Nutritional factors play an important role in the prevention and promotion of colorectal cancer. Vitamin E is a generic term that describes a group of lipid-soluble chain-breaking antioxidants that includes tocopherols and tocotrienols. Vitamin E occurs in nature as eight structurally related forms that include four tocopherols and four tocotrienols. Vitamin E is a potent membrane-soluble antioxidant. Antioxidants like vitamin E (tocopherols) may prevent colon cancer through several different cellular and molecular mechanisms. Vitamin E in the American diet is primarily available in plant-oil rich foods such as vegetable oils, seeds and nuts and these foods vary widely in their content of α-tocopherol and γ-tocopherol [1]. Vitamin E may help prevent colon cancer by decreasing the formation of mutagens arising from the oxidation of fecal lipids, by decreasing oxidative stress in the epithelial cells of the colon and by molecular mechanisms that influence cell death, cell cycle and transcriptional events. Most epidemiological, experimental and clinical studies have evaluated the α-isoform and not the γ-isoform of vitamin E. Recent epidemiological, experimental and mechanistic evidence suggests that γ-tocopherol may be a more potent cancer chemopreventive agent than α-tocopherol. The differences in chemical reactivity, metabolism and biological activity may contribute to these differences in the effects of γ-tocopherol when compared with α-tocopherol. The rationale supporting the development of γ-tocopherol as a colorectal cancer preventive agent is reviewed here.

This review will focus on the therapeutic uses of antioxidant liposomes. Antioxidant liposomes have a unique ability to deliver both lipid- and water-soluble antioxidants to tissues. This review will detail the varieties of antioxidants which have been incorporated into liposomes, their modes of administration, and the clinical conditions in which antioxidant liposomes could play an important therapeutic role. Antioxidant liposomes should be particularly useful for treating diseases or conditions in which oxidative stress plays a significant pathophysiological role because this technology has been shown to suppress oxidative stress. These diseases and conditions include cancer, trauma, irradiation, retinotherapy or prematurity, respiratory distress syndrome, chemical weapon exposure, and pulmonary infections.

The purpose of this investigation was to determine how dietary levels of α-tocopherol, γ-tocopherol and iron influence oxidative stress and ras-p21 levels in the colon. Rats were fed diets deficient in tocopherols (-E) or supplemented with either 0.156 mmol of α-tocopherol (AE)/kg diet or 0.156 mmol of γ-tocopherol (GE)/kg of diet. Half the rats in each of these three groups received dietary iron at a level of 35 mg/kg diet and the other half at eight times this level (280 mg/kg diet). Rats fed the AE diets had higher levels of Vitamin E in feces, colonocytes, plasma and liver than did rats fed the GE diets. Dietary iron levels did not influence tocopherol levels in plasma, liver or feces. For colonocytes, high dietary iron decreased tocopherol levels. The ratio of γ-tocopherol (in the GE groups) to α-tocopherol (in the AE groups) was 0.13 for plasma, 0.11 for liver, 0.28 for colonocytes and 0.51 for feces. The plasma ratio is not, therefore, predictive of the ratio in colonocytes and feces. High levels of dietary iron increased levels of fecal lipid hydroperoxides. Moreover, rats fed the GE diets had lower levels of fecal lipid hydroperoxides than rats fed the AE diets. The levels of ras-p21 were significantly lower in rats fed the GE diets compared with rats fed the AE diets. The γ-tocopherol may, therefore, play a significant role in preventing colon cancer. High levels of dietary iron were found to promote oxidative stress in feces and colonocytes.