Nagasawa H, Fujii Y, Kageyama Y, Segawa T, Ben-Amotz A
Experimental Animal Research Laboratory, Meiji University, Kanagawa, Japan.
Anticancer Res. 1991 Mar-Apr;11(2):713-7.
We previously found that beta-carotene-rich algae Dunaliella bardawil markedly inhibited spontaneous mammary tumourigenesis of mice. This study was carried out to clarify whether D. bardawil inhibits the development or the progression or both of mammary tumours. A high mammary tumour strain of SHN virgin mice were given vitamin A deficient AIN-76TM diet supplemented with D. bardawil during the limited period of 3 months between 1-4 months of age (Experiment I: the stage of tumour development), 4-7 months (Experiment II: the stage of initiation and progression) or 7-10 months (Experiment III: the stage of progression). The concentration of beta-carotene in the diet was 5.1 x 10(-5)%. The respective controls received AIN-76TM diet containing retinyl palmitate (2.2 x 10(-4)%) during the same periods as in the experimental groups. Both the experimental and the control mice were fed a commercial diet during all other periods. The diets and tap water were provided ad libitum. In Experiment I, mammary tumour incidence was higher in the experimental group than in the control at all months examined except at 5 months of age, while the cause is not clear at present. Meanwhile, mammary tumourigenesis was significantly suppressed in the experimental mice compared to the controls in Experiments II and III. Whereas tumorous mice were higher than non-tumorous mice in blood levels of lactic acid and glucose in the control, mice given D. bardawil maintained the levels of non-tumorous mice even after the development of tumours. D. bardawil feeding also induced a higher glucose tolerance. All results strongly suggest that D. bardawil can inhibit the progression of spontaneous mammary tumours of mice by increasing the homeostatic potential of the host animals as well as by the well-known antioxidant function of beta-carotene in D. bardawil.
我们之前发现，富含β-胡萝卜素的藻类巴氏杜氏藻能显著抑制小鼠自发性乳腺肿瘤的发生。本研究旨在阐明巴氏杜氏藻是抑制乳腺肿瘤的发生、发展还是两者皆抑制。将高乳腺肿瘤品系的SHN处女小鼠在1至4月龄之间的3个月有限期内（实验I：肿瘤发生阶段）、4至7月龄（实验II：起始和进展阶段）或7至10月龄（实验III：进展阶段）给予缺乏维生素A的AIN - 76TM饮食，并补充巴氏杜氏藻。饮食中β-胡萝卜素的浓度为5.1×10(-5)%。各对照组在与实验组相同的时期内接受含有棕榈酸视黄酯（2.2×10(-4)%）的AIN - 76TM饮食。在所有其他时期，实验小鼠和对照小鼠均喂食商业饮食。饮食和自来水随意供应。在实验I中，除5月龄外，实验组在所有检查月份的乳腺肿瘤发生率均高于对照组，而目前原因尚不清楚。同时，与实验II和III中的对照组相比，实验小鼠的乳腺肿瘤发生受到显著抑制。在对照组中，肿瘤小鼠的血液乳酸和葡萄糖水平高于非肿瘤小鼠，而给予巴氏杜氏藻的小鼠即使在肿瘤发生后仍维持非肿瘤小鼠的水平。喂食巴氏杜氏藻还诱导了更高的葡萄糖耐量。所有结果强烈表明，巴氏杜氏藻可通过提高宿主动物的稳态潜能以及巴氏杜氏藻中β-胡萝卜素的众所周知的抗氧化功能来抑制小鼠自发性乳腺肿瘤的进展。
