Nickel exposure induces gut microbiome disorder and serum uric acid elevation Original paper
Researched by:
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Dr. Umar
ID
Dr. Umar
Read MoreClinical Pharmacist and Clinical Pharmacy Master’s candidate focused on antibiotic stewardship, AI-driven pharmacy practice, and research that strengthens safe and effective medication use. Experience spans digital health research with Bloomsbury Health (London), pharmacovigilance in patient support programs, and behavioral approaches to mental health care. Published work includes studies on antibiotic use and awareness, AI applications in medicine, postpartum depression management, and patient safety reporting. Developer of an AI-based clinical decision support system designed to enhance antimicrobial stewardship and optimize therapeutic outcomes.
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Metals
Metals
Heavy metals play a significant and multifaceted role in the pathogenicity of microbial species.
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Microbes
Microbes
Microbes, short for microorganisms, are tiny living organisms that are ubiquitous in the environment, including on and inside the human body. They play a crucial role in human health and disease, functioning within complex ecosystems in various parts of the body, such as the skin, mouth, gut, and respiratory tract. The human microbiome, which is […]
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Dr. Umar
Read More
Researched by:
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Dr. Umar
ID
Dr. Umar
Read More
Microbiome Signatures identifies and validates condition-specific microbiome shifts and interventions to accelerate clinical translation. Our multidisciplinary team supports clinicians, researchers, and innovators in turning microbiome science into actionable medicine.
Dr. Umar
What was studied?
Nickel exposure induces gut microbiome disorder, and serum uric acid elevation was investigated to understand how chronic nickel exposure affects hyperuricemia through gut microbial and metabolic alterations in humans and mice. The study integrated human occupational exposure data, targeted microbial profiling, and metabolomic analyses to determine mechanistic links between nickel-associated dysbiosis, disrupted intestinal purine catabolism, and elevated serum uric acid. The research combined 16S rRNA sequencing and LC-MS/MS metabolomics to map microbial taxa changes and purine pathway perturbations, while mouse models validated causality and inflammatory consequences. The work also examined correlations between microbial shifts, bile acid metabolism, oxidative stress markers, and inflammation, revealing a multisystem disruption connecting heavy metal exposure to uric acid accumulation.
Who was studied?
A total of 109 human participants from an occupational cohort in Jinchang, China were examined, including 92 nickel-exposed workers and 17 unexposed controls. Inclusion criteria excluded kidney, liver, thyroid, or intestinal disease, ensuring uric acid elevations reflected exposure-related mechanisms rather than comorbidities. Fecal and serum samples were collected for microbiome and metabolomic profiling. Complementary mouse experiments used female Kun Ming mice receiving oral nickel chloride for 35 days to assess causal relationships between nickel exposure, microbiome disruption, purine metabolism, and systemic inflammation. Both populations showed consistent patterns, strengthening translational relevance.
Most important findings
Nickel exposure induced clear microbiome alterations strongly associated with disrupted purine metabolism and higher serum uric acid. Key purine-degrading taxa—including Lactobacillus, Lachnospiraceae_unclassified, and Blautia—were significantly reduced. These microbes normally degrade uric acid or reduce purine absorption, and their depletion paralleled elevated fecal purines and impaired intestinal purine breakdown. Pathogenic or inflammation-associated taxa, such as Parabacteroides, Escherichia-Shigella, Alistipes, and Mycoplasma, were enriched, contributing to intestinal inflammation and increased permeability. Metabolomic analyses showed elevated fecal adenine, guanine, inosine, and hypoxanthine, while serum uric acid was significantly higher. Mouse data confirmed increased serum uric acid, heightened pro-inflammatory cytokines, oxidative stress markers, and similar microbiome disruptions. Together, these findings identify a gut-driven mechanism in which nickel suppresses purine degradation, enhances systemic absorption of purines, and fosters inflammatory conditions that exacerbate uric acid accumulation.
| Microbial/Metabolic Change | Effect Associated with Nickel Exposure |
|---|---|
| ↓ Lactobacillus, Blautia | Reduced purine degradation and anti-inflammatory activity |
| ↑ Parabacteroides, Escherichia-Shigella | Increased pathogenic and inflammatory signaling |
| ↑ Fecal purines (adenine, inosine, etc.) | Impaired intestinal purine catabolism |
| ↑ Serum uric acid and TNF-α | Systemic inflammation and hyperuricemia |
Key implications
This study provides strong evidence that nickel-induced hyperuricemia is mediated not by impaired renal excretion alone but by microbiome-driven metabolic dysfunction. Heavy metal exposure disrupts the intestinal ecosystem, reduces key uricolytic microbes, suppresses purine catabolism, increases gut permeability, and intensifies inflammation. These findings expand the known environmental determinants of hyperuricemia and spotlight gut microbiome signatures—particularly reductions in Lactobacillus, Blautia, and Lachnospiraceae_unclassified and enrichment of inflammatory taxa—as potential biomarkers. Clinically, microbiome-targeted interventions may represent future therapeutic strategies for heavy-metal–associated hyperuricemia.
Citation
Yang J, Feng P, Ling Z, et al. Nickel exposure induces gut microbiome disorder and serum uric acid elevation. Environmental Pollution. 2023;324:121349. doi:10.1016/j.envpol.2023.121349
Nickel
Bacteria regulate transition metal levels through complex mechanisms to ensure survival and adaptability, influencing both their physiology and the development of antimicrobial strategies.