Effects of Vitamin E From Supplements and Diet on Colonicα- andγ-tocopherol Concentrations in Persons at Increased Colon Cancer Risk

Abstract

The available evidence indicates that γ-tocopherol has more potential for colon cancer prevention than α-tocopherol, but little is known about the effects of foods and supplements on tocopherol levels in human colon. This study randomized 120 subjects at increased colon cancer risk to either a Mediterranean or a Healthy Eating diet for six months. Supplement use was reported by 39% of the subjects, and vitamin E intake from supplements was 2-fold higher than that from foods. Serum α-tocopherol at baseline was positively predicted by dietary intakes of synthetic vitamin E in foods and supplements but not by natural α-tocopherol from foods. For serum γ-tocopherol, dietary γ-tocopherol was not a predictor, but dietary α-tocopherol was a negative predictor. Unlike with serum, the data supported a role for metabolic factors, and not a direct effect of diet, in governing concentrations of both α-and γ-tocopherol in colon. The Mediterranean intervention increased intakes of natural α-tocopherol, which is high in nuts, and decreased intakes of γ-tocopherol, which is low in olive oil. These dietary changes had no significant effects on colon tocopherols. The impact of diet on colon tocopherols therefore appears to be limited.

α-Tocopherol in breast milk of women with preterm delivery after a single postpartum oral dose of vitamin E

“…Maternal use of vitamin E supplements may also increase the body reserves of this micronutrient. Li et al (44) found that α-tocopherol supplements have a higher impact on tissue levels of α-tocopherol than dietary α-tocopherol. Studies on maternal supplementation of vitamin E after delivery and its effect on breast milk are scarce and inconclusive; some found a correlation between supplementation and breast milk α-tocopherol concentration and some did not (14) .…”

Association of serum γ-tocopherol levels with mortality: the Multiethnic Cohort Study

“…However, the IOM report points out the need for more research to determine the levels and types of tocopherols that are important for optimal nutrition and their mechanisms in the prevention of aging related chronic diseases. In particular, serum levels of γ-tocopherol appear to be independent of dietary intake and physiologically regulated [8], possibly as a consequence of chronic inflammation. This was suggested by the positive associations of γ-tocopherol with circulating C-reactive protein (CRP) and urinary isoprostane (both indicators of chronic inflammation) [9] as well as by animal and cell studies showing γ-tocopherol levels increase in response to inflammation [10, 11].…”

Tumour Microenvironment Stress Promotes the Development of Drug Resistance

“…The antioxidant approach aims at scavenging ROS in cancer cells, thus inhibiting pro-survival signalling [230]. This approach includes dietary and supplementary antioxidants [231][232][233][234][235], glutathione (GSH)-inducing phytochemicals [236,237], NADPH oxidase inhibitors [238] or modifying cyclic nitroxides, which present a group of stable radicals with strong antioxidant properties [239]. Conversely, a pro-oxidant approach boosts ROS to cytotoxic levels, overcoming antioxidant systems and inducing cancer cell death [230,240].…”

“…Antioxidant approach intake of antioxidants vitamins A [231], C [232] [233] and E [234], selenium [235] NADPH oxidase inhibition histamine [238] GSH induction sulforaphane [236,237] nitroxide compound manipulation tempol [239] Pro-oxidant approach ROS generation arsenic trioxide [249], imexon [248], doxorubicin, daunorubicin [250], cisplatin, oxaliplatin [251], sunitinib [252], gefitinib, erlotinib [253], trastuzumab [254], bevacizumab [255] GSH depletion β-phenylethyl isotiocyanate [241], buthionine sulfoximine [242] thioredoxin inhibition PX-12 [243], motexafin gadolinium [244] superoxide dismutase inhibition 2-methoxyestradiol [245], ATN-224 [246], disulfiram [247] In this regard, efforts have been made to develop anti-cancer therapeutics specifically targeting the HIF-1α regulation pathway, which is crucial for the survival of tumour cells. Multiple methods of targeting HIF-1α have been explored, including inhibition of HIF-1α (i) mRNA expression [257], (ii) protein synthesis [258][259][260][261][262][263][264][265][266], (iii) stabilisation [267][268][269][270], (iv) dimerization [271], (v) DNA binding [272], (vi) transcriptional activity…”