CANCER CELLS
Cell Studies
Apigenin
(1 micromole = one-thousandth of a gram-molecule)
1. This study suggests that 60 micromoles of the flavonoids apigenin, quercetin, myricetin, and kaempferol induced cell death in leukaemic cells.
Eur J Cancer 1999 Oct;35(10):151725
Induction of apoptosis by apigenin and related flavonoids through cytochrome c release and activation of caspase9 and caspase3 in leukaemia HL60 cells.
Wang IK, LinShiau SY, Lin JK
2. Dosages of apigenin in amounts (12.5 to 50 micromoles) may inhibit the growth of thyroid cancer cells.
Anticancer Res 1999 SepOct;19(5B):4297303
Signal pathways involved in apigenin inhibition of growth and induction of apoptosis of human anaplastic thyroid cancer cells (ARO).
Yin F, Giuliano AE, Van Herle AJ
ELLAGIC ACID
Animal Study
3. Rats were fed a diet comprised of 5 and 10% lyophilized black raspberries (LBRs) for 2 weeks before being exposed to a cancer inducing agent. This treatment lessened the proliferation of tumors. When LBRs were fed following the exposure to the carcinogen, proliferation of tumors was again inhibited, the number of tumors was reduced as was lesion development.
Cancer Res. 2001 Aug 15;61(16):6112-9.
Chemoprevention of esophageal tumorigenesis by dietary administration of lyophilized black raspberries.
Kresty LA, Morse MA, Morgan C, Carlton PS, Lu J, Gupta A, Blackwood M, Stoner GD.
4. Ellagic acid (100 mg/kilogram body weight per day) and Vitamin E (100 mg/kilogram body weight per day) were found to have an anticarcinogenic effect against toxin exposure in mice.
Cancer Letters ( CANCER LETT. ) (Ireland) 1995, 91/1 (139-144)
Inhibitory effects of vitamin E and ellagic acid on 8-hydroxydeoxyguanosine formation in liver nuclear DNA of rats treated with 2-nitropropane
Takagi A.; Sai K.; Umemura T.; Hasegawa R.; Kurokawa Y.
MILK THISTLE/SILYMARIN
(ppm = parts per million)
5. Rats were fed a diet containing silymarin (100 and 500 ppm)) for 1 week before being exposed to carcinogens which decreased cancer cell proliferation and increased cancer cell death.
Carcinogenesis. 2002 May;23(5):787-94. (Animal Study)
Dietary silymarin suppresses 4-nitroquinoline 1-oxide-induced tongue carcinogenesis in male F344 rats.
Yanaida Y, Kohno H, Yoshida K, Hirose Y, Yamada Y, Mori H, Tanaka T.
Animal Study
6. Doses of silibinin (100 and 200 mg/kilogram body weight/day) could have cancer preventive effects on liver, lung, stomach, skin and small bowel tissue in mice.
Carcinogenesis. 1999 Nov;20(11):2101-8.
Tissue distribution of silibinin, the major active constituent of silymarin, in mice and its association with enhancement of phase II enzymes: implications in cancer chemoprevention.
Zhao J, Agarwal R.
Animal Study
7. Doses of silymarin (3 mg, 6 mg and 12 mg), given prior to exposure to carcinogens resulted in fewer tumors, less proliferation of tumors and smaller tumor volume. Silymarin provided a significant level of protection from carcinogenics.
Cancer Res. 1999 Feb 1;59(3):622-32.
A flavonoid antioxidant, silymarin, affords exceptionally high protection against tumor promotion in the SENCAR mouse skin tumorigenesis model.
Lahiri-Chatterjee M, Katiyar SK, Mohan RR, Agarwal R.
N-acetyl L-cysteine (NAC)
(1 micromole = one-thousandth of a gram-molecule)
Cell Study
8. Administration of N-acetylcysteine (30 micromoles) protected cells from injury when exposed to ionizing radiation.
Cancer Res. 2003 Jun 15;63(12):3413-7.
2-Deoxy-D-glucose-induced cytotoxicity and radiosensitization in tumor cells is mediated via disruptions in thiol metabolism.
Lin X, Zhang F, Bradbury CM, Kaushal A, Li L, Spitz DR, Aft RL, Gius D.
Animal Study
9. Mice ingesting N-acetylcysteine (12.25 millimoles per kilogram body weight) were injected with malignant cells. Their survival time following injection was higher than the control group and there was less cancer cell proliferation and metastasis.
Inhibition by oral N-acetylcysteine of doxorubicin-induced clastogenicity and alopecia, and prevention of primary tumors and lung micrometastases in mice.
D'Agostini F, Bagnasco M, Giunciuglio D, Albini A, De Flora S.
Int J Oncol 1998 Aug;13(2):217-24 |
