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SECOND INTERNATIONAL SYMPOSIUM
ON THE ROLE OF SOY
IN PREVENTING AND TREATING CHRONIC DISEASESeptember 15-18, 1996
Brussells, Belgium
SCIENTIFIC PROGRAM
(Oral Abstracts)Soy and Cancer
Animal studiesSoy Isoflavone Extract Suppresses Fumonisin B1-Promoted Rat Hepatocarcinogenesis
Suzanne Hendrich, Zhibin Lu, Huei-Ju Wang, Ellen Hopmans, Patricia Murphy.
Food Science & Human Nutrition, Iowa State University, Ames, IA 50011.A soy isoflavone extract (1.0 or 2.0 mmol total isoflavones/kg diet) significantly suppressed early stages of diethylnitrosamine (DEN)-initiated, phenobarbital-promoted rat hepatocarcinogenesis (Lee, et. al. 1995, Nutr. & Cancer 24: 267-278). To further understand isoflavone effects on tumor promotions, four groups of 6 ten-day-old female F344/N rats were initiated with 15 mg DEN/kg body weight by intraperitoneal injection, and at weaning (at 4 weeks of age), were fed a diet containing soy isoflavone extract (1.0 mmol total isoflavones/kg diet, 60:40, genistein:daidzein), with and without 50 mg fumonisin B1(FB)/kg diet for 4 weeks. After 4 weeks of FB and isoflavone extract feeding, serum cholesterol was increased 1.8-fold by FB feeding and 1.6-fold by feeding FB+ isoflavone extract, compared with the control group (P<0.01). Serum glutamate/pyruvate transaminase (GPT) activity was significantly increased 1.8-fold by FB feeding, compared with the control group. Endogenous hepatic prostaglandin (PG) F2a and E2 levels were significantly increased 1.7-fold by FB feeding compared with the control group. Isoflavone extract feeding alone significantly suppressed hepatic PGF2a by 15% compared with the control group. The group fed FB+ isoflavone extract did not differ significantly from the control group in serum GPT or hepatic PG status. Isoflavone extract significantly suppressed development of placental glutathione S-transferase (PGST)-positive altered hepatic foci (AHF) in FB-fed rats by over 50%. Isoflavones did not suppress FB-promoted development of y-glutamyltransferase (GGT)-positive AHF. The control group and the group fed isoflavones alone showed no development of AHF. PGST is a more persistent marker of hepatic neoplasia than is GGT. Suppression of FB-promoted PGST-[+] AHF by isoflavone extract indicates an anticarcinogenic effect of the extract. The isoflavone extract is clearly antihepatotoxic, and its suppression of FB-stimulated prostaglandin production suggests that prostaglandin suppression is an anticarcinogenic mechanism of soy isoflavones.
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