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Associations between multiple essential trace metal concentrations and risk of hyperuricemia: insights from a central Chinese population.

Previous studies have indicated that levels of individual essential trace metals are related to hyperuricemia (HUA), but evidence on their combined effects is limited. To address this gap, the associations of individual and joint levels of 12 essential trace metals (manganese, selenium, nickel, chromium, cobalt, tin, iron, molybdenum, zinc, strontium, vanadium, and copper) with the risk of HUA were investigated in 2,021 adults recruited from Hunan Province, China. Inductively coupled plasma mass spectrometry (ICP-MS) was employed to determine urinary metal concentrations. Logistic regression, Bayesian kernel machine regression (BKMR), and quantile g calculation (Qgcomp) were applied to evaluate the associations of single and mixture metal concentrations with HUA. Of the participants, 516 (25.53%) were diagnosed with HUA. Inverse associations were found between vanadium, chromium, manganese, iron, cobalt, selenium, strontium, and molybdenum levels and HUA, with ORs ranging from 0.63 to 0.91. Conversely, a positive association was observed between zinc concentration and HUA [OR (95% CI): 1.17 (1.01, 1.37)]. Both BKMR and Qgcomp models showed a negative overall effect of essential trace metals on HUA risk, with strontium (- 43.6%) and vanadium (- 27.8%) being the main contributors. In addition, formal interaction tests revealed significant effect modification by age for tin and by BMI for zinc. In conclusion, the levels of essential trace metals were linked to a decreased risk of HUA, and these associations were modified by age and BMI only for specific metals.

Humans

Integration of metabolomics and proteomics reveals the toxicological mechanisms of environmentally relevant concentrations of cadmium on juvenile rockfish (Sebastes schlegelii).

As a highly toxic heavy metal, cadmium (Cd) is widely distributed in the coastal environments of the Bohai Sea, posing significant ecological and health risks. This is of particular concern for Sebastes schlegelii, a rockfish species commonly found along the Bohai coast and consumed by local populations. In this study, juvenile S. schlegelii were randomly assigned to three groups (control, 5 and 50&#xa0;&#x3bc;g/L Cd) for a 14-day exposure period, followed by analysis of Cd bioaccumulation, as well as metabolomic and proteomic profiling. ICP-MS analysis indicated dose-dependent Cd bioaccumulation in the whole body, with 0.11&#xa0;&#xb1;&#xa0;0.07&#xa0;&#x3bc;g/g dry weight in the 5&#xa0;&#x3bc;g/L group and 0.38&#xa0;&#xb1;&#xa0;0.09&#xa0;&#x3bc;g/g dry weight in the 50&#xa0;&#x3bc;g/L group (9.5-fold higher than the control, p&#xa0;<&#xa0;0.05). An iTRAQ-based proteomic analysis determined 168 differentially expressed proteins, while 1H NMR-based metabolomic profiling identified 34 metabolites with significant alterations. Integrated analysis of the proteomic and metabolomic data provided insights into the molecular responses of juvenile rockfish to Cd exposure. Specifically, metabolomic results indicated significant alterations in key metabolites, including lactate, phosphocholine, adenosine triphosphate, alanine, and inosine in the Cd-treated groups. Proteomic analysis further suggested that Cd exposure was associated with immune and oxidative stress responses, neurotoxicity, cellular damage, and disruptions in critical metabolic pathways, such as glycolysis, the tricarboxylic acid cycle, amino acid and lipid metabolism. Overall, this study demonstrates the utility of integrating proteomics and metabolomics to characterize molecular responses to Cd stress in juvenile S. schlegelii.

Animals

Attribution of PM2.5-Induced Transcriptomic Perturbation to Toxic Components.

Ambient fine particulate matter (PM2.5) is a chemically complex mixture whose health impacts are not fully captured by particle mass. Here, we developed an interpretable chemotranscriptomic framework to attribute PM2.5-induced molecular perturbations to toxicity-relevant components. PM2.5 collected from urban roadside and coastal environments was separated into whole, extractable, and unextractable fractions, characterized by LC/GC &#xd7; GC-HRMS-based nontarget analysis and inductively coupled plasma mass spectrometry (ICP-MS), and evaluated using cytotoxicity testing and transcriptomic profiling in human bronchial epithelial cells. Urban PM2.5 exhibited greater cytotoxic potency per unit mass than coastal PM2.5, with extractable fractions accounting for most cytotoxic and pathway-level responses. Transcriptomics revealed distinct site-specific modes of action: urban PM2.5 preferentially induced oxidative stress, xenobiotic metabolism, and cell cycle suppression, consistent with acute, nonapoptotic injury, whereas coastal PM2.5 elicited weaker cytotoxicity but stronger interferon-mediated immune and apoptosis-related signaling. Integrating chemical abundance with pathway activity using random forest regression, SHAP interpretation, and mechanistic corroboration reduced 5,033 detected features to 444 pathway-linked candidate drivers. Fewer than 5% of features explained &#x223c;95% of cumulative model contribution. Standard-confirmed contributors included plasticizer-related compounds, aromatic and heteroaromatic combustion products, and copper for urban PM2.5 and secondary/aged organics and nickel for coastal PM2.5. These findings support mechanism-informed prioritization of hazardous PM2.5 components beyond mass-based assessment.

Particulate Matter

Partners in root nodule symbiosis respond uniquely to heavy metal stresses in a host genotype-dependent manner.

The mutualistic symbiosis between legume roots and soil rhizobia culminates in the formation of root nodules, where nitrogen is fixed. Root nodule symbiosis is inhibited by heavy metal stress. In this study, we investigated the relative responses of the symbiotic partners to a non-essential heavy metal cadmium (Cd) and an essential heavy metal zinc (Zn) stress and identified patterns in gene expression. We performed dual transcriptomics in nodules, using the Medicago truncatula-Sinorhizobium meliloti symbiotic system. Phenotypes were measured in the wild-type Medicago truncatula and a mutant in an ABC transporter gene (Mtabcg36), which showed compromised nodule formation in control conditions and further after heavy metal treatment. We observed that the rhizobia were particularly sensitive to Zn in mutant nodules. The greatest degree of differential gene expression in the host plant were observed under Cd and Zn treatments in wild-type nodules. Most Cd-regulated host genes were also differentially regulated by Zn, revealing little discernment between an essential and a non-essential ion under increased exposure. Furthermore, the host response to both the stresses affected auxin and iron homeostasis genes in a host genotype-dependent manner. Our results suggested impaired cadmium export from the mutant nodules. These results have potential implications in agricultural management systems and bioremediation strategies.

Symbiosis