This study focused on the effects of oxidized tyrosine products (OTPs) and major component dityrosine (DT) on the brain and behavior of growing mice. Male and female mice were treated with daily intragastric administration of either tyrosine (Tyr; 420 μg/kg body weight), DT (420 μg/kg body weight), or OTPs (1909 μg/kg body weight) for 35 days. We found that pure DT and OTPs caused redox state imbalance, elevated levels of inflammatory factors, hippocampal oxidative damage, and neurotransmitter disorders while activating the mitochondrial apoptosis pathway in the hippocampus and downregulating the genes associated with learning and memory. These events eventually led to growing mice learning and memory impairment, lagging responses, and anxiety-like behaviors. Furthermore, the male mice exhibited slightly more oxidative damage than the females. These findings imply that contemporary diets and food-processing strategies of the modern world should be modified to reduce oxidized protein intake.
Scope: Recent studies have linked high consumption of red and processed meats to an increased risk of non-alcoholic fatty liver disease, and cooking-induced oxidation of proteins and amino acids might be contributing factors. Herein, this study investigates the influence of oxidized pork and the protein oxidation biomarker dityrosine (Dityr) on hepatic steatosis in mice. Methods and Results: Low-and high-oxidative injury pork (LOP and HOP) are freeze-dried to prepare mouse diets. Mice are fed a diet of either the control, LOP, HOP, LOP+Dityr, or Dityr for 12 weeks. HOP and Dityr intake induced oxidative stress and inflammation that impaired thyroid function and peripheral metabolism (reduced type 1 deiodinase activity) of thyroid hormones (THs). These lead to a decrease in the circulating as well as liver THs and induced hepatic steatosis. This process might be regulated through reduced TH levels and altered TH target genes and proteins related to hepatic lipid metabolism that ultimately inhibited hepatic energy metabolism, as indicated by increased hepatic lipid synthesis, decreased hepatic lipid catabolism, and fatty acid oxidation. Conclusion: HOP intake could induce hepatic steatosis by impairing TH function. Dityr plays an important role in the HOP-induced harmful effects.
Sea cucumber promotes multifaceted health benefits. However, the mechanisms of sea cucumber peptides (Scp) regulating the antifatigue capacity is still unknown. The present study is aimed at further elucidating the effects and mechanisms of Scp on the antifatigue capacity of mice. At first, C57BL/6J mice were assigned into four groups named Con, L-Scp, M-Scp, and H-Scp and received diets containing Scp (0%, 0.15%, 0.3%, and 0.5%, respectively) for continuous 30 days. On the 21th day, a fore grip test was conducted on mice. On the 25th day, a rotating rod test was conducted on mice. On the 30th day, the quantities of glycogen and mitochondrial DNA (mtDNA) were determined in 8 random mice and another 8 mice were forced to swim for 1 hour before slaughter for detecting biochemical indicators. It was observed that the Scp groups significantly prolonged the running time in rotarod, increased forelimb grip strength, improved lactic acid (LD) and urea nitrogen (BUN) levels in the serum, decreased lactic dehydrogenase (LDH) and glutamic oxalacetic transaminase (GOT) activities in the serum, increased blood glucose (BG) and glycogen (GN) levels in the liver and skeletal muscle after swimming, increased the activity of Na+-K+-ATPase and Ca2+-Mg2+-ATPase in the skeletal muscle and heart, and improved antioxidant capacity. Furthermore, Scp treatment significantly elevated the mRNA and protein relative levels of power-sensitive factors, lipid catabolism, and mitochondrial biogenesis and significantly upregulated mRNA levels of gluconeogenesis. Besides, mtDNA before the swimming test was increased in the three Scp groups. These results show that Scp treatment has antifatigue capacity. Furthermore, these results suggest that improved energy regulation and antioxidant capacity may be the result of improved mitochondrial function.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.