[Effects of tyrosine oxidation products on redox state in myocardium of rats].

Objective: To explore the effects of tyrosine oxidized products (TOP) on the redox state of rats myocardium and investigate the oxidative damage mechanism.

Methods: Male SD Rats were randomly assigned to three groups and treated respectively with normal diet (Group C), 440 mg/kg TOP (Group TOP), 440 mg/kg tyrosine oxidized products plus 5 mg/kg lipoic acid (Group TOP + LA). Indicators of oxidative stress in blood and myocardial were measured at the end of 6 weeks, 12 weeks and 24 weeks. RT-PCR was used to detect mRNA expression of Nrf2, Trx, NF-κB and AP-1 in myocardium.

Results: Compared to the control group (Group C), reactive oxygen species (ROS), carbonyl (PC), malondialdehyde (MDA), dityrosine (Dityr), 3-nitrotyrosine (3-NT) in rats blood and myocardium were all significantly increased in the TOP group (P < 0.05). Total antioxidant capacity (T-AOC), catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), reducing glutathione (GSH) and oxidized glutathione (GSSG) levels all decreased significantly (P < 0.05). The mRNA expression of Nrf2, Trx-1, NF-κB, AP-1 RNA significantly up-regulated (P < 0.05) in the TOP group compared to the control.

Conclusion: Tyrosine oxidized products impairs antioxidant defense system and lead to accumulation of protein oxidation products in rats myocardium. Moreover, lipoic acid performs a positive effect in the protective reaction, which may adjusted by regulation of redox signaling pathway.