Although carotenoids can be found in foods of animal origin, algae and microorganisms, plant foods represent the main source of carotenoids in the human diet. Only 40 carotenoids are significantly consumed by humans, however, only five are the most abundant carotenoids in human plasma (Desmarchelier and Borel, 2017). The most abundant carotenoids in green leafy vegetables are lutein and β-carotene (Table 1). Carotenes in green leafy vegetables can be found as proteincarotenoid complexes. The roots (e.g. sweet potatoes and carrots) are commonly rich in α- and β-carotene, with carrots being the most important source of β-carotene (where it accumulates as crystals) in human diet (Schweiggert and Carle, 2017). Fruits are rich in xanthophyll esters (e.g., β-cryptoxanthin, zeaxanthin and lutein) and β-carotene, which are in non-crystalline form in the chromoplasts. Lycopene accumulates in tomato fruit as big crystals. The carotenoid content in commonly consumed fruits is shown in Table 1.

Table 1
Carotenoid content (µg/g FW) in commonly consumed foods as affected by different factors.

*Values expressed in dry weight; FW: flesh weigh; Lyc: lycopene; αC: α-carotene; βC: β-carotene; Lut: lutein; Vio: violaxanthin; Zea: zeaxanthin; βCry: β-cryptoxanthin; CD: convective draying; B: boiling; R: roasted; S: steaming; MW: microwaving; H: heating; F: freezing; FD: freeze drying; HHP: high hydrostatic pressure; US: ultrasound treatment; HP: heat pasteurization; W: watts; PEF: pulsed electric fields; HPH: high-pressure homogenization. Sources: Condurso et al., 2012; Dhliwayo et al., 2014; Donado-Pestana et al., 2012; Jacobo-Velazquez and Hernandez-Brenes, 2012; Leong and Oey, 2012; Fernandez-Orozco et al., 2013; Ferioli et al., 2013; Reif et al., 2013, Samuolienė et al., 2013; Zhao et al., 2013; Kljak and Grbeša, 2015; Ma et al., 2015; Behsnilian and Mayer-Miebach, 2017; Cao et al., 2017; Ordonez-Santos et al., 2017; De Andrade Lima et al., 2019; Kourouma et al., 2019; Ranganath et al., 2018; Kulczyński and Gramza-Michałowska, 2019; Elizondo-Montemayor et al., 2020; Etzbach et al., 2020; Fratianni et al., 2020; Liang et al., 2020; Zhou et al., 2020; Cervantes-Paz et al., 2021; Diamante et al., 2021; Hu et al., 2021; Lara-Abia et al., 2021; Laurora et al., 2021; Lebaka et al., 2021; Lopez-Gamez, et al., 2021a; Viacava et al., 2021; Zhang et al., 2021; Suo et al., 2022; Szczepanska et al., 2022.

The carotenoid content in plant foods depends on many factors, especially on the ripening process. Ethylene, the ripening hormone, triggers carotenoid biosynthesis, causing in many cases, exponential increases in carotenoid content (Cervantes-Paz et al., 2012). This process involves the degradation of chlorophylls and the transformation of chloroplasts in chromoplasts rich in carotenoids (Cervantes-Paz et al., 2012). Any postharvest technology applied to preserve plant foods in postharvest may retard or compromise the biosynthesis of carotenoids. This is the case of the use of low temperatures, the modification of the gas composition surrounding the food (modified atmosphere packaging and controlled atmosphere storage), application of ripening inhibitors (e.g., KMnO₄ and 1-methylcyclopropene) or application of phytosanitary treatments with heat or ionizing energy (Table 1) (Ornelas-Paz et al., 2017; Yahia et al., 2018).

Carotenoids do not accumulate homogeneously in plant foods, and their content also depends on genotype (Kljak et al., 2015). The geographical origin of plant foods also alters the carotenoid content in foods, since it is influenced by environment temperature, exposition to light, and rain (Laurora et al., 2021). Processing also alters significantly the carotenoid content in plant foods because carotenoids are prone to degradation, transformation or isomerization under light exposition, heating and alkaline or acid conditions. New processing techniques (e.g., pulsed electric fields, ultrasound, high hydrostatic pressures, high pressure homogenization, etc.) reduce the negative effects of conventional processing techniques on carotenoid content (López-Gámez et al., 2021), however, mincing, chopping or homogenizing are enough to alter the carotenoid content in fruits and vegetables (Yahia et al., 2018). Undoubtedly, other factors can alter the content of carotenoids in plant foods (Table 1).

The first step of the carotenoid absorption process implies the release of these compounds from foods during digestion (Figure 1) (Cervantes-Paz et al., 2017). This step largely depends on the mechanical and chemical disruption of food by mastication, movements of the gastrointestinal tract, gastric acid, alkaline medium in the intestine, and digestive enzymes. Due to their lipophilic nature, the released carote-noids must then be incorporated into the lipids co-consumed with the carotenoidrich food (Yahia et al., 2018). The carotenoid-lipidic phase tends to emulsify with the aqueous content of the gastrointestinal tract. The lipid droplet size in this emulsion is large in the gastric phase, but it decreases in the intestinal phase of digestion due to the emulsifying action of bile salts secreted by gall bladder (Victoria-Campos et al., 2013; Desmarchelier and Borel, 2017). This reduction of lipid droplet size is very important for lipid digestion, since lipases are hydrosoluble and only exert their action on lipid droplet surface (Cervantes-Paz et al., 2017).

Figure 1
Overview of the carotenoid absorption process. Figura 1. Diagrama general del proceso de absorcion de carotenoides.

Lipid digestion influences the formation of micelles, which are structured by the products of lipid digestion (free fatty acids, diglycerides, monoglycerides, etc.), bile salts, phospholipids and cholesterol (Yahia et al., 2018). Micelles are required for transportation of carotenoids from the chime to the enterocyte. Only micellarized carotenoids can be absorbed by intestinal cells (Cervantes-Paz et al., 2017; Desmarchelier and Borel, 2017).

It must be stated that the distribution of carotenoids in lipid droplets depends on their polarity, with xanthophylls being located on droplet surface and carotenes in the core of the lipid droplets (Yahia et al., 2018). Thus, the lipid digestion starts on the surface of the lipid droplet and therefore xanthophylls are more efficiently released and micellarized than carotenes. Micellarized carotenoids are considered as bioaccessible and represent the amount of carotenoids available in the required form to be absorbed by intestinal cells (Victoria-Campos et al., 2013; Cervantes-Paz et al., 2017). Micellarized carotenoids are transported to the brush border of enterocytes through the aqueous medium. The acidic medium of the unstirred water layer adjacent to the brush border of the enterocytes causes the dissociation of micelles and the liberation of carotenoids, which are passively taken by the enterocytes and facilitated diffusion and unilamellar or multilamellar vesicles of phospholipids (Reboul, 2013).

Currently, the quantity of micellarized carotenoids (bioaccessible carotenoids) is used as a measure of carotenoid absorption (bioavailability). The passive diffusion process is quickly saturated causing that most carotenoids are incorporated into the enterocytes by protein transporters (e.g. SRBI, CD36, NPC1L1) (Reboul, 2013; Desmarchelier and Borel, 2017). Table 2 shows the bioaccessibility of carotenoids from several plant foods. In the enterocytes, the provitamin A carotenoids are converted in vitamin A esters. Then, the non-provitamin A carotenoids, vitamin A and other com-pounds are packed in chylomicrons, which are evacuated to the lymphatic system and then to the bloodstream. Several transporters are involved in the intracellular flux of carotenoi-ds, including CD36, NPC1L1, SR-BI, GSTP1, HR-LPB and fatty acid-binding proteins (Reboul, 2013). Chylomicrons exposed to the action of endothelial lipoprotein lipases in the bloods-tream, lead to chylomicrons remnants, which are taken by the liver (Schweiggert and Carle, 2017; Desmarchelier and Borel, 2017).

Table 2
Bioaccessibility (%) of carotenoids from commonly consumed fruits and vegetables.

Abbreviations: TC = total carotenoids; βC = β - carotene; αC = α - carotene; δC = δ - carotene; ϒC = ϒ - carotene; Lut = lutein; Lyc = lycopene; Zea= zeaxanthin; βCry = β - cryptoxanthin; Viol = violaxanthin; Phy = phytoene; Phyt = phytofluene; Carotenes includes αC, βC, Lyc. Sources: Ornelas - Paz et al., 2010; Jeffery et al., 2012; Schweiggert et al., 2012; Victoria-Campos et al., 2013; Li et al., 2016; Petry and Mercadante, 2017; Bergantin et al., 2018; Gonzalez-Casado et al., 2018; Mapelli-Brahm et al., 2018; Zhang et al., 2018; de la Fuente et al., 2019; Liu et al. 2019; Zhong et al., 2019; De Oliveira et al., 2020; Etzbach et al., 2020; Hayes et al., 2020; Cervantes-Paz et al., 2021; Iddir et al., 2021; Lara-Abia et al., 2021; Laurora et al., 2021; Lopez-Gamez et al., 2021a; Lopez-Gamez et al., 2021b; Schmidt et al., 2021.

Carotenoids are exported from liver to different tissues by lipoproteins. Carotenes (e.g., β-carotene and lycopene) are transported by low-density lipoproteins (LDL) and very low-density lipoproteins, while xanthophylls (e.g., lutein, zeaxanthin and β- cryptoxanthin) are transported by high-density lipoproteins and LDL (Desmarchelier and Borel, 2017; Meléndez-Martínez et al., 2017). Carotenoids that are being absorbed, metabolized, stored and/or employed by the organism are considered as bioavailable (Desmarchelier and Borel, 2017). The general process for carotenoids absorption is shown in Figure 1.

The micellarization of carotenoids, which is a key step for carotenoid bioavailability, is affected by many factors (Tables 3 and 4). The food matrix is the most important factor affecting the bioaccessibility/bioavailability of carotenoids (Victoria-Campos et al., 2013; Cervantes-Paz et al., 2017). The term “food matrix” refers to the combined effects of all factors associated with a food that improve or reduce the bioavailability of carotenoids (Cervantes-Paz et al., 2017). This explain why the bioaccessibility/bioavailability of carotenoids from simple foods (e.g., supplements) is higher than that of complex plant foods. The form in which carotenoids are present in foods determines their bioaccessibility/bioavailability.

Table 3
Effect of thermic and non-thermic food processing on carotenoid bioaccessibility (BA).

Abbreviations: UF = ultrafrozen; MW= microwave oven; PAST = Pasteurized; OH = Ohmic heating; PEF= Pulsed electric field; HPP= high pressure proces-sing; HHP = High hydrostatic pressurization; US = ultrasonication; HPH = high-pressure homogenization; HADϒ = hotϒ air drying; TT = thermally-treated; BA = bioaccessibility; TC = total carotenoids; βC = β-carotene; αC = α-carotene; ζC = ζ-carotene; δC = δ-carotene; C = -carotene; Lut = lutein; Lyc = lycopene; βCry = β-cryptoxanthin; Viol = violaxanthin; Ant = antheraxanthin; Phy = phytoene; Phyt = phytofluene. Sources: Victoria-Campos et al., 2013; Li et al., 2016; Eriksen et al., 2017; Mercado-Mercado et al., 2017; Dhuique-Mayer et al., 2018; González-Casado et al., 2018; Mapelli-Brahm et al., 2018; Zhang et al., 2018; Cano et al., 2019; Zhong et al., 2019; Zhang et al., 2019; de Oliveira et al., 2020; Etzbach et al., 2020; Lara-Abia et al., 2021; López-Gámez et al., 2021.

Table 4
Modifiers of carotenoid bioaccessibility (BA).

Abbreviations: BA = bioaccessibility; TC = total carotenoids; βC = β-carotene; αC = α-carotene; Lut = lutein; Lyc = lycopene; Zea = zeaxanthin; βCry = β-cryptoxanthin; Phy = phytoene; Phy t = phytofluene; RDA = recommended dietary allowance; WPI = Whey protein isolate; SPI = soy protein isolate; SC = sodium caseinate; GEL = gelatin. Sources: Corte-Real et al., 2017; da Costa and Mercadante 2017; García-Cayuela et al., 2017; Hempel et al., 2017; Corte-Real et al., 2018; González-Casado et al., 2018; Stinco et al., 2019; De Souza et al., 2020; Iddir et al., 2021.

Carotenoids present in foods as lipid-based forms, are readily released from the food and then incorporated into the oily phase of chime, as compared to carotenoid crystals or carotenoid-protein complexes (Schweiggert and Carle, 2017). That is the reason why β-carotene from some fruits (e.g., tomatoes and mango) is more bioavailable than β-carotene from carrots or spinach (Ornelas-Paz et al., 2010).

Food processing alters the effect of food matrix. Cooking and mincing favor carotenoid release from food during digestion, increasing the micellarization and absorption of these compounds (Table 3) (Li et al., 2016; Eriksen et al., 2017; De Oliveira et al., 2020). Industrial processing also increases the bioaccessibility of food carotenoids (Dhuique-Mayer et al., 2018; Mapelli-Brahm et al., 2018; Zhong et al., 2019). Non-thermic technologies (e.g., high hydrostatic pressurization, high pressure homogenization, pulsed electric fields and ultrasound) also increase the bioaccessibility of carotenoids (Lara-Abia et al., 2021; López-Gámez et al., 2021). The increase of carotenoid bioaccessibility is a consequence of the processing-mediated softening of food (cellular disruption). Ripening also causes softening of fruits, favoring the release of carotenoids during digestion. However, ripening also favors the esterification of carotenoids with fatty acids, reducing their polarity and, consequently, their micellarization rate and bioavailability (Cervantes-Paz, et al., 2012; Victoria-Campos et al. 2013).

On the other hand, the fiber from carotenoid-rich food or co-consumed foods alters the carotenoids micellarization and bioavailability (Table 4). Overall, fiber reduces the absorption of carotenoids by altering of the macro- and microviscosity of chime. This alteration reduces the emulsification of lipid droplets favoring the formation of large ones, and reduces the activity of lipase, formation of micelles, the transference of carotenoids from lipid droplets to micelles and the diffusion of carotenoidrich micelles to the enterocyte (Cervantes-Paz et al., 2016). Low concentrations of pectin in the chime (~ 2 %) can cause high reductions in carotenoid bioavailability (20 - 50 %) (Rock and Swendseid, 1992). This effect depends on the physicochemical characteristics of fibers (solubility, molecular weight, degree of esterification, etc.), with soluble fibers exerting the most negative effect on carotenoid absorption (Cervantes-Paz et al., 2016; Cano et al., 2019).

The amount and type of fat consumed with carotenoids alter the absorption rate of carotenoids (Table 4), since the latter are poorly absorbed in absence of fat. The minimum amount of fat required for carotenoid absorption is unknown. Some studies have suggested that at least 3-5 g of fat per meal are required for good carotenoid absorption, although higher quantities of fat per meal (e.g., 20 g) have also been proposed (Goltz et al., 2012). The positive effect of fat on carotenoid absorption depends on carotenoid type, with zeaxanthin, α -carotene, and β-carotene requiring more fat than lutein to reach the highest micellarization values (Hempel et al., 2017; González- Casado et al., 2018; De Souza et al., 2020). Fat consumption can increase the absorption of carotenoids by 2-3 times or even more, depending on carotenoid type. The beneficial effect of fat on carotenoid micellarization and absorption also depends on fat type, with monounsaturated and polyunsaturated fatty acids best promoting the bioaccessibility of carotenoids than saturated fatty acids (Goltz et al., 2012; Victoria-Campos et al., 2013).

Protein improves the bioaccessibility of dietary carotenoids due to its emulsifying properties (Iddir et al., 2021). The carotenoid dose also influences the carotenoid absorption rate, with low doses resulting in a higher carotenoid absorption than large doses (Yahia et al., 2018). Under gastrointestinal conditions, there is a competence among carotenoids for absorption, thus the inclusion of a new carotenoid in the diet will cause a reduction in the absorption of other carotenoids. In some cases, the inclusion of xanthophylls causes a decrease in carotene absorption while in other cases the opposite has been observed (Kopec and Failla, 2018). The effect of some modifiers on carotenoid bioaccessibility is shown in Table 4.

Carotenoids are able to neutralize free radicals, whichcan damage molecules in cells and cause degenerative diseases in humans. Abnormal levels of free radicals in the human body cause oxidative stress, which has been associated with the pathogenesis of more than 100 different diseases (Yahia et al., 2018). Carotenoids can neutralize several oxygen reactive species, including singlet oxygen and peroxyl radicals (Britton, 2020). This antioxidant activity depends on their number of conjugated double bonds and oxygenated substituents (Yahia et al., 2018), and involves the binding of carotenoids to free radicals and the transference of energy from the free radical to the carotenoid (Swapnil et al., 2021). Lycopene, canthaxanthin and astaxanthin show a higher antioxidant activity than β-carotene and zeaxanthin. Several studies have demonstrated that the antioxidant activity of carotenoid mixtures is higher than that of individual carotenoids, demonstrating the synergistic effects of carotenoids (Rowles and Erdman, 2020).

The consumption of some carotenoids has been associated with a reduced risk of some forms of cancer (Table 5). The carotenoid with the highest anticancer effect seems to be lycopene, independently if it is consumed in purified form or from tomato products. Lycopene is highly effective in the prevention of prostate cancer, although consumption of lycopene has also been related to the protection against other cancer forms (digestive tract, pancreatic, cervical, etc.) (Lu et al., 2015; Bakker et al., 2016; Van Hoang et al., 2018; Kim et al., 2018; Swapnil et al., 2021).

Table 5
Carotenoids and health.

*All effects in the table were reported as statistically significant trends (p < 0.05) in original papers. Abbreviations. TC = total carotenoids; βC = β-carotene; αC = α-carotene; Lut = lutein; Lyc = lycopene; Zea = zeaxanthin; βCry = β-cryptoxanthin; BMI = body mass index; baPWV = brachial ankle pulse wave velo-city; SBP = systolic blood pressure; DBP = diastolic blood pressure; HOMA−IR = Homeostatic Model Assessment for Insulin Resistance; FBG = fasting blood glucose; TG = triglyceride; HDL = high-density lipoprotein; LDL = low density lipoprotein; CRP = C-reactive protein; tHcy = total homocysteine. Sources: Karppi et al., 2013; Wang et al., 2014; Curhan et al., 2015; Lu et al., 2015; Sluijs et al., 2015; Munter et al., 2015; Bakker et al., 2016; Van Hoang et al., 2018; Kim et al., 2019; Matsumoto et al., 2020; Yuan et al., 2021.

The effects of other carotenoids in cancer prevention are less clear. There is some evidence that lycopene, β-carotene and β-cryptoxanthin prevent lung cancer (Iskandar et al., 2016). β-Carotene, α -carotene and lutein have shown protective effects against breast cancer (Bakker et al., 2016). β-Carotene, lycopene, β-cryptoxanthin, lutein and zeaxanthin prevent pharyngeal, laryngeal and pancreas cancers (Rowles and Erdman, 2020). Lycopene reduces the risk of gastric and prostate cancer (Van Hoang et al., 2018; Kim et al., 2018). β- cryptoxanthin, lycopene, α-carotene and β-Carotene reduce the risk of colorectal cancer (Lu et al., 2015). The anticancer effects of carotenoids have been attributed to their antioxidant properties, the alteration of genes expression involved in the pathogenesis, alterations in the levels of signaling molecules and other effects (Rowles and Erdman, 2020).

The effect on carotenoid consumption on cardiovascular diseases is unclear, as both positive and negative effects have been reported (Table 5). There are some evidences suggesting that β-carotene, lycopene, lutein, zeaxanthin, astaxanthin, among others, might prevent the development of cardiovascular diseases (Karppi et al., 2013; Wang et al., 2014; Kulczyński et al., 2017; Matsumoto et al., 2020). The effects of lycopene and β -carotene on cardiovascular diseases has been highly studied. The antioxidant activity of carotenoids seems to be associated with their beneficial effect on prevention of cardiovascular diseases, however, other mechanisms seem to be involved, including the carotenoid-related reduction of the inflammatory response caused by the tumor necrosis factor-α (TNF-α), maintaining endothelial nitric oxide bioavailability, altering the expression of some genes, inhibiting leucocyte adhesion and migration, reducing apoptosis, inhibiting macrophages activation, regulating cholesterol synthesis, inhibiting platelet activation, regulating the levels of lipoproteins, among others (Kulczyński et al., 2017). The consumption of β-carotene and α-carotene also is inversely related to type 2 diabetes risk (Sluijs et al., 2015). A neuro-protective effect was recently associated with the intake of total carotenoids, lutein, zeaxanthin, β-cryptoxanthin, and β-Carotene (Yuan et al., 2021).

Lutein and zeaxanthin are important components of macula and retina and their levels in these tissues have positively been associated with visual functions (García-Romera et al., 2022). These effects have been clearly demonstrated in clinical trials. Lutein and zeaxanthin absorb blue light, exert antioxidant effects, improve vision and prevent the development of cataracts and agerelated macular degeneration (Yahia et al., 2018). Interestingly, the levels of these carotenoids in the macule can be used as markers of their concentrations in the brain and cognitive functions (García-Romera et al., 2022).

β-Carotene, β-cryptoxanthin, zeaxanthin, lycopene, siphonaxanthin, fucoxanthin, astaxanthin, crocetin and crocin, and some of their conversion products, are able to reduce the adiposity in animals and humans (Bonet et al., 2020), by influencing adipocyte differentiation, oxidation rate of fatty acids and thermogenesis (Bonet et al., 2015).

Also, carotenoids can reduce liver damage, due to their antioxidant and anti-inflammatory effects as well as the modulation of the expression of genes (Yahia et al., 2018).

Other beneficial effects of carotenoids include the protection of photodamage of skin, cytoprotection against mycotoxins, human growth, reproduction and immune function, among other beneficial effects (Yahia et al., 2018; Swapnil et al., 2021). Table 5 summarizes the results of some recent epidemiological studies on the effect of carotenoids on human health.

^*Autor para correspondencia: José de Jesús Ornelas Paz. Correo electrónico: jornelas@ciad.mx