Abstract:Among several secondary metabolic products of Camellia oleifera the injury of saponin to Colletotrichum camelliae is the severest at 200-400μg/ml concentration, but the concentration is so high that it is indicated that saponin can not be regarded as physiologically active substance. However, after saponin is hydrolyzed by 6N HCl and forms sapogenin, the injury of sapogenin to C. camelliae is severer than saponin, for example, 0.05 mM saponin causes increasing of amino-acid which is leaked into medium by C. camelliae mycelium at 0.43 times more than control, and 0.05mM sapogenin causes increasing in amino-acid at 16.86 times more than con- trol. The leakage of large number of amino acid results in death of C. camelliae mycelium. Therefore Camellia oleifera sapogenin is the main compound to inhibit C. camelliae. In plant, saponin transforms into sapogenin, that is resulted in catabolized reaction by β-glucosidase. The experiments in vitro demonstrate that Camellia oleifera saponin transforms into sapogenin by β-glucosidase, and sapogenin injures C.camelliae and brings C. camelliae mycelium to leak off aminoacid. Therefore it may be conjectured that the metabolic process which saponin transforms into sapogenin by β-glucosidase will play an important role in resistance of Camellia oleifera to C. camelliae.