Suppression by beta-carotene-rich algae Dunaliella bardawil of the progression, but not the development, of spontaneous mammary tumours in SHN virgin mice.
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.
Nagasawa
H
H
Experimental Animal Research Laboratory, Meiji University, Kanagawa, Japan.
Fujii
Y
Y
Kageyama
Y
Y
Segawa
T
T
Ben-Amotz
A
A
D000311:Adrenal Glands / Q000503:physiopathology; D000818:Animals; D000970:Antineoplastic Agents; D001786:Blood Glucose / Q000378:metabolism; D002338:Carotenoids / Q000627:therapeutic use*; D000460:Chlorophyta; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005260:Female; D005527:Food, Fortified; D005951:Glucose Tolerance Test; D007328:Insulin / Q000097:blood; D007773:Lactates / Q000097:blood; D008099:Liver / Q000503:physiopathology; D008325:Mammary Neoplasms, Experimental / Q000473:pathology* / Q000503:physiopathology / Q000517:prevention & control; D051379:Mice; D008815:Mice, Inbred Strains; D009367:Neoplasm Staging; D009929:Organ Size; D010053:Ovary / Q000503:physiopathology; D010903:Pituitary Gland, Anterior / Q000503:physiopathology; D011230:Precancerous Conditions / Q000473:pathology; D019207:beta Carotene
D000970:Antineoplastic Agents; D001786:Blood Glucose; D005230:Fatty Acids, Nonesterified; D007328:Insulin; D007773:Lactates; D019207:beta Carotene; D002338:Carotenoids