# Anthocyanin Delivery Systems: A Critical Review of Recent Research Findings
## 1 Introduction
As mentioned already, though the potential of applications is significant, the stability issues associated with ACNs limit their utilization in processing applications [20]. The limitation of ACNs in terms of food applications is directly related to their bioavailability; as they undergo extensive presystemic degradation, and hence, are poorly absorbed [21]. The bioavailability of ACNs is reportedly very low, with recoveries of \(<\)1% of the ingested dose of ACNs [22]. Albeit higher recoveries have been reported as well in some in vitro studies, reaching values of 12.4% [23; 24]. ACNs are usually assimilated from the stomach and small intestine, although, a considerable proportion can reach the large intestine, where these ACNs are subjected to extensive catabolism, resulting in the formation of various metabolites, for instance, phenolic and propionic acids [22]. ACNs in their glycoside forms have demonstrated superior stability under low pH (1.5-4) conditions in the stomach, allowing for their absorption in the small intestine as intact molecules [25]. ACN aglycones, upon reaching intestinal epithelia, undergo metabolism before entering portal circulation, in two distinct phases, phase I metabolism (oxidation, reduction, and hydrolysis reactions), and phase II metabolism (conjugation reactions) [22]. Moreover, in the intestine, ACNs undergo sulfation, methylation, and glucuronidation under the influence of sulfotransferase, catechol-O-methyltransferase, and uridine-5\({}^{\prime}\)-diphospho-glucuronosyltransferase enzymes [26]. Alternatively, ACNs aglycones may undergo degradation and fragmentation induced by the action of deglycosylation enzymes produced by the colonic microbiota, resulting in the formation of aglycones that undergo further ring-opening, leading to the production of various aldehydes, and benzoic acids, such as vanillic, gallic, protocatechuic, and syringic acids [27]. Consequently, the proportion of phenolic acids increases, while that of ingested ACNs decreases, as they progress further along the gastrointestinal (GI) tract. The low in vivo bioavailability of ACNs can be attributed to their low permeability, low water solubility, inadequate gastric residence time, and high sensitivity to the GI environment, where they undergo substantial pH-dependent transformations [28]. Therefore, only a small portion of the consumed ACNs is recovered in plasma/urine, and \(<\)0.1% is excreted in the intact form [29]. This calls for the development of methods aimed at reducing the degradation of ingested ACNs, and therefore, enhancing their bioavailability [30]. ACNs can be stabilized by embedding them in nanocarriers systems to produce microcapsules, acylating their reactive groups, or forming copignments with other macromolecules [31]. A significant number of research studies have recorded the encapsulation of ACNs using different techniques and encapsulating materials [32; 33; 34; 35; 36; 37]. Encapsulation technology is focused on the entrapment of bioactive compounds and the formation of one stable form, either in a solid or liquid state, which can significantly enhance ACN stability, bioaccessibility, and bioavailability [38]. One of the most commonly used encapsulation materials for ACNs, among others such as chitosan and Gum Arabic, are cyclodext (CDs), whereby the apolar guest molecules (for instance, amphiphilic ACN aglycones) can be trapped within the torus-shaped apolar cavity of CDs through electrostatic interactions,hydrogen bonds, and van der Waals forces (utilizing techniques such as molecular inclusion or host-guest complexation) [39]. CDs owing to their hydrophobic interior, and hydrophilic exterior, allow them to form complexes with a wide range of organic components, thereby also permitting the selectivity of the organic compounds to be encapsulated, which can be attributed to the adaptable nature of the hydrophobic cavity of CDs, as well as its size [40].