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Updated: Oct 3, 2025
Experimental Protocol for Detecting Mitochondrial Function in Hepatocytes Exposed to Organochlorine Pesticides
Published on: September 16, 2020
Oral exposure to a hexafluoropropylene oxide trimer acid (HFPO-TA) disrupts mitochondrial function and biogenesis in
Xiaoxian Xie1, Jiafeng Zhou1, Luting Hu1
1College of Biotechnology and Bioengineering, Zhejiang University of Technology, Hangzhou 310032, China.
Abstract:
Hexafluoropropylene oxide trimer acid (HFPO-TA) is reported to have hepatotoxicity, lipotoxicity, and cytotoxicity. In this study, the toxicological effects of HFPO-TA on mitochondrial function and biogenesis were studied. Mice were exposed to drinking water which contained either 2, 20, or 200 μg/L HFPO-TA. Results showed exposure to HFPO-TA induced disadvantageous physiological changes in mice, including increases in liver weight, altered cell morphology, and inflammatory responses. Specifically, exposure to 200 μg/L HFPO-TA increased mitochondria number, relative mitochondrial DNA (mtDNA) content, and mRNA levels of mitochondrial genes encoded by mtDNA. Significant increases in TFAM mRNA and protein levels were also observed. Liver metabolome analysis also showed exposure to 200 μg/L HFPO-TA further enhanced increases in metabolites and altered metabolic pathways that correlated with mitochondrial function, especially the production of ATP. HFPO-TA exposure increased protein expression of mitochondrial complex I-V, and the activities of key enzymes involved in TCA cycle (α-ketoglutarate dehydrogenase, citrate synthase, and succinate dehydrogenase). Furthermore, exposure to 200 μg/L HFPO-TA significantly up-regulating mRNA and protein levels of Opa1, Mfn1, Mfn2, Fis1, and Mff, but did not change Drp1. These findings suggest HFPO-TA could have detrimental effects on health of animals, particularly it was associated with disrupted mitochondrial energy metabolism.
Insights
Hexafluoropropylene oxide trimer acid (HFPO-TA) exposure disrupted mitochondrial energy metabolism in mice, increasing liver weight and altering cellular functions. This highlights potential health risks associated with HFPO-TA contamination.
Area of Science:
- Toxicology
- Mitochondrial Biology
- Environmental Health
Background:
- Hexafluoropropylene oxide trimer acid (HFPO-TA) is a chemical contaminant with known toxic effects.
- Previous studies suggest HFPO-TA may cause hepatotoxicity, lipotoxicity, and cytotoxicity.
- The impact of HFPO-TA on mitochondrial function and biogenesis requires further investigation.
Purpose of the Study:
- To investigate the toxicological effects of HFPO-TA on mitochondrial function and biogenesis in a mouse model.
- To assess the physiological and metabolic changes induced by HFPO-TA exposure.
- To elucidate the mechanisms underlying HFPO-TA's detrimental health effects.
Main Methods:
- Mice were exposed to varying concentrations of HFPO-TA (2, 20, 200 μg/L) in drinking water.
- Evaluated liver weight, cellular morphology, and inflammatory responses.
- Analyzed mitochondrial number, mitochondrial DNA (mtDNA) content, and gene/protein expression related to mitochondrial function and biogenesis.
- Conducted liver metabolome analysis to assess metabolic pathway alterations.
Main Results:
- HFPO-TA exposure led to increased liver weight, altered cell morphology, and inflammatory responses.
- High-dose HFPO-TA (200 μg/L) increased mitochondrial number, mtDNA content, and expression of mtDNA-encoded mitochondrial genes.
- Significant upregulation of TFAM, mitochondrial complexes I-V, TCA cycle enzymes, and proteins involved in mitochondrial dynamics (Opa1, Mfn1, Mfn2, Fis1, Mff) was observed.
- Metabolome analysis revealed altered metabolic pathways linked to mitochondrial function and ATP production.
Conclusions:
- HFPO-TA exposure induces significant physiological and metabolic disruptions in animals.
- The chemical is associated with altered mitochondrial biogenesis and energy metabolism, particularly ATP production.
- These findings suggest HFPO-TA poses detrimental health risks due to its impact on cellular energy processes.
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