Table 1.
Summary of the known and potential vitamin E effects on some non-communicable pathological conditions.
| Pathological Conditions | Reported Effect | References |
|---|---|---|
| Oxidative stress | Antioxidant by scavenging free radicals, especially peroxyl radicals, and singlet oxygen. | [2] |
| To maintain the integrity of long-chain polyunsaturated fatty acids in the membranes of cells and thus maintain their bioactivity. Maintaining the membranes integrity by inhibiting long-chain polyunsaturated fatty acids oxidation |
[10] | |
| Preserving mitochondrial efficiency | [4,6,15] | |
| Inflammation | Inhibition of inflammation mediators and related enzymes | [3,4,18,19] |
| Dysbiosis | Modulatory effect on gut microbiota | [30,31] |
| CVD | Reduction in atherosclerotic plaque formation, CVD outcomes, myocardial infraction, and ischemic stroke risks | [12,36] |
| Lowering of CD36 expression | [3,12,37] | |
| Elevation of blood pressure by αT or mixed tocopherols | [4] | |
| Reduction in platelets coagulation and aggregation with αT or γT supplementation | [4] | |
| Reduction in atherosclerosis progression with vitamin E and coenzyme Q supplementation | [4] | |
| Reduction in oxidized HODE in the hearts of α-TOH-treated mice | [36] | |
| αT administration causes anti-oxidative response following I/R damage | [36] | |
| Protective effect of αT on mitochondrial integrity | [12,36] | |
| Inhibition of COXs and 5-LOX by 13′-COOHs and αT | [3,4,7] | |
| Reduction in lipids oxidation in the myocardium by αT | [36,37] | |
| Reduction in CVD risk factors with vitamin E, C and L-arginine | [12] | |
| Reduction in ischemic heart disease risk using vitamin E, C, and/or vitamin A | [12] | |
| Reduction in apoptotic activity with vitamin E | [12] | |
| Diabetes | No relationship with αT serum levels | [43] |
| Lower αT plasma levels in subjects with T2DM | [44] | |
| No protective effect of vitamin E supplementation | [43,44,45] | |
| Protective effect against diabetes-induced complications | [46] | |
| Protective effect against diabetes-induced atherosclerosis | [49,50] | |
| Conflicting result about the protective effect against diabetes-induced atherosclerosis | [51] | |
| Protective effect against diabetes-induced nephropathy | [53,54] | |
| Protective effect against diabetes-induced retinopathy | [55,56,57,58] | |
| Lower vitamin E serum levels in people with diabetes-induced retinopathy | [56] | |
| Asthma | Protective effect of vitamin E maternal intake | [19,61,62] |
| Protective effect of vitamin E | [19,63,64] | |
| Breast cancer | Possible protective effect of vitamin E | [67] |
| Inverse association with breast cancer risk only for vitamin E dietary intake in postmenopausal women | [68] | |
| Inverse relationship between αT serum levels and ER+ breast cancer risk, but positive relationship with serum ẟT and conjugated γT. | [69] | |
| Lung cancer | No relationship with αT serum levels | [71] |
| No protective effect of vitamin E supplementation | [72] | |
| Inverse relationship between αT serum basal levels and lung cancer risk | [73] | |
| No protective effect of vitamin E supplementation | [73] | |
| Colorectal cancer | Lower vitamin E plasma levels in subjects with colorectal cancer (for Caucasian population) | [74] |
| No protective effect of vitamin E | [75,76] | |
| Inverse relationship between vitamin E intake and colorectal cancer risk, but no relationship with αT serum levels | [77] | |
| Prostate Cancer | Inverse relationship between αT serum levels and prostate risk, no relationship with γT | [79] |
| No protective effect of αT supplementation | [80] |