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題名 | 攝取類胡蘿蔔素對雄性倉鼠口腔癌化與抗氧化酵素之影響=Effects of Carotenoid Consumption on Oral Carcinogenesis and Antioxidative Enzymes in Male Hamsters |
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作者 | 錢信; 黃士懿; 林永和; 謝穎欣; 謝孟志; 謝明哲; | 書刊名 | 中華民國營養學會雜誌 |
卷期 | 26:3 2001.09[民90.09] |
頁次 | 頁171-180 |
分類號 | 412.7 |
關鍵詞 | 檳榔嚼塊萃取物; 類胡蘿蔔素; 倉鼠; 口腔頰囊癌; Betel quid extract; Carotenoids; Hamster; Buccal pouch carcinoma; |
語文 | 中文(Chinese) |
中文摘要 | 本研究係探討類胡蘿蔔素的攝取對檳榔萃取物誘發倉鼠口腔癌症的預防效果。58隻6~8週齡大雄性倉鼠隨機分配於6組,對照組(control, n=9)以AIN-76標準飲食配方為基準,其他各組額外添加0.1%的不同類胡蘿蔔素,分別為β-胡蘿蔔素組(β-carotene, n=12),蕃茄紅素組(lycopene, n=10)木質黃素組(lutein, n=8),4,4'-二酮-β-胡蘿蔔素組(canthaxanthin, n=9)和混合組(mixed carotenoids, n=10, 0.025% each)。第1至4週各組先以0.5%DMBA(9,10-dimethyl 1,2-benz-anthracene)礦物油為誘癌物質,塗抹於倉鼠右側口頰內側,每週各塗抹三次,每次塗抹0.3毫升,第5週至第16週致癌物的投予改為檳榔嚼塊萃取物,投予劑量亦為0.3毫升。實驗結果顯示實驗組血漿及肝臟各組類胡蘿蔔素濃度皆顯著上升。在抗氧化酵素(SOD & GPx)活性方面,蕃茄紅素組和混合組紅血球超氧化歧化?活性顯著低於對照組(p<0.05),木質黃素組,4,4'-二酮-β胡蘿蔔素和混合組肝臟麩胱甘?過氧化?活性顯著低於對照組;此外,在脂質過氧化產物(malondialdehyde, MDA)方面,混合組血漿MDA濃度顯著小於對照組(p<0.05),而肝臟MDA濃度則為類胡蘿蔔素各組皆小於對照組(p<0.05)。綜合上述,攝取類胡蘿蔔素能降低誘發性口腔癌症倉鼠體內脂質過氧化產物(malondialdehyde, MDA)的濃度,特別是蕃茄紅素、4,4'-二酮-β-胡蘿蔔素和混合類胡蘿蔔素。以口腔腫瘤數目及腫瘤負荷(tumor burden)之觀點評估類胡蘿蔔素的預防效果,蕃茄紅素、4,4'-二酮-β-胡蘿蔔素和混合類胡蘿蔔素有較佳的抑制效果。 |
英文摘要 | This study investigated the effects of consumption of various carotenoids on oral carcinogenesis and the activity of antioxidative enzymes in male hamsters. In the first 4 weeks, the right buccal pouch of each animal was daubed with 9,1 0-dimethyl-l ,2-benz-anthracene (DMBA) three times a week, and in the following 12 weeks the right buccal pouch was daubed with betel quid extract (BOE) and the rats were fed different experimental diets. Diets of the experimental groups were individually supplemented with 0, 1 % of β-carotene, lycopene, lutein, canthaxanthin, or equal amount of these four carotenoids (0,025% each) during the following 12 weeks. The results indicate that plasma and liver carotenoid levels of experimental groups were significantly higher than those of the control group (p < 0,05). Red blood cell (RBC) superoxide dismutase (SOD) activities of the lycopene and mixture groups were significantly lower than the control group, as was liver SOD activity of the canthaxanthin and mixture groups. Liver glutathione peroxidase (GPx) activities of the lutein, canthaxanthin, and mixture groups were significantly lower than that of the control group; however there was no difference between the activity of RBC GPx in each group. The plasma malondialdehyde (MDA) level in the mixture group was significantly lower than in the control group (p < 0.05); furthermore, hepatic MDA levels of the carotenoid treated groups were all significantly lower than that of the control group (p < 0,05). The number and volume of the tumor burden of the experimental groups were significantly lower than those of the control group. In conclusion, carotenoids provide an inhibitory capability on BQE-induced hamster oral carcinogenesis. The carotenoids significantly reduced the plasma and liver MDA levels and decreased the BQE-induced tumor burden in hamsters, especially in groups treated with lycopene, canthaxanthin, and a mixture of carotenoids. |
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