Effects of beta-carotene-rich algae Dunaliella bardawil on the dynamic changes of normal and neoplastic mammary cells and general metabolism in mice.
As a possible step to estimate the mechanism of the inhibitory role of Dunaliella bardawil (Db) in the initial progression of spontaneous mammary tumours of SHN virgin mice, the DNA synthesizing enzyme activities and the in vivo 31P-NMR spectroscopy of normal and neoplastic mammary cells were examined in mice fed Db. The blood levels of glucose and free fatty acids and 1H-NMR spectroscopy of serum or urine were also studied in these animals to check the general metabolic background. Beginning at 4 months of age, the experimental and the control mice were given a vitamin A deficient AIN-76TM diet supplemented with Db (the concentration of beta-carotene was 5.1 x 10(-5)%) and AIN-76TM diet containing retinyl palmitate (2.2 x 10(-4)%), respectively, until 3 weeks after mammary tumour appearance (tumourous) or 9 months of age (non-tumourous). An increasing rate of thymidine kinase activity in mammary tumour was decreased by Db, while the thymidylate synthetase activity was affected little by the treatment. Lipid synthesis was accelerated by Db in normal mammary cells; however, no difference was observed between the experimental and the control groups in energy and lipid metabolism of mammary tumour cells. The growth of preneoplastic mammary hyperplastic alveolar nodules was also enhanced by Db. Db prevented an increase of blood levels of glucose and free fatty acids and a decrease of cholin plus phosphorylcholin level after tumour appearance. Liver weights of mice given Db were greater than those of the control in both the tumourous and non-tumourous groups. Db had little effect on the urinary component levels before and after the appearance of mammary tumours. These results indicate that Db promotes the growth of normal mammary gland cells, but inhibits that of neoplastic cells, and that the inhibitory effect of Db on mammary tumour progression is due to its normalizing both the organ specific and the general metabolism.
Fujii
Y
Y
Experimental Animal Research Laboratory. Meiji University, Kanagawa, Japan.
Sakamoto
S
S
Ben-Amotz
A
A
Nagasawa
H
H
D000818:Animals; D016588:Anticarcinogenic Agents / Q000627:therapeutic use*; D001786:Blood Glucose / Q000378:metabolism*; D002338:Carotenoids / Q000032:analysis / Q000627:therapeutic use*; D000460:Chlorophyta / Q000737:chemistry*; D004247:DNA / Q000096:biosynthesis; D005230:Fatty Acids, Nonesterified / Q000097:blood*; D005260:Female; D008099:Liver / Q000033:anatomy & histology / Q000187:drug effects; D009682:Magnetic Resonance Spectroscopy / Q000379:methods; D008321:Mammary Glands, Animal / Q000187:drug effects* / Q000201:enzymology / Q000378:metabolism; D008325:Mammary Neoplasms, Experimental / Q000201:enzymology / Q000378:metabolism / Q000517:prevention & control*; D051379:Mice; D008815:Mice, Inbred Strains; D009929:Organ Size / Q000187:drug effects; D010758:Phosphorus; D011230:Precancerous Conditions / Q000201:enzymology / Q000378:metabolism / Q000517:prevention & control; D013937:Thymidine Kinase / Q000378:metabolism; D013940:Thymidylate Synthase / Q000378:metabolism; D014556:Urine / Q000737:chemistry; D019207:beta Carotene
D016588:Anticarcinogenic Agents; D001786:Blood Glucose; D005230:Fatty Acids, Nonesterified; D019207:beta Carotene; D010758:Phosphorus; D002338:Carotenoids; D004247:DNA; D013940:Thymidylate Synthase; D013937:Thymidine Kinase