ArticleFree radical biology & medicine2019
Low-dose cadmium disrupts mitochondrial citric acid cycle and lipid metabolism in mouse lung.
Article in Free radical biology & medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 71 citations in OpenAlex.
- Single-cell RNA sequencing reveals dysregulation of innate immune signaling in early-life respiratory syncytial virus infection with subsequent low-level cadmium exposure.Toxicology reports · 2026Article
- Proteomic Insights into Molybdenum-Induced Pancreatic Injury in Goats.Biological trace element research · 2026Article
- Carvacrol Modulates Cadmium-Induced Behavioral, Biochemical, Histopathological, and Metabolomic Alterations in rats.Biological trace element research · 2026Article
- Integrated Network Toxicology and Metabolomics Elucidate Mechanisms of Carbosulfan-Induced Respiratory Toxicity in Rats.International journal of molecular sciences · 2026Article
- Cadmium induces ferroptosis in mouse spermatocytes by activating the ROS-TCA pathway.Scientific reports · 2026Article
- Single-Cell Multiome Impact of Prenatal Heavy Metal Exposure on Early Airway Development.American journal of respiratory cell and molecular biology · 2026Article
- Cadmium exposure at low environmental levels induces cognitive decline in aged male mice.Neurotoxicology · 2026Article
- The effects of combined low-dose cadmium and deltamethrin on mitochondrial bioenergetics and metabolism in human lung fibroblasts.Toxicology reports · 2025Article
- Cadmium exposure following early-life respiratory syncytial virus infection promotes lung fibrosis through autophagy inhibition.Toxicological sciences : an official journal of the Society of Toxicology · 2025Article
- Pyrimidine Biosynthesis in Branching Morphogenesis Defects Induced by Prenatal Heavy Metal Exposure.American journal of respiratory cell and molecular biology · 2024Article
- Co-exposure effects of urinary polycyclic aromatic hydrocarbons and metals on lung function: mediating role of systematic inflammation.BMC pulmonary medicine · 2024Article
- Integrating Transcriptomics and Proteomics to Characterize the Intestinal Responses to Cadmium Exposure Using a Piglet Model.International journal of molecular sciences · 2024Article
- The Protective Effects ofToxics · 2024Article
- Redox organization of living systems.Free radical biology & medicine · 2024Review
- Protein S-palmitoylation enhances profibrotic signaling in response to cadmium.Toxicology and applied pharmacology · 2024Article
- Dandelion (Foods (Basel, Switzerland) · 2023Article
- Study on the relationship between selenium and cadmium in diseased human lungs.Advances in redox research · 2023Article
- Low-Dose Cadmium Potentiates Metabolic Reprogramming Following Early-Life Respiratory Syncytial Virus Infection.Toxicological sciences : an official journal of the Society of Toxicology · 2022Article
- Article
- Protective effects of vitexin on cadmium-induced renal toxicity in rats.Saudi journal of biological sciences · 2021Article
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
Cadmium (Cd) causes acute and chronic lung toxicities at occupational exposure levels, yet the impacts of Cd exposure at low levels through dietary intake remain largely uncharacterized. Health concerns arise because humans do not have an effective Cd elimination mechanism, resulting in a long (10- to 35-y) biological half-life. Previous studies showed increased mitochondrial oxidative stress and cell death by Cd yet the details of mitochondrial alterations by low levels of Cd remain unexplored. In the current study, we examined the impacts of Cd burden at a low environmental level on lung metabolome, redox proteome, and inflammation in mice given Cd at low levels by drinking water (0, 0.2, 0.6 and 2.0 mg Cd/L) for 16 weeks. The results showed that mice accumulated lung Cd comparable to non-smoking humans and showed inflammation in lung by histopathology at 2 mg Cd/L. The results of high resolution metabolomics combined with bioinformatics showed that mice treated with 2 mg Cd/L increased levels of lipids in the lung, accompanied by disruption in mitochondrial energy metabolism. In addition, targeted metabolomic analysis showed that these mice had increased accumulation of mitochondrial carnitine and citric acid cycle intermediates. The results of redox proteomics showed that Cd at 2 mg/L stimulated oxidation of isocitrate dehydrogenase, malate dehydrogenase and ATP synthase. Taken together, the results showed impaired mitochondrial function and accumulation of lipids in the lung with a Cd dose response relevant to non-smokers without occupational exposures. These findings suggest that dietary Cd intake could be an important variable contributing to human pulmonary disorders.
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