The growth-inhibitory activity of Cassia tora seed-derived materials against seven intestinal bacteria was examined in vitro, and compared with that of anthraquinone, anthraflavine, anthrarufin, and 1-hydroxyanthraquinone. The active constituent of C. tore seeds was characterized as quinizarin, using various spectroscopic analyses. The growth responses varied depending on the compound, dose, and bacterial strain tested. At 1 mg/disk, quinizarin exhibited a strong inhibition of Clostridium perfringens and moderate inhibition of Staphylococcus aureus without any adverse effects on the growth of Bifidobacterium adolescentis, B. bifidum, B. longum, and Lactobacillus casei. Furthermore, the isolate at 0.1 mg/disk showed moderate and no activity against C. perfringens and S. aureus. The structure-activity relationship revealed that anthrarufin, anthraflavine, and quinizarin moderately inhibited the growth of S. aureus. However. anthraquinone and 1-hydroxyanthraquinone did not inhibit the human intestinal bacteria tested. As for the morphological effect of 1 mg/disk quinizarin, most strains of C. perfringens were damaged and disappeared, indicating that the strong activity of quinizarin was morphologically exhibited against C. perfringens. The inhibitory effect on aflatoxin $B_1$ biotransformation by anthraquinones revealed that anthrarufin ($IC_50,;11.49mu extrm{M}$) anthraflavine ($IC_50,;26.94mu extrm{M}$), and quinizarin ($IC_50,;4.12mu extrm{M}$), were potent inhibitors of aflatoxin ${B_1}-8,9-epoxide$ formation. However, anthraquinone and 1-hydroxyanthraquinone did not inhibit the mouse liver microsomal sample to convert aflatoxin $B_1$ to aflatoxin ${B_1}-8,9-epoxide$. These results indicate that the two hydroxyl groups on A ring of anthraquinones may be essential for inhibiting the formation of aflatoxin ${B_1}-8,9-epoxide$. Accordingly, as naturally occurring inhibitory agents, the C. tora seed-derived materials described could be useful as a preventive agent against diseases caused by harmful intestinal bacteria, such as clostridia, and as an inhibitory agent for the mouse liver microsomal conversion of aflatoxin $B_1$ to aflatoxin ${B_1}-8,9-epoxide$.