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Retinoic Acid Vitamin A, Beta Carotine


1. 2/5/02 Vitamin A Healthwell Notes What does it do? Vitamin A helps cells reproduce normally-a process called differentiation. Cells that have not properly differentiated are more likely to undergo precancerous changes. Vitamin A, by maintaining healthy cell membranes, helps prevent invasion by disease-causing microorganisms. Vitamin A also stimulates immunity and is needed for formation of bone, protein, and growth hormone. Beta-carotene is a substance from plants that the body can convert to vitamin A.
   
   
2. 2/5/02 Beta Carotine - Healthwell Notes What does it do? Beta-carotene is a substance from plants the body converts into vitamin A; it also acts as an antioxidant and an immune system booster. Other members of the antioxidant carotene family include cryptoxanthin, alpha-carotene, zeaxanthin, lutein, and lycopene. However, unlike beta-carotene, most of these nutrients do not convert to significant amounts of vitamin A How do natural and synthetic beta-carotene differ? Most beta-carotene in supplements is synthetic, consisting of only one molecule called all trans beta-carotene. Natural beta-carotene found in food is made of two molecules-all trans beta-carotene and 9-cis beta-carotene Despite the overlap between natural and synthetic forms, natural beta-carotene may possibly have activity that is distinct from the synthetic form. For example, the natural form has antioxidant activity the synthetic form has been reported to lack in both animals9 and people.10 Also, in one trial, pre-cancerous changes in people reverted to normal tissue with natural beta-carotene supplements, but not with synthetic supplements.11
   
   
3. 2/5/02 Avoiding Vitamin A Toxicity LEF
   
   
4. 2/5/02 Source of Natural Beta Carotine
   
   
5. 2/5/02 Inhibition of Caco-2 cell proliferation by all-trans retinoic acid: role of insulin-like growth factor binding protein-6. J Cell Physiol 2002 Jan;190(1):92-100 PMID: 11807815 The present study examined the effects of all-trans retinoic acid (tRA) on proliferation and expression of the IGF system in Caco-2 human colon adenocarcinoma cells. tRA inhibited Caco-2 cell proliferation in a dose-dependent manner, with a 40 +/- 2% decrease in cell number observed 48 h after the addition of 1 microM tRA Increased expression of IGFBP-6, which has a high binding affinity for IGF-II, following tRA treatment suggests that the decreased proliferation caused by tRA may result, at least in part, from IGFBP-6-mediated disruption of the IGF-II autocrine loop in these colon cancer cells.
   
   
6. 2/5/02 Retinoic acids reduce matrilysin (matrix metalloproteinase 7) and inhibit tumor cell invasion in human colon cancer Tumour Biol 2001 Jul-Aug;22(4):247-53 PMID: 11399950 All-trans retinoic acid (ATRA), 9-cis retinoic acid and 13-cis retinoic acid are naturally occurring retinoids used in the prevention and therapy of various preneoplastic and neoplastic diseases. It was previously reported that matrilysin, one of the matrix metalloproteinases (MMP-7), plays a critical role in the invasion and metastasis of gastrointestinal cancers. Moreover, it has been shown that ATRA downregulates matrilysin expression and prevents in vitro invasion by colon cancer cells These data support the use of retinoic acids as useful reagents to manage patients with colorectal carcinoma
   
   
7. 2/5/02 Differential effects of retinoic acid on growth and apoptosis in human colon cancer cell lines associated with the induction of retinoic acid receptor beta Biochem Pharmacol 2000 Mar 1;59(5):485-96 PMID: 10660115 Retinoids are well known as potential chemopreventive and chemotherapeutic agents against a variety of human cancers. Here, we report that retinoic acid (RA) induced differential growth inhibition in human colon cancer cell lines: while DLD-1, HT-29, and WiDr were relatively resistant, HCT-15 and Colo201 were relatively sensitive. All-trans-retinoic acid caused morphological and biochemical changes such as membrane shrinkage, chromatin condensation, and DNA cleavage, which are typical features of cells undergoing apoptosis in sensitive cell lines
   
   
8. 2/5/02 Effect of retinoids on AOM-induced colon cancer in rats: modulation of cell proliferation, apoptosis and aberrant crypt foci. Carcinogenesis 1999 Feb;20(2):255-60 PMID: 10069462 We have previously reported that the retinoids, 4-(hydroxyphenyl)retinamide (4-HPR) and 9-cis-retinoic acid (RA) prevented azoxymethane (AOM)-induced colon tumors and along with 2-(carboxyphenyl)retinamide (2-CPR) prevented aberrant crypt foci (ACF). In this study, we evaluated the effect of 2-CPR on AOM-induced colon tumors and the effect of the three retinoids on apoptosis and cell proliferation. Unlike the demonstrated prevention of colon cancer by the other two retinoids, both dosing schedules of 2-CPR resulted in an approximate doubling of the yield of colon tumors. Hence, unlike the other two retinoids, 2-CPR, although very potent in preventing ACF, enhanced rather than prevented AOM-induced colon cancer. Furthermore, our results suggest that the effect of 2-CPR on tumor yield is different from 4-HPR and 9-cis-RA because, unlike them, it does not enhance apoptosis
   
   

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