Scope: Dityrosine (DT), a marker of protein oxidation, is widely found in many high-protein foods. Dietary intake of DT induces myocardial oxidative stress injury and impairs energy metabolism. Lycopene is a common dietary supplement with antioxidant and mitochondrial-lipid homeostasis modulating abilities. This study aimed to examine the effects of lycopene on DT-induced disturbances in myocardial function and energy metabolism. Methods and Results: Four-week-old C57BL/6J mice received intragastric administration of either tyrosine (420 µg kg −1 BW), DT (420 µg kg −1 BW), or lycopene at high (10 mg kg −1 BW) and low (5 mg kg −1 BW) doses for 35 days. Lycopene administration effectively reduced oxidative stress, cardiac fatty acid accumulation, and cardiac hypertrophy and improved mitochondrial performance in DT-induced mice. In vitro experiments in H9c2 cells showed that DT directly inhibited the activity of the respiratory chain complex, whereas oxidative phosphorylation and 𝜷-oxidation gene expression is upregulated. Lycopene enhanced the activity of the complexes and inhibited ROS production caused by compensatory regulation. Conclusion: Lycopene improves DT-mediated myocardial energy homeostasis disorder by promoting the activity of respiratory chain complexes I and IV and alleviates the accumulation of cardiac fatty acids and myocardial hypertrophy.

To assess the effects of digestion on the functional components of walnut pigment and their bioactivities, we developed an in vitro model simulating gastro-intestinal digestion. Results showed an increase in the contents of flavonoids and conjugated phenols (with retention rates higher than 100%) in husk pigment after digestion. The lowest of the 2,2 -azino-bis(3-ethylbenzothiazoline-6-sulfonic acid) (ABTS) radical scavenging abilities was reached in the group with the minimum flavonoid content after digestion. Close correlation was observed between free phenol content and total reducing power, as the reducing power among different groups of husk pigment was in consistent with free phenols changes. The inhibitory effect of walnut pigment on α-amylase with/without digestion enzyme was similar. However, shell pigment showed improved inhibitory effect on α-glucosidase activity, with an increased inhibitory rate of 5.42%. In general, the antioxidant activity and hypoglycemic ability of walnut pigment were prone to chemical and enzymatic changes during simulated digestion, which were also related to the alteration of flavonoids and phenols.

Scope Dityrosine (DT) is a protein oxidation marker present in many high‐protein foods, such as dairy and meat products. Chronic dietary intake of DT induces oxidative stress damage in the liver and impairs energy metabolism. This study aims to investigate the mechanisms underlying the effects of DT on disrupted hepatic energy metabolism. Methods and results The study investigates hepatic lipid accumulation, redox status imbalance, mitochondrial dysfunction, and energy metabolism disorders in 4‐week‐old C57BL/6J mice after 35 days of DT (420 µg kg−1 body weight) treatment. Transcriptome sequencing and quantitative real‐time PCR in HepG2 cells show that DT mainly acted via miR‐144‐3p. miR‐144‐3p targets immune responsive gene 1 (IRG1) and decreases the fumaric acid level in the tricarboxylic acid (TCA) cycle, thereby decreasing nuclear factor erythroid 2‐related factor 2 (Nrf2) expression and antioxidant activity. Conclusion Administration of lycopene, a strong antioxidant, alleviates DT‐induced damage in mice, confirming the involvement of the Nrf2 pathway in DT‐induced abnormal hepatic lipid metabolism and energy homeostasis.