**4. Vitamin E**

Vitamin E (C29H50O2) is known as the generic of a derived set of tocols, with α-tocopherol the most active form for humans. Tocopherols possess a functional phenolic group in a chromanol ring and an isoprenoid side- chain of 16 carbons; it is saturated with three double links. There are two groups of compounds with vitamin E activity, and the tocopherols (with a 16-carbon isoprenoid side-chain) and the tocotrienols (with the same 16-carbon chain, but with three double links); both groups present vitameres that differ in the number

The Protective Effect of Antioxidants in Alcohol Liver Damage 105

acids (PUFA) have methylene groups localized between two double links; this renders PUFA sensitive to auto-oxidation; the initial reaction produces the lipid radical, a conjugated diene radical (L●), which reacts rapidly with the oxygen molecule, giving rise to a peroxyl free radical L-OO. In turn, this FR can act upon another PUFA, which will reinitiate the entire process and which would give rise to the peroxidation chain. The FR chain reaction is broken when α-tocopherol, present in the membrane, transfers a hydrogen to a peroxyl FR, transforming it into a hydroperoxide and giving rise to a tocopherol radical. The latter can react with different electron donors, among which ascorbate (vitamin C) is highlighted, for regenerating the tocopherol. In general, each α-tocopherol molecule can

Oligoelements comprise nine micronutrients that are found in the organism in amounts of <0.01% of body weight, and are the following: iron; zinc; selenium; manganese; iodine; chromium; fluorine; copper, and molybdenum. Oligoelements are very important for the organism because they perform functions such as serving as co-factors in enzymatic systems

Selenium is localized within the group of micronutrients constituting a trace element or an essential micronutrient for all mammals. Selenium is defined as a non-volatile micromineral that fulfills numerous biological functions; thus, its best known function is its role as part of the glutathione peroxidase enzyme that protects cells from oxidative damage. Its presence in tissues such as liver, heart, lung, and pancreas is essential because it promotes the breakdown of toxic peroxides formed during metabolism, impeding cell membrane damage. Selenium protects against toxicity by means of mercury, cadmium, and silver (Morales-

Absorption is mainly carried out in the duodenum. This element enters into the body in two principal ways depending on its source: selenocysteine (in animals), and selenomethionine (in plants); once in the organism, sulfur replacement takes place in cysteine and methionine for the formation of amino acids and selenoproteins. It is excreted through the urine and when consumed in high quantities, it also can be eliminated through the breath

Selenium (Se) possesses a potent antioxidant power, which is associated with the so-called selenoenzymes. To date, approximately 35 selenoenzymes have been described; these are proteins contain a selenocysteine residue in their active site and in which Se constitutes their enzymatic co-factor. Among the selenoenzymes, the best characterized and studied are Glutathione peroxidase (GPx) and Selenoprotein P (SePP). Another two very important enzymes are thioredoxin reductase, whose function is to reduce nucleotides during DNA synthesis, and iodothyronine deiodinase, which is responsible for the peripheral conversion

react with two peroxyl radicals (Morales-González, 2009; Sayago, 2007).

or as vital molecular components (Morales-González, 2009).

González, 2009; Manzanares-Castro, 2007).

**5.1.1 Absorption and metabolism** 

(Manzanares-Castro, 2007).

**5.1.2 Antioxidant action** 

**5. Oligoelements** 

**5.1 Selenium (Se)** 

and position of the methyl groups in the chromanol ring, designated as α, β, ∂, and (Figure 3) (Morales-González, 2009).

This vitamin forms part of the essential vitamins; thus, it should be acquired by means of its consumption in the daily diet. The distinct forms of vitamin E are not interchangeable among themselves in humans; in addition, they present distinct metabolic behaviors; therefore, other existing forms do not convert into α-tocopherol at any time and do not contribute to covering the vitamin E requirement. One of the main functions of α-tocopherol is that of its being a lipid antioxidant; on the other hand, it diminishes the production of thromboxanes and prostaglandins, is capable of inducing apoptosis directly or indirectly in tumor cells, modulates microsomal enzyme activity, inhibits protein kinase C activity, functions as a genetic regulator at the messenger RNA (mRNA) level, modulates the immunitary response during oxidative stress, and intervenes in the processes of fetal development and gestation, as well as in the processes of the formation of elastic and collagen fibers of the connective tissues, and in addition promotes the normal formation of erythrocytes; thus, the importance of this vitamin (Morales-González, 2009; Sayago, 2007).

**α- Tocopherol**

Fig. 3. In tocopherol structure, the alpha (α) homologue possesses four methyl groups in positions 2, 5, and 7.

#### **4.1 Absorption and metabolism**

Vitamin E is principally absorbed in the small intestine, with biliary secretion and micelle solubilization as indispensible. The bile acids, proceeding from the liver and segregated in the small intestine, favor the formation of micelles and facilitate the action of pancreatic lipases on lipids. Absorption of vitamin E within the erythrocyte is a passive process; αtocopherol and non-esterized -tocopherol are incorporated into the kilomicrons and for transport to the liver, in which the alpha-Tocopherol transfer protein (α-TTP) binds to the natural α-tocopherol stereoisomer or to the Golgi apparatus to incorporate it into Very-lowdensity lipoproteins (VLDL), from which is transferred to other circulating lipoproteins such as High-density (HDL) and Low-density lipoproteins (LDL) during their catabolism by the Lipoprotein lipase (LPL). LPL can also act on HDL and LDL in order for vitamin E to be able to accede to the peripheral tissues (Morales-González, 2009; Sayago, 2007).

#### **4.2 Antioxidant activity**

α-Tocopherol inhibits lipid oxidation by means of two mechanisms. On the one hand, it eliminates the FR produced during peroxidation, thus inhibiting the oxidation chain reaction and, on the other hand, it acts as a singlet oxygen chelator. Polyunsaturated fatty acids (PUFA) have methylene groups localized between two double links; this renders PUFA sensitive to auto-oxidation; the initial reaction produces the lipid radical, a conjugated diene radical (L●), which reacts rapidly with the oxygen molecule, giving rise to a peroxyl free radical L-OO. In turn, this FR can act upon another PUFA, which will reinitiate the entire process and which would give rise to the peroxidation chain. The FR chain reaction is broken when α-tocopherol, present in the membrane, transfers a hydrogen to a peroxyl FR, transforming it into a hydroperoxide and giving rise to a tocopherol radical. The latter can react with different electron donors, among which ascorbate (vitamin C) is highlighted, for regenerating the tocopherol. In general, each α-tocopherol molecule can react with two peroxyl radicals (Morales-González, 2009; Sayago, 2007).
