Summary
This in vitro study examined how hexavalent chromium perturbs macrophage polarization, immunometabolic programming, and mitochondrial integrity in RAW264.7 mouse macrophage cells exposed to 0.63 to 20.00 micromol/L Cr(VI) for 24 hours. Cr(VI) drove a shift toward M1-type (pro-inflammatory) polarization, reduced cellular ATP production, redirected metabolism toward less efficient glycolysis despite increased glucose uptake, and caused mitochondrial membrane potential collapse. The study provides mechanistic detail on Cr(VI)-induced immune dysfunction relevant to the toxicology section of the hexavalent chromium wiki page.
Key numbers
| Measurement | Value | Condition | Source location |
|---|---|---|---|
| Cr(VI) concentrations tested | 0.63, 1.25, 2.50, 5.00, 10.00, 20.00 micromol/L | 24 h exposure | Methods section 2.2 |
| Cell viability at 2.50 micromol/L | approximately 80% | 24 h, CCK-8 assay | Results section 3.1 |
| Cell viability at 5.00 micromol/L | approximately 50% | 24 h, CCK-8 assay | Results section 3.1 |
| Genes uniquely expressed after Cr(VI) | 273 | 2.50 micromol/L vs. control, RNA-seq | Results section 3.4 |
| RNA-seq dose used | 2.50 micromol/L | Transcriptome-wide analysis | Methods section 2.2 |
Qualitative findings reported as concentration-dependent with statistical significance but without published numeric effect sizes for all endpoints: TNF-alpha, CD36, and CD80 mRNA increased; VEGFb mRNA decreased; ROS levels elevated by DCFH-DA; MDA elevated; ATP production decreased; Slc2a1 (GLUT1) expression approximately tripled in the 5.00 micromol/L group relative to control.
Evidence Fitness
Context only. This is an in vitro study using a mouse macrophage cell line under a 24-hour exposure window. It characterises mechanistic pathways at concentrations spanning the cytotoxic range (50% viability at 5.00 micromol/L) and does not translate to human dietary exposure estimates or food occurrence data. The findings inform the mechanistic toxicology of Cr(VI) and are cited accordingly.
Methods (brief)
RAW264.7 mouse macrophage cells (ATCC-derived) maintained in DMEM with 10% FBS. Potassium dichromate (K2Cr2O7, purity 90% or higher) dissolved in ultrapure water used as Cr(VI) source. Cell viability by CCK-8 and calcein-AM/PI live-dead staining. Polarization markers assessed by RT-qPCR (45 cycles) and Western blotting. Cytokine secretion by ELISA. Transcriptome by RNA-seq. ATP by luminescent assay. Glucose uptake by 2-NBDG fluorescence. ROS by DCFH-DA flow cytometry. Mitochondrial membrane potential by JC-1. Lipid peroxidation by MDA assay. LOD/LOQ, CRM and recovery for the chromium exposure concentrations are not reported; this is a cell-dosing study rather than an analytical measurement study.
Implications
- Certification: no direct application; provides mechanistic context for the immunotoxic basis of Cr(VI) hazard designation.
- Courses: illustrates the macrophage polarization mechanism at the cellular level, connecting to the broader inflammatory basis of metal toxicity.
- App: no contamination_profile data; not applicable.
- Microbiome: Cr(VI)-induced M1 macrophage polarization in intestinal macrophage populations is a potential metal-microbiome interaction thread for WikiBiome.
Provenance notes
Open access, CC BY 4.0. First and second authors (Li C and Zhang R) contributed equally. Affiliation: School of Engineering Medicine, Beihang University, Beijing; collaborating affiliations at Peking University School of Public Health and Henan Third People’s Hospital. No retraction or correction flags at time of ingest. See Chromium, Hexavalent for the page this source informs.
Update history
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