ArticleJournal of toxicology and environmental health. Part A2015
In Vivo Exposures to Particulate Matter Collected from Saudi Arabia or Nickel Chloride Display Similar Dysregulation of Metabolic Syndrome Genes.
Article in Journal of toxicology and environmental health. Part A, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
9 citing papers in PubMed, 18 citations in OpenAlex.
- Particulate matter inhalation and the exacerbation of cardiopulmonary toxicity due to metabolic disease.Experimental biology and medicine (Maywood, N.J.) · 2021Review
- β-carotene oxygenase 2 deficiency-triggered mitochondrial oxidative stress promotes low-grade inflammation and metabolic dysfunction.Free radical biology & medicine · 2021Article
- Assessment of particulate matter toxicity and physicochemistry at the Claim 28 uranium mine site in Blue Gap, AZ.Journal of toxicology and environmental health. Part A · 2021Article
- Article
- Air pollution-derived particulate matter dysregulates hepatic Krebs cycle, glucose and lipid metabolism in mice.Scientific reports · 2019Article
- Associations forYonsei medical journal · 2019Article
- Association between Exposure to Ambient Air Particulates and Metabolic Syndrome Components in a Saudi Arabian Population.International journal of environmental research and public health · 2017Article
- Targeted Metabolomics Reveals Abnormal Hepatic Energy Metabolism by Depletion of β-Carotene Oxygenase 2 in Mice.Scientific reports · 2017Article
- Lack of β, β-carotene-9', 10'-oxygenase 2 leads to hepatic mitochondrial dysfunction and cellular oxidative stress in mice.Molecular nutrition & food research · 2017Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
Particulate matter (PM) exposures have been linked to mortality, low birth weights, hospital admissions, and diseases associated with metabolic syndrome, including diabetes mellitus, cardiovascular disease, and obesity. In a previous in vitro and in vivo study, data demonstrated that PM(10μm) collected from Jeddah, Saudi Arabia (PMSA), altered expression of genes involved in lipid and cholesterol metabolism, as well as many other genes associated with metabolic disorders. PMSA contains a relatively high concentration of nickel (Ni), known to be linked to several metabolic disorders. In order to evaluate whether Ni and PM exposures induce similar gene expression profiles, mice were exposed to 100 μg/50 μl PM(SA) (PM-100), 50 μg/50 μl nickel chloride (Ni-50), or 100 μg/50 μl nickel chloride (Ni-100) twice per week for 4 wk and hepatic gene expression changes were determined. Ultimately, 55 of the same genes were altered in all 3 exposures. However, where the two Ni groups differed markedly was in the regulation (up or down) of these genes. Ni-100 and PM-100 groups displayed similar regulations, whereby 104 of the 107 genes were similarly modulated. Many of the 107 genes are involved in metabolic syndrome and include ALDH4A1, BCO2, CYP1A, CYP2U, TOP2A. In addition, the top affected pathways, such as fatty acid α-oxidation, and lipid and carbohydrate metabolism, are involved in metabolic diseases. Most notably, the top diseased outcome affected by these changes in gene expression was cardiovascular disease. Given these data, it appears that Ni and PM(SA) exposures display similar gene expression profiles, modulating the expression of genes involved in metabolic disorders.
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