Toward the bioactive potential of myricitrin in food production: state-of-the-art green extraction and trends in biosynthesis.

Myricitrin is a member of flavonols, natural phenolic compounds extracted from plant resources. It has gained great attention for various biological activities, such as anti-inflammatory, anti-cancer, anti-diabetic, as well as cardio-/neuro-/hepatoprotective activities. These effects have been demonstrated in both in vitro and in vivo models, making myricitrin a favorable candidate for the exploitation of novel functional foods with potential protective or preventive effects against diseases. This review summarized the health benefits of myricitrin and attempted to uncover its action mechanism, expecting to provide a theoretical basis for their application. Despite enormous bioactive potential of myricitrin, low production, high cost, and environmental damage caused by extracting it from plant resources greatly constrain its practical application. Fortunately, innovative, green, and sustainable extraction techniques are emerging to extract myricitrin, which function as alternatives to conventional techniques. Additionally, biosynthesis based on synthetic biology plays an essential role in industrial-scale manufacturing, which has not been reported for myricitrin exclusively. The construction of microbial cell factories is absolutely an appealing and competitive option to produce myricitrin in large-scale manufacturing. Consequently, state-of-the-art green extraction techniques and trends in biosynthesis were reviewed and discussed to endow an innovative perspective for the large-scale production of myricitrin.

From polyphenol to o-quinone: Occurrence, significance, and intervention strategies in foods and health implications.

Polyphenol oxidation is a chemical process impairing food freshness and other desirable qualities, which has become a serious problem in fruit and vegetable processing industry. It is crucial to understand the mechanisms involved in these detrimental alterations. o-Quinones are primarily generated by polyphenols with di/tri-phenolic groups through enzymatic oxidation and/or auto-oxidation. They are highly reactive species, which not only readily suffer the attack by nucleophiles but also powerfully oxidize other molecules presenting lower redox potentials via electron transfer reactions. These reactions and subsequent complicated reactions are capable of initiating quality losses in foods, such as browning, aroma loss, and nutritional decline. To attenuate these adverse influences, a variety of technologies have emerged to restrain polyphenol oxidation via governing different factors, especially polyphenol oxidases and oxygen. Despite tremendous efforts devoted, to date, the loss of food quality caused by quinones has remained a great challenge in the food processing industry. Furthermore, o-quinones are responsible for the chemopreventive effects and/or toxicity of the parent catechols on human health, the mechanisms by which are quite complex. Herein, this review focuses on the generation and reactivity of o-quinones, attempting to clarify mechanisms involved in the quality deterioration of foods and health implications for humans. Potential innovative inhibitors and technologies are also presented to intervene in o-quinone formation and subsequent reactions. In future, the feasibility of these inhibitory strategies should be evaluated, and further exploration on biological targets of o-quinones is of great necessity.

Polyphenol mediated non-enzymatic browning and its inhibition in apple juice.

Non-enzymatic browning is a severe problem in juice industry. Here, polyphenol mediated non-enzymatic browning and its inhibition in apple juice were investigated. Epicatechin (R = -0.83), catechin (CAT, R = -0.79), chlorogenic acid (CGA, R = 0.65) and caffeic acid (CAF, R = 0.65) were strongly correlated with browning. CAT and chlorogenic acid quinone (CGAQ) decreased during storage with the fastest CAT degradation rate (kCGA-enriched = 1.97 × 10-3 mg·L-1·h-1 and kCAT-enriched = 2.09 × 10-3 mg·L-1·h-1) at the initial stage, but CGA and catechin quinone (CATQ) hardly changed. It was possible that CGAQ oxidized CAT at initial stage, leading to the generation of CATQ but less browning. Then the formed CATQ reacted with CAT through the complex reactions, leading to the accumulation of yellow polymers, which might explain why browning increased faster during the secondary and tertiary stages. In addition, glutathione could effectively inhibit browning compared to ascorbic acid and oxygen blocking methods.