Antioxidant; DL-alpha-Tocopherol does not bind to a specific protein receptor but rather exerts its primary effects through non-specific interactions with lipid bilayers and free radical species. Its primary mechanism involves scavenging reactive oxygen species (ROS) and reactive nitrogen species (RNS), thereby preventing oxidative damage to polyunsaturated fatty acids within cell membranes. Additionally, DL-alpha-tocopherol has been associated with the ferroptosis pathway, where it functions as an inhibitor of lipid peroxidation, a key process in ferroptotic cell death. It also modulates gene expression and enzyme activities involved in inflammation and cell signaling, though these effects are indirect consequences of its antioxidant function.

In vitro studies have demonstrated multiple activities of DL-alpha-tocopherol. At 20 μM, it inhibits brominated diphenyl ether-47-induced increases in reactive oxygen species (ROS) and prostaglandin E2 (PGE2) production in HTR-8/SVneo cells. In HepG2 cells, DL-alpha-tocopherol inhibits lipid peroxidation with an IC50 of 24.5 μM. It protects human skin fibroblasts from UVB-induced cytotoxicity in a dose-dependent manner at concentrations of 10-1000 μg/mL, increasing the mean lethal dose (D0) of UV radiation. This protective effect is attributed to inhibition of UV-induced lipid peroxidation, as evidenced by reduced malondialdehyde (MDA) production. In human umbilical vein endothelial cells (HUVECs), DL-alpha-tocopherol (50-200 μmol/L) inhibits oxidized low-density lipoprotein (oxLDL)-induced expression of intercellular adhesion molecule-1 (ICAM-1) at both protein and mRNA levels in a concentration-dependent manner.

---

The effect of dl-alpha-tocopherol on ultraviolet light, 280-320 nm (UVB)-induced damage of human skin fibroblasts was studied by measuring the colony-forming ability, unscheduled DNA synthesis (UDS) and malondialdehyde (MDA) production. Regarding the cell toxicity, the values of the mean lethal dose (D0) of UV in fibroblast strains from 5 normal subjects were examined. D0 increased dose-dependently when the cells were cultured in the presence of dl-alpha-tocopherol at the concentration of 10-1000 micrograms/ml. UDS induced by 500 J/m2 UVB irradiation was not altered by treatment of 100 micrograms/ml dl-alpha-tocopherol. MDA did not increase after 500 J/m2 UVB irradiation in the fibroblasts cultured with 100 micrograms/ml dl-alpha-tocopherol, while MDA in the fibroblasts cultured without dl-alpha-tocopherol increased after irradiation. These results suggest that dl-alpha-tocopherol protects human skin fibroblasts against the cytotoxic effect of UVB, and its mechanism seems to be related to inhibition of UV-induced lipid peroxidation or to the antioxidation effect of dl-alpha-tocopherol [1].

In vivo studies have established that DL-alpha-tocopherol effectively increases alpha-tocopherol concentrations in plasma and various tissues. In sheep fed dl-alpha-tocopheryl acetate-supplemented diets (200-600 mg/sheep), tocopherol concentrations were significantly higher in all tissues (P < 0.001) compared to basal diet controls, with liver vitamin E storage showing a linear response to dietary vitamin E levels. In piglet studies, supplementation with DL-alpha-tocopherol resulted in measurable alpha-tocopherol accumulation in serum, muscle, subcutaneous fat, and liver, although natural D-alpha-tocopherol (RRR stereoisomer) demonstrated higher bioavailability and preferential tissue retention compared to the synthetic racemic mixture. Comparative studies in sheep showed that dl-alpha-tocopherol acetate has greater bioavailability than dl-alpha-tocopherol nicotinate, and the route of administration significantly affects availability (P < 0.001).

---

To investigate the in vivo effect of short-term, moderate dosage synthetic dl-alpha-tocopherol acetate supplementation on platelet aggregation, coagulation profile, and simulated bleeding time in healthy individuals. alpha-tocopherol is the most biologically active isomer of Vitamin E, traditionally promoted as an antioxidant and therapeutic agent in cardiovascular disease. In vitro studies have suggested that alpha-tocopherol plays a role in the inhibition of platelet aggregation. However, further investigations into the effect of alpha-tocopherol on bleeding in vivo have not duplicated these findings. A total of 42 healthy volunteers complied with a 2-week abstinence period from the use of anti-platelet agents followed by determination of baseline platelet aggregation properties and coagulation studies using citrated whole blood. Moderate dosage Vitamin E (800 IU of dl-alpha-tocopherol acetate) was then self-administered for 14 days with reevaluation of platelet aggregation and coagulation profile, and simulated bleeding time after 14 days of Vitamin E supplementation. Forty subjects completed the 4-week study period. All 40 subjects demonstrated normal baseline coagulation studies and all had collagen-stimulated platelet aggregation assessment performed in triplicate. After Vitamin E supplementation, no significant difference was demonstrated in any study parameter. Dietary supplementation with moderate dosage synthetic dl-alpha-tocopherol acetate did not significantly prolong bleeding or platelet aggregation in vivo. The affect of Vitamin E on platelet aggregation in vitro does not appear to be reproducible in vivo. Therefore, peri-operative discontinuation of Vitamin E may not be necessary [2].

DL-alpha-Tocopherol is not typically evaluated in conventional enzyme/receptor binding assays due to its primary mechanism of action as a free radical scavenger rather than a specific enzyme inhibitor. However, cell-free antioxidant activity can be assessed using chemical assays such as the DPPH (2,2-diphenyl-1-picrylhydrazyl) radical scavenging assay, ABTS (2,2'-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid)) assay, or lipid peroxidation inhibition assays in artificial membrane systems. A typical protocol for assessing lipid peroxidation inhibition: Prepare liposomes from soybean phosphatidylcholine, induce lipid peroxidation using Fe²⁺/ascorbate or AAPH (2,2'-azobis(2-amidinopropane) dihydrochloride), and measure malondialdehyde (MDA) production using the thiobarbituric acid reactive substances (TBARS) assay. DL-alpha-Tocopherol is added at varying concentrations (1-100 μM) to determine IC50 values.

A standard protocol for evaluating DL-alpha-tocopherol in cell culture is as follows: Seed cells (e.g., HTR-8/SVneo, HepG2, or HUVECs) in appropriate culture medium at 37°C in 5% CO₂. After reaching 70-80% confluence, treat cells with DL-alpha-tocopherol at concentrations ranging from 10-200 μM (or 10-1000 μg/mL) for 24-48 hours. For oxidative stress studies, pre-incubate cells with DL-alpha-tocopherol for 2-24 hours before exposure to oxidative stressors such as UVB radiation, oxLDL (50 μg/mL), or brominated diphenyl ether-47. Assess cellular oxidative stress markers including ROS production (using DCFH-DA probe), MDA levels (TBARS assay), and PGE2 production (ELISA). Cell viability can be evaluated using MTT assay or colony-forming ability assay. For IC50 determination, treat HepG2 cells with increasing concentrations of DL-alpha-tocopherol and measure lipid peroxidation inhibition.

A typical in vivo protocol for DL-alpha-tocopherol involves dietary supplementation studies in animal models. For sheep studies: Administer dl-alpha-tocopheryl acetate mixed into the basal diet at doses ranging from 25-600 mg/sheep/day for 8 weeks. Collect blood samples at baseline and twice weekly thereafter. At the end of the study (8 weeks), euthanize animals and collect tissues (liver, heart, muscle, adipose tissue) for alpha-tocopherol analysis using HPLC. For piglet studies: Supplement sows with either natural micellized D-alpha-tocopherol (low dose) or synthetic DL-alpha-tocopherol (threefold higher dose) in feed during gestation and lactation. Collect serum samples from piglets at days 2, 14, and 28 postpartum, and tissue samples (muscle, subcutaneous fat, liver) at day 39 of age for stereoisomer analysis by HPLC. For bioavailability comparisons: Administer a single dose of dl-alpha-tocopherol acetate or nicotinate via intraruminal or intraperitoneal routes, collect blood samples over 180 hours, and fit curves to plasma alpha-tocopherol concentration values.

---

A total of 42 healthy volunteers complied with a 2-week abstinence period from the use of anti-platelet agents followed by determination of baseline platelet aggregation properties and coagulation studies using citrated whole blood. Moderate dosage Vitamin E (800 IU of dl-alpha-tocopherol acetate) was then self-administered for 14 days with reevaluation of platelet aggregation and coagulation profile, and simulated bleeding time after 14 days of Vitamin E supplementation. Results: Forty subjects completed the 4-week study period. All 40 subjects demonstrated normal baseline coagulation studies and all had collagen-stimulated platelet aggregation assessment performed in triplicate. After Vitamin E supplementation, no significant difference was demonstrated in any study parameter. Conclusions: Dietary supplementation with moderate dosage synthetic dl-alpha-tocopherol acetate did not significantly prolong bleeding or platelet aggregation in vivo. The affect of Vitamin E on platelet aggregation in vitro does not appear to be reproducible in vivo. Therefore, peri-operative discontinuation of Vitamin E may not be necessary.[2]

Absorption, Distribution and Excretion
The 2R-stereoisomer is the only form of α-tocopherol that can be maintained in human plasma and tissues. An equal weight of natural or naturally sourced α-tocopherol (RRR α-tocopherol) has at least twice the activity of synthetic α-tocopherol. This is primarily because the half-stereoisomer of synthetic α-tocopherol cannot be maintained in human plasma and therefore lacks bioavailability.

---

DL-alpha-Tocopherol exhibits distinct pharmacokinetic properties as a fat-soluble vitamin. Absorption occurs in the small intestine and requires dietary fat, bile salts, and pancreatic enzymes for micelle formation. Following absorption, it is incorporated into chylomicrons and transported via the lymphatic system to the liver, where it is packaged into very-low-density lipoproteins (VLDL) for distribution to peripheral tissues. The synthetic DL form is less bioavailable than natural D-alpha-tocopherol due to the presence of non-RRR stereoisomers, which are preferentially metabolized and excreted. In piglet studies, supplementation with DL-alpha-tocopherol resulted in accumulation of RRS-, RSS-, and RSR-α-tocopherol stereoisomers, whereas natural D-alpha-tocopherol produced predominantly RRR-α-tocopherol (P < 0.001). The plasma elimination half-life of alpha-tocopherol ranges from approximately 48-72 hours in humans. Tissue distribution is widespread, with the highest concentrations found in the liver, adipose tissue, and adrenal glands. Excretion occurs primarily via the bile into feces, with minor urinary excretion of metabolites.

Toxicity Summary
Identification and Uses: dl-α-tocopherol is a slightly viscous, pale yellow oil. It is the synthetic form of α-tocopherol. An equal weight of natural α-tocopherol has at least twice the activity of the synthetic form. dl-α-tocopherol is used as an antioxidant in oils and animal feed. It is also used as an experimental drug and dietary supplement. Human Exposure and Toxicity: In a patch study of 23,908 patients, 219 (0.9%) had sunscreen as their allergen. The three most common allergens in sunscreen were benzophenone-3, dl-α-tocopherol, and fragrance blends. In healthy volunteers, supplementation with moderate doses of synthetic dl-α-tocopherol acetate did not significantly prolong bleeding or platelet aggregation time. Multiple studies have shown that dl-α-tocopherol can protect healthy volunteers from exercise-induced oxidative damage. In vitro studies have shown that dl-α-tocopherol broadly inhibits cell proliferation, with breast cancer cells and prostate cancer cells showing significantly higher sensitivity than erythroleukemia cells. Animal experiments: Chicks exposed to dl-α-tocopherol acetate for 3-8 weeks showed prolonged prothrombin time, increased reticulocyte count, and decreased hematocrit. Dl-α-tocopherol supplementation increased α-tocopherol concentration in dairy cows, but had little effect on reproductive efficiency. Adding dl-α-tocopherol to leukocyte cultures reduced the number of chromosome breaks induced by 7,12-dimethylbenzanthracene. Dl-α-tocopherol significantly reduced the mutagenic effects of malondialdehyde and β-propiolactone on five strains of Salmonella Typhimurium, all of which exhibited frameshift mutations.

---

Effects during pregnancy and lactation
◉ Overview of medication use during lactation
Vitamin E is a normal component of breast milk. Maternal obesity, smoking, and preterm birth (premature delivery before 37 weeks of gestation) are all associated with reduced vitamin E levels in breast milk. Lactating mothers may need vitamin E supplementation to reach the recommended daily intake of 19 mg. Compared to no vitamin E supplementation, daily administration of prenatal multivitamin supplements can safely and effectively increase vitamin E levels in breast milk and improve vitamin E status in breastfed infants. Higher daily doses have not been studied.
◉ Effects on breastfed infants
No relevant published information found as of the revision date.
◉ Effects on lactation and breast milk
No relevant published information found as of the revision date.

---

Interactions
Inflammatory bowel disease is often accompanied by iron deficiency anemia, which may require oral iron supplementation. However, iron supplementation may increase oxidative stress through the Fenton reaction, thereby exacerbating the condition. This study aimed to determine whether oral iron supplementation increased intestinal inflammation and oxidative stress in a rat model of colitis induced by dextran sulfate sodium (DSS), and whether the addition of the antioxidant vitamin E could mitigate this harmful effect. Rats were divided into four groups, each receiving water containing 50 g/L DSS for 7 days. Rats were fed the following diets: control group (unpurified diet containing 270 mg/kg iron and 49 mg/kg dl-α-tocopherol acetate); diet + iron group (containing 3000 mg/kg iron); diet + vitamin E group (containing 2000 mg/kg dl-α-tocopherol acetate); and diet + iron and vitamin E (at the same concentrations as the previous groups). Changes in body weight, rectal bleeding volume, histological score, plasma and colonic lipid peroxide (LPO), plasma 8-isoprostan, colonic glutathione peroxidase (GPx), and plasma vitamin E levels were measured in each group. Results showed that iron supplementation increased disease activity, manifested as increased histological score and rectal bleeding volume. This was associated with increased colonic and plasma LPO and 8-isoprostan levels, and decreased colonic GPx levels. Vitamin E supplementation reduced colonic inflammation and rectal bleeding but had no effect on oxidative stress, suggesting the existence of other mechanisms to reduce inflammation. In conclusion, oral iron supplementation led to increased disease activity in this colitis model. Vitamin E can mitigate this harmful effect on disease activity. Therefore, adding vitamin E to oral iron supplements may be beneficial. Previous studies have shown that β-carotene and α-tocopherol can synergistically inhibit the growth of experimentally induced oral cancer. Initial research on the synergistic anticancer activity of antioxidants has been extended to reduced glutathione and ascorbic acid. Sixty male hamsters (4-5 weeks old) were divided into six equal groups. Groups 1-6 were treated with 7,12-dimethylbenzo[a]anthracene (DMBA) (0.5% solution). Group 2 animals were orally administered an equal amount of a mixture of β-carotene, dl-α-tocopherol (vitamin E), glutathione, and L-ascorbic acid (vitamin C) (12.5 μg). Groups 3-6 were treated individually with β-carotene (50 μg), vitamin E (50 μg), glutathione (50 μg), and vitamin C (50 μg), respectively. Animals were sacrificed at weeks 12 and 14. Tumor size was counted and measured, and tumor burden was calculated for each experimental group. The antioxidant mixture significantly reduced tumor burden, while treatments with β-carotene, vitamin E, and reduced glutathione also reduced tumor burden. The chemopreventive effects of β-carotene and glutathione were superior to vitamin E alone. In contrast, vitamin C treatment did not produce an antitumor effect and instead led to an increase in tumor burden at week 14. This antioxidant mixture produced a significant synergistic chemopreventive effect against oral cancer.
Ferrous triacetate (Fe-NTA) is a potent nephrotoxic substance. This study investigated the regulatory effects of DL-α-tocopherol (vitamin E) on ferric triacetate (Fe-NTA)-induced oxidative stress, toxicity, and hyperproliferative responses in rat kidneys. Fe-NTA treatment enhanced the sensitivity of renal microsomal membranes to iron-ascorbic acid-induced lipid peroxidation and hydrogen peroxide production, accompanied by decreased activity of renal antioxidant enzymes (catalase, glutathione peroxidase, glutathione reductase, and glutathione S-transferase) and decreased renal glutathione levels. Parallel to these changes, a sharp increase in blood urea nitrogen and serum creatinine levels was observed. Furthermore, Fe-NTA treatment enhanced the activity of renal ornithine decarboxylase (ODC) and increased the incorporation of [(3)H]thymidine into renal DNA. Daily prophylactic treatment with vitamin E for one week prior to Fe-NTA administration reduced Fe-NTA-mediated damage. The sensitivity of renal microsomal membrane lipid peroxidation induced by iron-ascorbic acid and hydrogen peroxide generation was significantly reduced (P < 0.05). In addition, the decrease in glutathione levels and the inhibition of antioxidant enzyme activity were significantly restored to normal levels (P < 0.05). Similarly, the elevated blood urea nitrogen and serum creatinine levels, indicative of renal injury, decreased by approximately 50% under high-dose vitamin E treatment. Pretreatment of rats with vitamin E reduced Fe-NTA-mediated ODC activity induction and the enhancement of [(3)H]thymidine incorporation into DNA. The protective effect of vitamin E was dose-dependent. In summary, our data suggest that vitamin E is a potent nephrochemopreventive agent and may inhibit Fe-NTA-induced nephrotoxicity. Ultraviolet (UV) irradiation of C3H/HeN mice induces skin cancer and immunosuppression, thereby preventing host rejection of antigenic UV-induced tumors. This study evaluated the ability of topical vitamin E (dl-α-tocopherol) to prevent UV-induced photocarcinogenesis or immunosuppression. At 33 weeks after initial UV irradiation, the incidence of skin cancer in UV-irradiated mice was 81%; application of 25 mg vitamin E three times weekly to mice during the first three weeks of UV irradiation and throughout the experiment reduced the tumor incidence to 42% (p = 0.0065, log-rank test). The immunomodulatory effect of vitamin E was assessed by comparing the immunosuppressive levels of spleen cells from normal and UV-irradiated mice (regardless of whether topical vitamin E treatment was received). Transferring spleen cells from UV-irradiated mice to unirradiated mice prevented the recipient mice from rejecting UV-induced tumor attacks; however, spleen cells from UV-irradiated mice treated with vitamin E did not prevent the recipient mice from rejecting similar tumor attacks. Phenotypic analysis of spleen cells used in passive transfer experiments was performed using biotin-avidin-immunopyroxidase technology. The results showed that vitamin E treatment in mice exposed to ultraviolet (UV) radiation prevented UV-induced downregulation of Ia expression in spleen cells and increased the proportion of Lyt-2+ and L3T4+ spleen cells. Therefore, long-term vitamin E administration can effectively reduce UV-induced cancer incidence and immunosuppression. Inhibition of UV-induced downregulation of Ia expression may contribute to this immunomodulatory effect. For more complete data on interactions of dl-α-tocopherols (9 in total), please visit the HSDB record page.

---

: DL-alpha-Tocopherol is generally recognized as safe (GRAS) when used at recommended doses. The World Health Organization's Joint FAO/WHO Expert Committee on Food Additives (JECFA) established a group acceptable daily intake (ADI) of 0.15-2 mg/kg body weight for dl-alpha-tocopherol and d-alpha-tocopherol concentrate, singly or in combination. The lower value represents the daily dietary allowance recommended by the US National Academy of Sciences, while the upper value represents the maximum ADI. No-observed-adverse-effect levels (NOAEL) are significantly higher than the ADI. However, very high doses (typically >1000 mg/day in humans) may cause adverse effects including nausea, diarrhea, abdominal cramps, fatigue, and increased risk of bleeding due to antiplatelet activity. In animal studies, no apparent signs of toxicity have been observed at supplementation levels up to 600 mg/sheep/day or at the doses used in piglet studies. DL-alpha-Tocopherol has a wide safety margin, and acute toxicity is very low, with LD50 values in rodents exceeding 5000 mg/kg orally.

[1]. Protective effect of dl-alpha-tocopherol on the cytotoxicity of ultraviolet B against human skin fibroblasts in vitro. Photodermatol Photoimmunol Photomed. 1990 Aug;7(4):173-7.

[2]. Short-term, moderate dosage Vitamin E supplementation may have no effect on platelet aggregation, coagulation profile, and bleeding time in healthy individuals. J Surg Res. 2006 May;132(1):121-9.

2,5,7,8-Tetramethyl-2-(4,8,12-trimethyltetrazyl)-3,4-dihydro-2H-1-benzopyran-6-ol is a tocopherol. DL-α-Tocopherol has been reported in Albifimbria verrucaria, Sida acuta, and other organisms with relevant data. DL-α-Tocopherol is the synthetic form of vitamin E, a fat-soluble vitamin with powerful antioxidant properties. DL-α-Tocopherol is considered essential for stabilizing biological membranes, especially those rich in polyunsaturated fatty acids. It is a potent superoxide radical scavenger and can non-competitively inhibit cyclooxygenase activity in various tissues, thereby reducing prostaglandin production. Vitamin E can also inhibit angiogenesis and tumor dormancy by suppressing vascular endothelial growth factor (VEGF) gene transcription. (NCI04)
See also: α-Tocopherol (note moved to); Tocopherol (note moved to); Vitamin E (note moved to).

---

Therapeutic Use
Exploratory Treatment We evaluated the effect of vitamin E (dl-α-tocopherol) on mutagenicity levels in a randomized, placebo-controlled pilot trial. Briefly, we randomized outpatients with no clinical history of melanoma to receive either a daily vitamin E dietary supplement or placebo for 3 months. Plasma vitamin E and mutagenicity levels were measured at baseline and at the end of the 3-month trial. At baseline, we found no significant differences in plasma vitamin E and mutagenicity levels between the two groups. We also measured dietary intake at baseline and found that dietary vitamin E did not predict plasma vitamin E levels well. After 3 months of vitamin E supplementation, we found a significant increase in plasma α-tocopherol levels in the vitamin E supplementation group compared to the placebo group (P = 0.0005). We also found that, compared with the placebo group, plasma γ-tocopherol concentrations decreased in the vitamin E supplementation group, but the difference was not significant and the decrease was persistent. At baseline or 3 months after supplementation, we found no significant difference in mutagenic sensitivity levels between the vitamin E group and the placebo group. We conclude that short-term vitamin E supplementation, while increasing blood α-tocopherol levels, does not prevent bleomycin-induced chromosomal damage.
Exploratory treatment epidemiological studies have shown a negative correlation between vitamin E intake and cardiovascular disease (CVD) risk. In contrast, randomized controlled trials have yielded conflicting results regarding whether vitamin E supplementation can slow the progression of atherosclerosis and the incidence of cardiovascular events. This study included men and women aged ≥40 years with low-density lipoprotein cholesterol (LDL-C) levels ≥3.37 mmol/L (130 mg/dL) and no clinical signs or symptoms of cardiovascular disease. Eligible participants were randomly assigned to receive 400 IU DL-α-tocopherol daily or a placebo and were followed up every 3 months for a mean follow-up of 3 years. The primary endpoint was the rate of change in carotid intima-media thickness (IMT) of the distal common carotid artery, assessed using computed tomography-guided B-mode ultrasound. A mixed-effects model was used to test the hypothesis of differences in IMT rate of change between treatment groups using all IMT measurements. Compared with placebo, α-tocopherol supplementation significantly increased plasma vitamin E levels (P<0.0001), decreased circulating oxidized low-density lipoprotein (LDL) levels (P=0.03), and reduced LDL oxidative sensitivity (P<0.01). However, vitamin E supplementation did not slow the progression of carotid intima-media thickness (IMT) over 3 years compared with subjects randomly assigned to the placebo group. These results are consistent with previous randomized controlled trials and extend the conclusion that vitamin E supplementation has no effect on IMT progression in healthy men and women with low cardiovascular disease risk to IMT progression.
Exploratory treatment of elevated protein glycation and triglyceride (TG) levels are two major risk factors for the development of diabetic complications. Previous studies have found that supplementation with pharmacological doses (900-2000 IU/day) of vitamin E has certain benefits for patients with type 2 diabetes. This study aimed to investigate whether adequate vitamin E supplementation (100 IU/day) affects blood glucose, glycated hemoglobin (GHb), triglycerides (TG), or red blood cell count in patients with type 1 diabetes. A double-blind clinical trial enrolled 35 diabetic patients, who were given either DL-α-tocopherol (vitamin E) capsules (100 IU/day) or a placebo for 3 months. Fasting blood samples were collected from each diabetic patient before and after vitamin E supplementation or placebo administration. Paired t-tests and Wilcoxon signed-rank tests were used for data analysis. GHb levels (mean ± standard error) were 11.5 ± 0.4% and 12.8 ± 0.9%, respectively (p < 0.05); blood glucose levels were 8.8 ± 1.2 mM and 11.6 ± 1.3 mM, respectively; after vitamin E supplementation, triglyceride (TG) levels were 2.2 ± 0.2 mM and 2.9 ± 0.3 mM, respectively (p < 0.03), while there was no significant change before supplementation. These parameters showed no significant difference after placebo supplementation. Blood red blood cell count, hematocrit, and hemoglobin levels did not change after vitamin E or placebo supplementation. There were also no significant differences between the placebo group and the vitamin E supplementation group in terms of age and duration of diabetes. This study indicates that adequate vitamin E supplementation (100 IU/day) can significantly reduce blood glycated hemoglobin (GHb) and triglyceride (TG) levels in patients with type 1 diabetes, without affecting red blood cell parameters.
Exploratory Treatment: Dietary components may play both pathogenic and protective roles in the development and progression of pancreatic cancer, but the preventive potential of single components has not been evaluated. This study reports the effects of α-tocopherol and β-carotene supplementation on pancreatic cancer incidence and mortality in a randomized controlled trial. The α-tocopherol-β-carotene Cancer Prevention (ATBC) study included 29,133 male smokers aged 50–69 years who were randomly assigned to one of four intervention groups: dl-α-tocopherol (AT; 50 mg/day), β-carotene (BC; 20 mg/day), a combination of AT and BC, and a placebo. Daily supplementation continued for 5–8 years. New cancer cases were identified through death certificates from the Finnish National Cancer Registry and Statistics Finland. The effects of supplementation on pancreatic cancer incidence and mortality were analyzed using a Cox regression model. The results showed no statistically significant difference between the two supplements. Men taking beta-carotene supplements (n = 38) had a 25% lower incidence of pancreatic cancer than men not taking beta-carotene (n = 51) (95% CI, -51% to 14%). Men taking alpha-tocopherol supplements (n = 51) had a 34% higher incidence of pancreatic cancer than men not taking alpha-tocopherol (95% CI, -12% to 105%). During follow-up, after adjusting for tumor stage and anatomical location, men taking beta-carotene had a 19% lower pancreatic cancer mortality rate than men not taking supplements (95% CI, -47% to 26%), while men taking alpha-tocopherol had an 11% higher pancreatic cancer mortality rate than men not taking supplements (95% CI, -28% to 72%). Supplementation with either beta-carotene or alpha-tocopherol did not have a statistically significant effect on the incidence or mortality of pancreatic cancer. For more complete data on the therapeutic uses of dl-α-tocopherol (7 types in total), please visit the HSDB record page.

C29H50O2

430.7061

430.381

10191-41-0

DL-alpha-Tocopherol-13C3;DL-alpha-Tocopherol-d9;131230-17-6

2116

Colorless to light yellow liquid

0.9±0.1 g/cm3

485.9±0.0 °C at 760 mmHg

2-4°C

210.2±24.4 °C

0.0±1.2 mmHg at 25°C

1.495

11.9

1

2

12

31

503

0

O1C2C(C([H])([H])[H])=C(C([H])([H])[H])C(=C(C([H])([H])[H])C=2C([H])([H])C([H])([H])[C@@]1(C([H])([H])[H])C([H])([H])C([H])([H])C([H])([H])[C@]([H])(C([H])([H])[H])C([H])([H])C([H])([H])C([H])([H])[C@]([H])(C([H])([H])[H])C([H])([H])C([H])([H])C([H])([H])C([H])(C([H])([H])[H])C([H])([H])[H])O[H]

GVJHHUAWPYXKBD-UHFFFAOYSA-N

InChI=1S/C29H50O2/c1-20(2)12-9-13-21(3)14-10-15-22(4)16-11-18-29(8)19-17-26-25(7)27(30)23(5)24(6)28(26)31-29/h20-22,30H,9-19H2,1-8H3

2,5,7,8-tetramethyl-2-(4,8,12-trimethyltridecyl)-3,4-dihydrochromen-6-ol

DL-ALPHA-TOCOPHEROL; 10191-41-0; alpha-tochopherol; dl-; A-tocopherol; TOCOPHEROL; Ephanyl; Tocopheroxy radical;

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: This product requires protection from light (avoid light exposure) during transportation and storage.

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

H2O : ~100 mg/mL (~232.17 mM)
DMSO : ~100 mg/mL (~232.17 mM)

Solubility in Formulation 1: ≥ 2.5 mg/mL (5.80 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

---

Solubility in Formulation 2: 2.5 mg/mL (5.80 mM) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), suspension solution; with ultrasonication.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

---

View More

Solubility in Formulation 3: ≥ 2.5 mg/mL (5.80 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

---

Solubility in Formulation 4: 100 mg/mL (232.17 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with ultrasonication.

---

 (Please use freshly prepared in vivo formulations for optimal results.)