**Abstract**

Vitamin A refers to a group of related compounds with all-trans retinol biological activity and includes retinol, retinal, retinoic acid as well as the retinyl esters. Dietary source of vitamin A ranges from animal-based or plant-based foods, fortified food products and supplements. The vital biological roles of vitamin A compounds include normal cell growth, cell differentiation, vision and immunology. Vitamin A status is monitored to prevent occurrence of both subclinical deficiency and toxicity. Vitamin deficiency or excess is determined through the measure of vitamin A status. Prolonged vitamin A intake at high doses is shown to be toxic, which leads to various health symptoms. Xerophthalmia, a dry eye condition is the most severe clinical effects known to be caused by vitamin A deficiency. The resulting deleterious effects on human health led to efforts of supplementation, food fortification and dietary diversification in combating vitamin A deficiency. In brief, this chapter covers on vitamin A, with focus on its general information, dietary recommendations, biological roles, vitamin A status assessment, deficiency or excess effects to human health as well as the prevention measures.

**Keywords:** vitamin A, biological roles, deficiency, excess, human health

### **1. Introduction**

 Vitamin A in health and disease chapter intends to introduce general information of vitamin A with specific focus mainly on its dietary recommendations and its importance to human health. In line with this, continuous monitoring of vitamin A status that determines deficiency or toxicity state that could significantly affect human health along with prevention efforts is also described.

 Vitamin A is a fat-soluble vitamin and also comprises of a group of unsaturated nutritional organic compounds. These compounds include preformed vitamin A that exist in the form of retinol (alcohol), retinal (aldehyde), retinoic acid (irreversibly oxidized form of retinol) and several pro-vitamin A carotenoids (mainly β–carotene). The preformed vitamin A can only be obtained from the diet in food of animal origin and is the most abundant form of vitamin A in the human body. Retinol is a yellow fat-soluble substance, an absorbable form of vitamin A present in animal food sources. This chemical structure makes it poorly soluble in water but easily transferable through membrane lipid bilayers. Retinol is an alcohol and is known to be unstable. Vitamin A is mainly found in human tissues in the form of retinyl esters, which explains why the vitamin is commercially produced and administered as esters of retinyl acetate or palmitate. Retinyl esters will subsequently be converted into retinols in the small intestine [1, 2]. The pro-vitamin A comes from plant-derived

#### *Vitamin A*

 foods primarily in oils, fruits and vegetables. β-Carotene is the major source of vitamin A precursor from plants and is represented as two connected retinyl groups. The molecules contribute to the body's total vitamin A level. All forms of vitamin A have a β-ionone ring, which is attached to an isoprenoid chain (retinyl group). Both of these structural moieties are essential for the vitamin to exert biological activity. The β-ionone ring containing carotenoids include α-carotene, β-carotene and the xanthophyll β-cryptoxanthin [2].

Vitamin A can be found in a variety of foods. The bioavailability of carotenoids in food is variable because the efficacy of metabolic processes that convert carotene into retinol varies from one person to another. **Table 1** shows important dietary sources of vitamin A. Foods rich in retinol include meat, butter, retinol-enriched margarine, dairy products and eggs, while foods rich in β-carotene include vegetables and fruits (e.g. sweet potatoes, carrots, dark-green leafy vegetables, sweet red peppers, mangoes, melons). Several processed foods have been fortified with vitamin A and are good sources of the vitamin, such as cornflakes, malted milk powder and milk powder [2–4]. Foods containing pro-vitamin A carotenoids tend to have less biologically available vitamin A but are more affordable than animal products especially in the diets of economically deprived populations.

Retinol, in the form of retinyl esters, and pro-vitamin A carotenoids enter the human body as a component of nascent chylomicrons secreted into the lymphatic system. Most dietary retinol (in chylomicrons and chylomicron remnants) is taken up by the liver, which is the major site of retinol metabolism and storage. Once circulating retinol is absorbed from the intestine, it will bind primarily to a protein


**Table 1.** 

*Dietary sources of vitamin A and retinol activity equivalences (adapted from [5, 6]).* 

#### *Vitamin A in Health and Disease DOI: http://dx.doi.org/10.5772/intechopen.84460*

 called retinol-binding protein (RBP). The RBP will enter and leave the liver several times daily due to its lipophilic properties in a process known as retinol recycling. The retinol will bind to a cellular RBP (CRBP-I or CRBP-II) and can then be esterified by enzyme lecithin: retinol acyltransferase (LRAT), which enables the vitamins to be interconvertible, i.e. the stored ester and circulating retinol form. The storage efficiency and retinol catabolism are dependent on vitamin A status. Low retinol stores are associated with reduced storage efficiency and decrease the absolute catabolic rate [2].

To express the vitamin A activity of carotenoids in diets on a common basis, a concept of the retinol equivalent (RE) was introduced [7]. Based on this concept, the relationships among food sources of vitamin A were established as shown below:


 A new term, retinol activity equivalent (RAE), was introduced in order to express the activity of carotenoids after taking into account new research on vitamin A activity of carotenoids [8, 9]. Specific carotenoids/retinol equivalence ratios are defined for pro-vitamin A carotenoids, which account for the less efficient absorption of carotenoids and their bioconversion to retinol. Recent work has shown that the absorption of carotenoids, the vitamin A precursors, is only half of as much as that previously considered. Institute of Medicine established the following conversion factor equivalents:


The use of SI units (weight and molar) is strongly recommended to replace the use of IU in many databases to decrease confusion and overcome limitations in the nonequivalence of the IU values for retinol and β-carotenes. The conversion factors to be used are as follows:

