We explore the feasibility of the long-term transportation of live large yellow croakers (Pseudosciaena crocea) using the combined method of CO₂ anesthesia and hypothermia hibernation, and its effect on the quality of recovered fish stored at 4 °C. Fish treated with CO₂ anesthesia at a 2 ppm/s aeration rate were cooled at 3 °C/h to hibernate survived for 36 h at 8 °C in seawater. This method resulted in better survival rates and time, and a lower operational time than hypothermia hibernation or CO₂ anesthesia methods. The results of a blood analysis indicated that the stress experienced by the fish during hibernation was mitigated, but existent after recovery. The drip loss rate of the ordinary muscle of hibernated fish was significantly different from that of the control group at 4 °C, but there was no significant difference in the pH, lactic acid content, and color during early storage. Furthermore, hibernation did not affect springiness and chewiness. Thus, the combination of CO₂ anesthesia and hibernation may improve the survival and operation efficiency of fish in long-term transportation. However, this method affects the quality of fish after long-term storage. Thus, hibernated fish should be consumed after appropriate domestication or immediately after recovery.

It has been strongly suggested that selenium deficiency and T-2 toxin contamination have a strong relationship with the occurrence and development of Kashin–Beck disease (KBD). In order to provide information for understanding the high prevalence of KBD in Tibet, this study collected the responses to a cubital venous blood and dietary questionnaire of 125 subjects including 75 KBD patients and 50 healthy controls in a KBD-prevalent county (Luolong County) in Tibet, China. A total of 10 household local families were randomly selected in this area, and local diet samples of brick tea, Zanba powder, milk residue, and hulless Barley were collected from these residents. Selenium content in blood was detected by inductively coupled plasma mass spectrometry (ICP-MS). The T-2 toxin contamination level in food sample was assayed using an ELISA kit. The selenium levels of patients and controls were 42.0 ± 19.8 and 56.06 ± 22.4 μg/L, respectively. The serum selenium level in controls was higher than that in patients, but there was no significant difference, and the serum selenium level both in patients and controls in Tibet was lower than the normal range. The results of the dietary survey showed that the number of respondents who consumed butter tea was large; 46.67% of patients indicated that they drank buttered tea every day, which was significantly higher than in controls. The contents of T-2 toxin in Zanba powder, milk residue, hulless barley and drinking water samples were below the detection limit (0.05 μg/kg); this result was labeled Tr. Unexpectedly, the contents of T-2 toxin in brick tea were higher, with average levels of 424 ± 56 μg/kg in Detong village and 396 ± 24 μg/kg in Langcuo village. For the first time, we report the presence of an extremely high concentration of T-2 toxin in brick tea of Tibet.

Objectives: We aimed to explore the possible effects of Kashin–Beck disease (KBD) on the risk of sarcopenia and its possible interaction in the association between the risk of sarcopenia and element concentration. Methods: This cross-sectional study was conducted among individuals 18–75 years old in Qamdo, a KBD-endemic area. All individuals received physical and radiological examinations before recruitment. Patients with KBD were enrolled in the KBD group based on a diagnosis of national criteria WS/T 207-2010. Healthy individuals without KBD were enrolled in the non-KBD group. Participants with a history of element supplements, other severe musculoskeletal diseases, or organ dysfunctions were excluded. We adopted WOMAC scores for the assessment of musculoskeletal conditions and SARC-F scores for the risk of sarcopenia. Patients with SARC-F ≥ 4 were at risk of sarcopenia. Serum element concentrations were analyzed by inductively coupled plasma mass spectrometry. Dose–relationship effects of clinical scores and element concentrations on the risk of sarcopenia were determined in correlation analysis. Risk factors were identified using univariate and multivariate regression. Statistical analysis was conducted using R software. Results: A total of 65 patients with KBD and 38 participants without KBD were enrolled in the analysis. After propensity score matching, population characteristics were comparable in the two groups, and the incidence of SARC-F ≥ 4 was determined to be higher in the KBD group (p = 0.002). The WOMAC scores were correlated with SARC-F scores in the KBD group (p < 0.001) and non-KBD (p < 0.001) group, respectively. Further analysis proved that KBD was the independent risk factor for the risk of sarcopenia (p = 0.014). Moreover, high Selenium concentrations were associated with a low risk of sarcopenia in the non-KBD group (p = 0.047), while this association was not observed in the KBD group (p = 0.239). Conclusions: KBD as an independent risk factor increased the risk of sarcopenia for patients. Although high Se concentration was associated with a low risk of sarcopenia in participants without KBD, this association was not observed in those with KBD.

Background: Under oxidative stress conditions, the increased levels of reactive oxygen species (ROS) within cells disrupt the intracellular homeostasis. Tartary buckwheat peptides exert their effects by scavenging oxidative free radicals, such as superoxide anion and hydrogen peroxide, thereby reducing oxidative damage within cells. Meanwhile, these peptides safeguard mitochondria by maintaining the mitochondrial membrane potential, decreasing the production of mitochondrial oxygen free radicals, and regulating mitochondrial biogenesis and autophagy to preserve mitochondrial homeostasis. Through these mechanisms, Tartary buckwheat peptides restore the intracellular redox balance, sustain cellular energy metabolism and biosynthesis, and ensure normal cellular physiological functions, which is of great significance for cell survival and adaptation under oxidative stress conditions. Objectives: In this experiment, a classical cellular oxidative stress model was established. Indicators related to antioxidant capacity and mitochondrial membrane potential changes, as well as pathways associated with oxidative stress, were selected for detection. The aim was to elucidate the effects of Tartary buckwheat oligopeptides on the metabolism of cells in response to oxidative stress. Methods: In this study, we established an oxidative damage model of mouse skeletal muscle myoblast (SOL8) cells using hydrogen peroxide (H₂O₂), investigated the pre-protective effects of Tartary buckwheat oligopeptides on H₂O₂-induced oxidative stress damage in SOL8 cells at the cellular level, and explored the possible mechanisms. The CCK-8 method is a colorimetric assay based on WST-8-[2-(2-methoxy-4-nitrophenyl)-3-(4-nitrophenyl)-5-(2,4-disulfophenyl)-2H-tetrazolium, monosodiumsalt], which is used to detect cell proliferation and cytotoxicity. Results: The value of CCK-8 showed that, when the cells were exposed to 0.01 mmol/L H₂O₂ for 1 h and 10 mg/mL Tartary buckwheat oligopeptides intervention for 48 h, these were the optimal conditions. Compared with the H₂O₂ group, the intervention group (KB/H₂O₂ group) showed that the production of ROS was significantly reduced (p < 0.001), the malondialdehyde (MDA) content was significantly decreased (p < 0.05), and the activity of catalase (CAT) was significantly increased (p < 0.01); the mitochondrial membrane potential in the KB/H₂O₂ group tended to return to the level of the control group, and they all showed dose-dependent effects. Compared with the H₂O₂ group, the mRNA expression of KEAP1 in the KB/H₂O₂ group decreased, while the mRNA expression of NRF2α, HO-1, nrf1, PGC-1, P62, and PINK increased. Conclusions: Therefore, Tartary buckwheat oligopeptides have a significant pre-protective effect on H₂O₂-induced SOL8 cells, possibly by enhancing the activity of superoxide dismutase, reducing ROS attack, balancing mitochondrial membrane potential, and maintaining intracellular homeostasis.