Effects of supplemental alpha-tocopherol and beta-carotene on colorectal cancer: results from a controlled trial (Finland)
ABSTRACT Some epidemiological investigations suggest that higher intake or biochemical status of vitamin E and beta-carotene might be associated with reduced risk of colorectal cancer.
We tested the effects of alpha-tocopherol and beta-carotene supplementation on the incidence of colorectal cancer in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) Study, a double-blind, placebo-controlled trial among 29,133 50-69-year-old male cigarette smokers. Participants were randomly assigned to receive alpha-tocopherol (50 mg), beta-carotene (20 mg), both agents, or a placebo daily for 5-8 years. Incident colorectal cancers (n = 135) were identified through the nationwide cancer registry, and 99% were histologically confirmed. Intervention effects were evaluated using survival analysis and proportional hazards models.
Colorectal cancer incidence was somewhat lower in the alpha-tocopherol arm compared to the no alpha-tocopherol arm, but this finding was not statistically significant (relative risk (RR) = 0.78, 95% confidence interval (CI) 0.55-1.09; log-rank test p = 0.15). Beta-carotene had no effect on colorectal cancer incidence (RR = 1.05, 95% CI 0.75-1.47; log-rank test p = 0.78). There was no interaction between the two substances.
Our study found no evidence of a beneficial or harmful effect for beta-carotene in colorectal cancer in older male smokers, but does provide suggestive evidence that vitamin E supplementation may have had a modest preventive effect. The latter finding is in accord with previous research linking higher vitamin E status to reduced colorectal cancer risk.
- SourceAvailable from: fresenius-kabi.es
Article: sobre el GALT
- [Show abstract] [Hide abstract]
ABSTRACT: Valproic acid (VPA) is a widely used antiepileptic medication and has teratogenic effects in both animals and humans. The objective of the current study was to investigate the effects of vitamin E (Vit-E) on VPA induced cytogenotoxicity and hepatotoxicity in male albino mice (Mus musculus). Genotoxicity and cytotoxicity were evaluated by bone marrow chromosomal aberration assay and mitotic index respectively, while hepatic dysfunctions were evaluated by light and electron microscopy. 80 mice were used, they were divided into eight groups, group one (G1) served as negative control group and the other seven groups were administered VPA and Vit-E as follows: G2 received VPA (100 mg/kg) and G3–G5 received Vit-E at doses 50, 100 and 200 mg/kg respectively for 21 days. While the treated groups (G6–G8) were administrated with Vit-E in concomitant with VPA for 21 days. The positive control animals administered VPA alone showed toxic histological and genetical manifestations (at P < 0.05). All the histological alterations in liver were greatly abated using Vit-E with significant reduction in chromosomal aberrations and elevation in mitotic index (P < 0.05). On the basis of the present results, Vit-E at dose 100 mg/kg appeared more potent in exerting the ameliorative effect.The Journal of Basic & Applied Zoology. 05/2014;
- [Show abstract] [Hide abstract]
ABSTRACT: Background Obesity and related metabolic abnormalities, including excess oxidative stress and chronic inflammation, are associated with colorectal carcinogenesis. Astaxanthin, a xanthophyll carotenoid found in aquatic animals, is known to possess antioxidant, anti-inflammatory, and antineoplastic properties. The present study examined the effects of astaxanthin on the development of azoxymethane (AOM)-induced colonic premalignant lesions in C57BL/KsJ-db/db (db/db) obese mice.Method Male db/db mice were administered 4 weekly subcutaneous injections of AOM (15 mg/kg body weight) from 5 weeks of age and subsequently, from 1 week after the last injection of AOM, were fed a diet containing 200 ppm astaxanthin throughout the experiment (8 weeks).ResultThe development of colonic premalignant lesions, i.e., aberrant crypt foci and ß-catenin accumulated crypts, was significantly inhibited in mice treated with astaxanthin than in mice fed the basal diet. Astaxanthin administration markedly reduced urinary levels of 8-OHdG and serum levels of d-ROMs, which are oxidative stress markers, while increasing the expression of mRNA for the antioxidant enzymes GPx1, SOD1, and CAT in the colonic mucosa of AOM-treated db/db mice. The expression levels of IL-1ß, IL-6, F4/80, CCL2, and CXCL2 mRNA in the colonic mucosa of AOM-treated mice were significantly decreased by astaxanthin. Dietary feeding with astaxanthin also resulted in a reduction in the numbers of NF-¿B- and PCNA-positive cells that were increased by AOM exposure, in the colonic epithelium.Conclusion These findings suggest that astaxanthin inhibits the development of colonic premalignant lesions in an obesity-related colorectal carcinogenesis model by reducing oxidative stress, attenuating chronic inflammation, and inhibiting NF-¿B activation and cell proliferation in the colonic mucosa. Astaxanthin, therefore, may be a potential candidate as a chemoprevention agent against colorectal carcinogenesis in obese individuals.BMC Gastroenterology 12/2014; 14(1):212. · 2.11 Impact Factor