Effects of Dietary Vitamin B2 on the Metabolism of S-adenosylmethionine and Polyamines During Long-term High Selenium Consumption

• Main Authors: Gwo-Shyong Tarn, 談國雄
• Other Authors: 楊駱菲莉
• Format: Others
• Language: zh-TW
• Published: 2000
• Online Access: http://ndltd.ncl.edu.tw/handle/41436133275893689008

碩士 === 輔仁大學 === 食品營養學系 === 88 === The purpose of this study was to investigate the effect of dietary vitamin B2 and selenium levels on SAM and polyamines metabolism of rats during long term selenium consumption. After 1 weeks of adaptation on normal diet (0.1 mg Se/kg diet, 6 mg vit. B2/kg diet), weanling male Wistar rats were randomly assigned to receive a AIN-93G diet with various levels of Se (0.1, 3, 5 mg Se/kg diet)and vitamin B2 (3, 6, 12 mg vit. B2/kg diet)for 12 weeks. Results indicated that hepatic SAM and SAH concentrations decreased significantly as dietary selenium level increased (p<0.05). Vitamin B2 levels tended to raise hepatic SAM and SAH concentrations, SAM : SAH ratio not effected. Hepatic putrescine, spermidine, spermine concentration and spermidine : spermine ratio increased significantly as dietary selenium level increased (p<0.05). However hepatic putrescine, spermidine concentration in 12 mg vit.B2/kg diet not significantly change. Long-term high selenium consumption significantly elevated glutathione-S-transferase activity, which was reduced by dietary vitamin B2 level. During long-term high selenium consumption, hepatic, kidney, and erythrocyte selenium concentration increased significantly (p<0.05). Hepatic, kidney selenium concentration increased as dietary vitamin B2 level increased. Liver morphology of rats in 5 mg Se/kg diet, 3 mg vitamin B2/kg diet group was the worst. However, increased dietary vitamin B2 levels reduced pathological damage in rat liver. In summary, long term consumption of high selenium diet caused growth retardation and hair loss, alter hepatic SAM, SAH and polyamines metabolism. A diet provided 2 folds of vitamin B2 level in AIN-93G diet may reduce selenium toxicity thus maintaining optimal growth of rats.