxicity was alleviated with KA by converting CTN to the CTN-KA adduct.