Lycopene Regulates Dietary Dityrosine‐Induced Mitochondrial‐Lipid Homeostasis by Increasing Mitochondrial Complex Activity

Abstract

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.

Hydroxysafflor yellow A triggered a fast-to-slow muscle fiber-type conversionviaregulating FoxO1 in myocytes

“…The mitochondrial copy number was assessed using the ratio of mt-ND2 to nβ2M measured by RT-PCR. 27 Consistently, HSYA significantly increased the mitochondrial copy number (Fig. 5E and J).…”

Lycopene alleviates multiple-mycotoxin-induced toxicity by inhibiting mitochondrial damage and ferroptosis in the mouse jejunum

“…LYC is a common dietary supplement with antioxidant properties that also modulates the homeostasis of mitochondrial lipids. As previously reported, LYC supplementation promotes dityrosine-induced reductions in the activities of respiratory chain complexes, 43 inhibits ethanol/palmitoleic acid-induced mitochondrial dysfunction and ROS production in pancreatic acinar cells, 44 and suppresses oxidative stress and mitochondria-dependent apoptosis to enhance embryonic development in pigs. 45 Our results show that LYC treatment significantly repaired mitochondrial injury by maintaining the redox status and the balance of the mitochondrial morphological dynamics, suggesting that LYC alleviated the effects of ZEN + DON + AFB1-induced mitochondrial toxicity in the mouse jejunum.…”

Dityrosine in food: A review of its occurrence, health effects, detection methods, and mitigation strategies

“…Cell experiments using dityrosine and T3 in H9c2 cells (to elucidate the suppression of T3 function in myocardia by dityrosine) indicate that dityrosine interferes with the T3 regulation of the myocardium, causing myocardial-mitochondrial damage and energy-metabolism disorders (Lu et al, 2020). Similar research by Wang et al (2022) indicates that dityrosine administration induces a myocardial-energy-homeostasis disorder by inhibiting the activity of the respiratory chain complexes I and IV, increasing the accumulation of cardiac fatty acids and myocardial hypertrophy. Therefore, dietary dityrosine induces myocardial injury and can be used as an indicator of heart disease.…”

“…In particular, lycopene has been shown to improve dityrosine-induced myocardial energy homeostasis disorder by reducing oxidative stress and promoting energy metabolism in mice (J. Wang et al, 2022). Tea is another rich source of antioxidants.…”