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題名 | 慢性中度餵食乙醇影響大白鼠組織對硒之利用=Chronic Ethanol Administration Affected Tissue Selenium Utilization in Rats |
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作 者 | 李文欽; 楊駱菲莉; | 書刊名 | 中華民國營養學會雜誌 |
卷期 | 26:2 2001.06[民90.06] |
頁次 | 頁109-118 |
分類號 | 361.13 |
關鍵詞 | 硒; 乙醇; 硒之營養狀況; 硒之生物可獲性; 麩胱苷冴過氧化酶; MDA含量; Selenium; Ethanol; Selenium status; Selenium bioavailability; Glutathione peroxidase; MDA; |
語文 | 中文(Chinese) |
中文摘要 | 為暸解長期中度餵食乙醇是否促進大白鼠體內過氧化物的生成或影響硒的利用,本研究使用75隻三週齡之雄性離乳Wistar大白鼠,先餵予五週的缺硒飼料(0.01 mg Se/kg diet, 硒消耗期),以消耗動物體內的硒。五週的硒消耗期結束後,犧牲12隻動物,檢測其硒營養狀況指標,以確定硒消耗之目的已達成。之後將其餘63隻動物隨機分成9組,分別接受硒含量為每公斤含0.01mg﹑0.042mg或0.105mg硒,及乙醇提供總熱量0%﹑10%或20%的九種飼料組合之一,為期五週(硒補充期)。研究結果顯示硒耗盡後給予不同硒含量的飼料,使動物的硒營養狀況呈現明顯的劑量效應;長期硒耗盡使動物肝藏、血漿及紅血球產生靈敏且一致的硒營養狀況指標之變化,而心臟則仍保有27%的SeGPX活性。中度餵食乙醇五週可能因干擾硒的生物可獲性而明顯降低腎臟與紅血球的硒含量及SeGPX活性。長期硒缺乏使大白鼠血漿MDA含量上升,五週的乙醇餵食使血漿MDA含量下降,但二者皆不影響組織MDA濃度,顯示各組織抗氧化系統的成員可能發揮代償作用,以因應硒缺乏與乙醇氧化代謝的影響。然而確切的變化機轉有待未來研究證實。 |
英文摘要 | In order to investigate the influence of chronic moderate ethanol consumption on peroxide generation and tissue selenium (Se) utilization, 75 weanling male Wistar rats were given a Sa-deficient diet containing 0.01 mg Se/kg diet for 5 weeks ( Se depletion period) to deplete bodily Se resources. Twelve rats were sacrificed to confirm their Se status at the end of the 5th week. The remaining 63 animals were randomly assigned to receive a diet with a Se level of 0.01 mg (deficient), 0.042 mg (marginal) and 0.105 mg (adequate) of Se per kg diet and each with an ethanol level providing 0%, 10%, or 20% of total energy for another 5 weeks (5e repletion period). Selenium depletion successfully lowered plasma and hepatic Se contents in the animals to 26-27% of normal rats. Results at the end of the Se repletion period showed that various degrees of Se repletion restored the Se status in a dose-dependent manner. The responses and sensitivity of Se status indices from erythrocytes, plasma and liver strongly correlated with one another, whereas cardiac Se status index was the most resistant to long term Se depletion among the tissues analyzed. Chronic moderate ethanol feeding significantly reduced the Se content and SeGPX activities of the kidney and erythrocytes probably through lowering the bioavailability of Se, thus rendering these tissues to elevated oxidative stress. Long term Se depletion raised plasma MDA levels. However, 5 weeks of moderate ethanol feeding lowered plasma MDA content without altering tissue MDA content. These results suggest that other members of the antioxidant defense system may be induced to compensate for the oxidative challenge caused by Se depletion and oxidative metabolism of ethanol. However, the exact mechanism of the compensatory response awaits further investigation. |
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