T-2 toxin induces cardiac fibrosis by causing metabolic disorders and up-regulating Sirt3/FoxO3α/MnSOD signaling pathway-mediated oxidative stress.

T-2 toxin, an omnipresent environmental contaminant, poses a serious risk to the health of humans and animals due to its pronounced cardiotoxicity. This study aimed to elucidate the molecular mechanism of cardiac tissue damage by T-2 toxin. Twenty-four male Sprague-Dawley rats were orally administered T-2 toxin through gavage for 12 weeks at the dose of 0, 10, and 100 nanograms per gram body weight per day (ng/(g·day)), respectively. Morphological, pathological, and ultrastructural alterations in cardiac tissue were meticulously examined. Non-targeted metabolomics analysis was employed to analyze alterations in cardiac metabolites. The expression of the Sirt3/FoxO3α/MnSOD signaling pathway and the level of oxidative stress markers were detected. The results showed that exposure to T-2 toxin elicited myocardial tissue disorders, interstitial hemorrhage, capillary dilation, and fibrotic damage. Mitochondria were markedly impaired, including swelling, fusion, matrix degradation, and membrane damage. Metabonomics analysis unveiled that T-2 toxin could cause alterations in cardiac metabolic profiles as well as in the Sirt3/FoxO3α/MnSOD signaling pathway. T-2 toxin could inhibit the expressions of the signaling pathway and elevate the level of oxidative stress. In conclusion, the T-2 toxin probably induces cardiac fibrotic impairment by affecting amino acid and choline metabolism as well as up-regulating oxidative stress mediated by the Sirt3/FoxO3α/MnSOD signaling pathway. This study is expected to provide targets for preventing and treating T-2 toxin-induced cardiac fibrotic injury.

Association between Body Mass Index and Serum Uric Acid: mediation analysis involving liver enzymes indicators.

BACKGROUND: Numerous studies have indicated a growing prevalence of hyperuricemia. Elevated levels of serum uric acid (SUA) have been established as influential factors in conditions such as obesity, metabolic syndrome, diabetes mellitus, gout, and cardiovascular disease. Overweight and obesity are closely related to an increase in SUA. Our objective is to demonstrate the mediating role of liver enzyme in the correlation between body mass index (BMI) and SUA. METHODS: A total of 5925 adults aged 18 to 65 were included in this cross-sectional study. Logistic regression and mediation analysis were used to investigate the relationship between BMI and hyperuricemia as well as liver enzyme levels. Standard methods were used to determine the biochemical indexes, including SUA, liver enzymes, and blood lipids in the collected samples. RESULTS: The study revealed that the prevalence of hyperuricemia was 28.0%. Furthermore, the prevalence of overweight and obesity was as high as 48.5%, with 70.7% of this subgroup presenting with hyperuricemia. There was a positive correlation between BMI and hyperuricemia, and elevated levels of liver enzymes (ALT, AST, GGT) were associated with a higher risk of hyperuricemia. The study also observed a positive correlation between BMI and liver enzymes (ALT, AST, GGT). The study findings suggested that ALT, AST, and GGT played significant mediating roles in the relationship between BMI and SUA. Specifically, the unadjusted model revealed that ALT and GGT accounted for 22.12% and 18.13% of the mediation effects, respectively. CONCLUSIONS: The study found that BMI is associated with hyperuricemia, where liver enzyme abnormalities may have a mediating role. It is suggested that being overweight or obese may affect liver enzyme levels, leading to increased SUA levels. Controlling weight and liver enzyme levels may help prevent and treat hyperuricemia.

An untargeted metabolomics study of cardiac pathology damage in rats caused by low selenium diet alone or in combination with T-2 toxin.

T-2 toxin is a highly cardiotoxic environmental contaminant. Selenium can uphold the cardiovascular system's functionality. Selenium insufficiency is common. The aim of this study was to elucidate the effects of low selenium diet alone or in combination with T-2 toxin on myocardial tissue damage. Thirty-two Sprague-Dawley rats of 3 weeks of age were randomized into control, low selenium diet, low selenium diet combined with T-2 toxin groups (at doses of 10 ng/g and 100 ng/g body weight) for 12-weeks intervention. Pathohistology and ultrastructural changes in cardiac tissue were observed. Changes in cardiac metabolites were analyzed using untargeted metabolomics. The findings demonstrated that cardiac tissue abnormalities, interstitial bleeding, inflammatory cell infiltration, and mitochondrial damage can be brought on by low selenium diet alone or in combination with the T-2 toxin. A low selenium diet alone or in combination with the T-2 toxin affected cardiac metabolic profiles and resulted in aberrant modifications in many metabolic pathways, including the metabolism of amino acids, cholesterol, and thiamine. Accordingly, low selenium diet and T-2 toxin may have a synergistic effect. Our findings provide fresh insights into the processes of cardiac injury by revealing the effects of low selenium diet and T-2 toxin on cardiac metabolism.

The Association between Serum Copper and Bone Mineral Density among Adolescents Aged 12 to 19 in the United States.

Bone mineral density (BMD) is a key parameter widely used in the assessment of bone health. Although many investigations have explored the relationship between trace elements and BMD, there are fewer studies focused on serum copper and BMD, especially for adolescents. Using data extracted from the National Health and Nutrition Examination Survey, we applied a multiple-linear regression and smooth curve fitting to assess the relationship between serum copper and BMD. A total of 910 participants were finally included in this study. After adjusting for relevant covariates, serum copper was negatively associated with lumbar spine BMD (ß = -0.057, 95% CI: -0.109 to -0.005), trunk bone BMD (ß = -0.068, 95% CI: -0.110 to -0.026), pelvis BMD (ß = -0.085, 95% CI: -0.145 to -0.024), subtotal BMD (ß = -0.072, 95% CI: -0.111 to -0.033), and total BMD (ß = -0.051, 95% CI: -0.087 to -0.016) (p < 0.05). In quartile analysis, the highest level of serum copper was associated with decreased BMD when compared with those at the lowest quartile (p < 0.05). The stratified analysis revealed a significant interaction between age and the effects of serum copper on trunk bone BMD (p = 0.022) and pelvis BMD (p = 0.018). Meanwhile, the higher level of serum copper was negatively associated with BMD in males, and gender modified the relationship (p < 0.001). Future longitudinal studies will be necessary for a more definitive interpretation of our results.