The Role of Microencapsulation in Food Application.

Modern microencapsulation techniques are employed to protect active molecules or substances such as vitamins, pigments, antimicrobials, and flavorings, among others, from the environment. Microencapsulation offers advantages such as facilitating handling and control of the release and solubilization of active substances, thus offering a great area for food science and processing development. For instance, the development of functional food products, fat reduction, sensory improvement, preservation, and other areas may involve the use of microcapsules in various food matrices such as meat products, dairy products, cereals, and fruits, as well as in their derivatives, with good results. The versatility of applications arises from the diversity of techniques and materials used in the process of microencapsulation. The objective of this review is to report the state of the art in the application and evaluation of microcapsules in various food matrices, as a one-microcapsule-core system may offer different results according to the medium in which it is used. The inclusion of microcapsules produces functional products that include probiotics and prebiotics, as well as antioxidants, fatty acids, and minerals. Our main finding was that the microencapsulation of polyphenolic extracts, bacteriocins, and other natural antimicrobials from various sources that inhibit microbial growth could be used for food preservation. Finally, in terms of sensory aspects, microcapsules that mimic fat can function as fat replacers, reducing the textural changes in the product as well as ensuring flavor stability.

Environmentally Friendly Techniques and Their Comparison in the Extraction of Natural Antioxidants from Green Tea, Rosemary, Clove, and Oregano.

Many current food and health trends demand the use of more ecological, sustainable, and environmentally friendly techniques for the extraction of bioactive compounds, including antioxidants. However, extraction yields and final antioxidant activities vary between sources and are highly influenced by the given extraction method and nature and ratio of the employed solvent, especially for total polyphenols, flavonoids, and anthocyanins, which are well recognized as natural antioxidants with food applications. This review focused on the most common extraction techniques and potential antioxidant activity in the food industry for various natural antioxidant sources, such as green tea, rosemary, clove, and oregano. Green extraction techniques have been proven to be far more efficient, environmentally friendly, and economical. In general, these techniques include the use of microwaves, ultrasound, high hydrostatic pressure, pulsed electric fields, enzymes, and deep eutectic solvents, among others. These extraction methods are described here, including their advantages, disadvantages, and applications.

Effect of the addition of microcapsules with avocado peel extract and nisin on the quality of ground beef.

This study evaluated the incorporation of microcapsules containing nisin and avocado peel extract on the shelf life of ground beef. Ten treatments were studied and divided into two groups: one packaged under vacuum and the other in permeable packaging. Each group contained: (a) control, (b) extract, (c) nisin, (d) empty microcapsules (only wall microcapsule system), and (e) microcapsules with extract and nisin. The samples containing the microcapsules presented lower bacterial growth and less oxidation. On day 10, the vacuum-packaged samples with microencapsulated preservative presented a reduction in the oxidation of proteins of approximately 45%, of 30% in the growth of mesophiles, and of 38% in the growth of coliforms, as well as a reduction in the changes in the pH and ɑ W that occur during storage, compared with the permeable control. The combination of microcapsules with vacuum packaging reduced the physicochemical and microbiological changes that occur in the controls.

Protective effect of sulforaphane against oxidative stress: recent advances.

Sulforaphane [1-isothiocyanate-(4R)-(methylsulfinyl)butane] is a natural dietary isothiocyanate produced by the enzymatic action of the myrosinase on glucopharanin, a 4-methylsulfinylbutyl glucosinolate contained in cruciferous vegetables of the genus Brassica such as broccoli, brussel sprouts, and cabbage. Studies on this compound is increasing because its anticarcinogenic and cytoprotective properties in several in vivo experimental paradigms associated with oxidative stress such as focal cerebral ischemia, brain inflammation, intracerebral hemorrhage, ischemia and reperfusion induced acute renal failure, cisplatin induced-nephrotoxicity, streptozotocin-induced diabetes, carbon tetrachloride-induced hepatotoxicity and cardiac ischemia and reperfusion. This protective effect also has been observed in in vitro studies in different cell lines such as human neuroblastoma SH-SY5Y, renal epithelial proximal tubule LLC-PK1 cells and aortic smooth muscle A10 cells. Sulforaphane is considered an indirect antioxidant; this compound is able to induce many cytoprotective proteins, including antioxidant enzymes, through the Nrf2-antioxidant response element pathway. Heme oxygenase-1, NAD(P)H: quinone oxidoreductase, glutathione-S-transferase, gamma-glutamyl cysteine ligase, and glutathione reductase are among the cytoprotective proteins induced by sulforaphane. In conclusion, sulforaphane is a promising antioxidant agent that is effective to attenuate oxidative stress and tissue/cell damage in different in vivo and in vitro experimental paradigms.

Curcumin protects from cardiac reperfusion damage by attenuation of oxidant stress and mitochondrial dysfunction.

This study was designed to investigate whether the pretreatment with curcumin, a yellow pigment from turmeric (Curcuma longa) known for its potent antioxidant capacity, was able to protect against the oxidant damage and mitochondrial dysfunction induced by reperfusion injury in isolated hearts. Rats were treated with a daily intragastric dose of curcumin (200 mg/kg) for 7 days prior to experimental ischemia (30 min) and reperfusion (60 min) (I/R). Cardiac mechanical work was measured during periods of stabilization, ischemia, and reperfusion. Oxidant stress and activity of antioxidant enzymes were measured in both homogenates of cardiac tissue and in isolated mitochondria. In addition, oxygen consumption was measured in isolated mitochondria. It was found that curcumin pretreatment attenuates the I/R injury as evidenced by (a) loss of cardiac mechanical work, (b) oxidant stress (increase in lipid peroxidation and decrease in reduced glutathione content) and (c) decrease in the activity of the antioxidant enzymes superoxide dismutase and glutathione reductase in both cardiac tissue and isolated mitochondria, and (d) decrease in mitochondrial respiratory capacity. In conclusion, the protective effect of curcumin was associated with the attenuation of oxidant stress and mitochondrial dysfunction secondary to I/R injury.

Protective effect of sulforaphane pretreatment against cisplatin-induced liver and mitochondrial oxidant damage in rats.

In the present work was analyzed whether sulforaphane (SFN) may protect against cisplatin (CIS)-induced hepatic damage, oxidant stress and mitochondrial dysfunction. Four groups of male Wistar rats were studied: control, CIS, CIS+SFN and SFN. SFN was given i.p. (500 µg/kg/d × 3 days) before CIS administration (single i.p. injection, 10mg/kg). Rats were sacrificed 3 days after CIS injection to evaluate hepatic damage (histological analysis, liver/body weight ratio and serum activity of aspartate aminotransferase and alanine aminotransferase), oxidant stress (lipid peroxidation and protein carbonyl and glutathione content), antioxidant enzymes (catalase, glutathione reductase, glutathione peroxidase, glutathione-S-transferase and superoxide dismutase) in liver homogenates and isolated mitochondria and mitochondrial function (oxygen consumption using either malate/glutamate or succinate as substrates and the activity of mitochondrial complex I, II, II-III, IV and V). Furthermore it was evaluated if SFN is able to scavenge some reactive oxygen species in vitro. It was found that SFN prevents CIS-induced (a) hepatic damage, (b) oxidant stress and decreased activity of antioxidant enzymes in liver and mitochondria and (c) mitochondrial alterations in oxygen consumption and decreased activity of mitochondrial complex I. It was also found that the scavenging ability of SFN for peroxynitrite anion, superoxide anion, singlet oxygen, peroxyl radicals, hydrogen peroxide and hydroxyl radicals was very low or negligible. The hepatoprotective effect of SFN was associated to the preservation of mitochondrial function, antioxidant enzymes and prevention of liver and mitochondrial oxidant stress.

Protective effect of sulforaphane against cisplatin-induced mitochondrial alterations and impairment in the activity of NAD(P)H: quinone oxidoreductase 1 and γ glutamyl cysteine ligase: studies in mitochondria isolated from rat kidney and in LLC-PK1 cells.

This work was designed to further study the mechanism by which sulforaphane (SFN) exerts a renoprotective effect against cisplatin (CIS)-induced damage. It was evaluated whether SFN attenuates the CIS-induced mitochondrial alterations and the impairment in the activity of the cytoprotective enzymes NAD(P)H: quinone oxidoreductase 1 (NQO1) and γ glutamyl cysteine ligase (γGCL). Studies were performed in renal epithelial LLC-PK1 cells and in isolated renal mitochondria from CIS, SFN or CIS+SFN treated rats. SFN effectively prevented the CIS-induced increase in reactive oxygen species (ROS) production and the decrease in NQO1 and γGCL activities and in glutathione (GSH) content. The protective effect of SFN on ROS production and cell viability was prevented by buthionine sulfoximine (BSO), an inhibitor of γGCL, and by dicoumarol, an inhibitor of NQO1. SFN was also able to prevent the CIS-induced mitochondrial alterations both in LLC-PK1 cells (loss of membrane potential) and in isolated mitochondria (inhibition of mitochondrial calcium uptake, release of cytochrome c, and decrease in GSH content, aconitase activity, adenosine triphosphate (ATP) content and oxygen consumption). It is concluded that the protection exerted by SFN on mitochondrial alterations and NQO1 and γGCL enzymes may be involved in the renoprotection of SFN against CIS.

The alpha-mangostin prevention on cisplatin-induced apoptotic death in LLC-PK1 cells is associated to an inhibition of ROS production and p53 induction.

Cisplatin (CDDP) is a widely useful chemotherapeutic agent for the treatment of tumors including lung, ovary and testis. Acute renal injury, however, is the main side effect observed after CDDP treatment. This side effect is related to the apoptotic death in proximal tubular cells in the kidney and p53 protein has a central role in this process. On the other hand, alpha-mangostin (alpha-M), a xanthone derived from the pericarp of mangosteen, exerts a renoprotective effect against cisplatin-induced renal damage in rats. The aim of this study was to evaluate whether alpha-M protects proximal tubule renal epithelial cells (LLC-PK1) from CDDP-induced apoptotic death. Cells were co-incubated with 5 microM alpha-M and 100 microM CDDP for 24h. It was found that alpha-M attenuated the following alterations: the apoptotic cell death, the increase in reactive oxygen species (ROS), the glutathione depletion and the increase in p53 expression induced by CDDP. In conclusion, the preventive effect of alpha-M on CDDP-induced apoptotic death is associated to the inhibition of p53 expression and ROS generation.

Sulforaphane protects against cisplatin-induced nephrotoxicity.

Cisplatin (cis-diamminedichloroplatinum II, CDDP) is a chemotherapeutic agent that induces nephrotoxicity associated with oxidative/nitrosative stress. Sulforaphane (SFN) is an isothiocyanate produced by the enzymatic action of myrosinase on glucorophanin, a glucosinolate contained in cruciferous vegetables. SFN is able to induce cytoprotective enzymes through the transcription factor Nrf2. The purpose of this study was to evaluate whether SFN induces a cytoprotective effect on the CDDP-induced nephrotoxicity. Preincubation of LLC-PK1 cells with 0.5-5 microM SFN by 24 h was able to prevent, in a concentration-dependent way, CDDP-induced cell death. Immunofluorescent staining confirmed the nuclear translocation of Nrf2 after treatment with SFN. In the in vivo studies, CDDP was given to Wistar rats as a sole i.p. injection at a dose of 7.5 mg/kg. SFN (500 microg/kg i.v.) was given two times (24 h before and 24 after CDDP-injection). Animals were killed three days after CDDP-injection. SFN attenuated CDDP-induced renal dysfunction, structural damage, oxidative/nitrosative stress, glutathione depletion, enhanced urinary hydrogen peroxide excretion and the decrease in antioxidant enzymes (catalase, glutathione peroxidase and glutathione-S-transferase). The renoprotective effect of SFN on CDDP-induced nephrotoxicity was associated with the attenuation in oxidative/nitrosative stress and the preservation of antioxidant enzymes.