Multiplexed quantitative evaluation on mitochondrial toxicity of tris (2,3-dibromopropyl) phosphate in hepatocyte
The frequent detection of (2,3-dibromopropyl) phosphate (TDBPP) in environment has led to a consistent risk to organisms. However, little is known about the toxicity of TDBPP exclusive for its carcinogen. Mitochondrion that tightly relates to adverse outcomes once deteriorated is referred as a targ...
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| Format: | Article |
| Language: | English |
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Elsevier
2021-09-01
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| Series: | Ecotoxicology and Environmental Safety |
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| Online Access: | http://www.sciencedirect.com/science/article/pii/S0147651321005376 |
| _version_ | 1818723752968454144 |
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| author | Xiaochun Ma Dezhao Lu Ying Liu Yifei Le Hang Chen Xiaowen Li Cui Wang |
| author_facet | Xiaochun Ma Dezhao Lu Ying Liu Yifei Le Hang Chen Xiaowen Li Cui Wang |
| author_sort | Xiaochun Ma |
| collection | DOAJ |
| description | The frequent detection of (2,3-dibromopropyl) phosphate (TDBPP) in environment has led to a consistent risk to organisms. However, little is known about the toxicity of TDBPP exclusive for its carcinogen. Mitochondrion that tightly relates to adverse outcomes once deteriorated is referred as a target of environmental pollutants. Here, we investigated the role of mitochondrial abnormality in development of cellular pathobiology especially lipid deposition when response to TDBPP in mitochondria-rich hepatocyte (AML12) at the same order of magnitude as the environmental concentrations (10−6 mol/L or below) via multiplexed quantitative high content analytic system. The present study claimed TDBPP shifted mitochondria from fusion morphology to fission phenotype charactering by less mitochondrial networks, larger mitochondrial areas and shorter branch length at 10−7 mol/L or above. This dynamic imbalance was triggered by high levels of fis and drp1 genes when treated with TDBPP. The deformation caused by TDBPP reciprocally influenced biogenesis through PGC1α and electron transport chains via ectopic expression of genes encoding for mitochondria complex I and III subunits. Accordingly, we observed high mitoROS level and low mitochondria membrane potential. Consequently, cells contained those abnormal mitochondria were predisposed to accumulating lipids after exposure to TDBPP. Here we showed that TDBPP deteriorated mitochondrial morphology and function, which may induce lipid generation. As for a banned while still emerged contaminant, our study also claimed further exploration on the non-carcinogenic toxicity of TDBPP. |
| first_indexed | 2024-12-17T21:15:31Z |
| format | Article |
| id | doaj.art-b21ec664a92c4cf7b85446206baf8ca1 |
| institution | Directory Open Access Journal |
| issn | 0147-6513 |
| language | English |
| last_indexed | 2024-12-17T21:15:31Z |
| publishDate | 2021-09-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Ecotoxicology and Environmental Safety |
| spelling | doaj.art-b21ec664a92c4cf7b85446206baf8ca12022-12-21T21:32:22ZengElsevierEcotoxicology and Environmental Safety0147-65132021-09-01221112425Multiplexed quantitative evaluation on mitochondrial toxicity of tris (2,3-dibromopropyl) phosphate in hepatocyteXiaochun Ma0Dezhao Lu1Ying Liu2Yifei Le3Hang Chen4Xiaowen Li5Cui Wang6Academy of Chinese Medical Science, Zhejiang Chinese Medical University, Hangzhou 310053, Zhejiang, People’s Republic of China; School of Life Science, Zhejiang Chinese Medical University, Hangzhou 310053, Zhejiang, People’s Republic of ChinaAcademy of Chinese Medical Science, Zhejiang Chinese Medical University, Hangzhou 310053, Zhejiang, People’s Republic of China; School of Life Science, Zhejiang Chinese Medical University, Hangzhou 310053, Zhejiang, People’s Republic of ChinaAcademy of Chinese Medical Science, Zhejiang Chinese Medical University, Hangzhou 310053, Zhejiang, People’s Republic of China; School of Life Science, Zhejiang Chinese Medical University, Hangzhou 310053, Zhejiang, People’s Republic of ChinaAcademy of Chinese Medical Science, Zhejiang Chinese Medical University, Hangzhou 310053, Zhejiang, People’s Republic of China; School of Life Science, Zhejiang Chinese Medical University, Hangzhou 310053, Zhejiang, People’s Republic of ChinaAcademy of Chinese Medical Science, Zhejiang Chinese Medical University, Hangzhou 310053, Zhejiang, People’s Republic of China; School of Life Science, Zhejiang Chinese Medical University, Hangzhou 310053, Zhejiang, People’s Republic of ChinaCangzhou Medical College, Cangzhou 061001, Hebei, People’s Republic of China; Corresponding author.Academy of Chinese Medical Science, Zhejiang Chinese Medical University, Hangzhou 310053, Zhejiang, People’s Republic of China; School of Life Science, Zhejiang Chinese Medical University, Hangzhou 310053, Zhejiang, People’s Republic of China; Corresponding author at: School of life science, zhejiang chinese medical university, Hangzhou 310053, Zhejiang, People's Republic of China.The frequent detection of (2,3-dibromopropyl) phosphate (TDBPP) in environment has led to a consistent risk to organisms. However, little is known about the toxicity of TDBPP exclusive for its carcinogen. Mitochondrion that tightly relates to adverse outcomes once deteriorated is referred as a target of environmental pollutants. Here, we investigated the role of mitochondrial abnormality in development of cellular pathobiology especially lipid deposition when response to TDBPP in mitochondria-rich hepatocyte (AML12) at the same order of magnitude as the environmental concentrations (10−6 mol/L or below) via multiplexed quantitative high content analytic system. The present study claimed TDBPP shifted mitochondria from fusion morphology to fission phenotype charactering by less mitochondrial networks, larger mitochondrial areas and shorter branch length at 10−7 mol/L or above. This dynamic imbalance was triggered by high levels of fis and drp1 genes when treated with TDBPP. The deformation caused by TDBPP reciprocally influenced biogenesis through PGC1α and electron transport chains via ectopic expression of genes encoding for mitochondria complex I and III subunits. Accordingly, we observed high mitoROS level and low mitochondria membrane potential. Consequently, cells contained those abnormal mitochondria were predisposed to accumulating lipids after exposure to TDBPP. Here we showed that TDBPP deteriorated mitochondrial morphology and function, which may induce lipid generation. As for a banned while still emerged contaminant, our study also claimed further exploration on the non-carcinogenic toxicity of TDBPP.http://www.sciencedirect.com/science/article/pii/S0147651321005376(23-dibromopropyl) phosphateMitochondria dynamicsMitochondria dysfunctionLipid accumulation |
| spellingShingle | Xiaochun Ma Dezhao Lu Ying Liu Yifei Le Hang Chen Xiaowen Li Cui Wang Multiplexed quantitative evaluation on mitochondrial toxicity of tris (2,3-dibromopropyl) phosphate in hepatocyte Ecotoxicology and Environmental Safety (2 3-dibromopropyl) phosphate Mitochondria dynamics Mitochondria dysfunction Lipid accumulation |
| title | Multiplexed quantitative evaluation on mitochondrial toxicity of tris (2,3-dibromopropyl) phosphate in hepatocyte |
| title_full | Multiplexed quantitative evaluation on mitochondrial toxicity of tris (2,3-dibromopropyl) phosphate in hepatocyte |
| title_fullStr | Multiplexed quantitative evaluation on mitochondrial toxicity of tris (2,3-dibromopropyl) phosphate in hepatocyte |
| title_full_unstemmed | Multiplexed quantitative evaluation on mitochondrial toxicity of tris (2,3-dibromopropyl) phosphate in hepatocyte |
| title_short | Multiplexed quantitative evaluation on mitochondrial toxicity of tris (2,3-dibromopropyl) phosphate in hepatocyte |
| title_sort | multiplexed quantitative evaluation on mitochondrial toxicity of tris 2 3 dibromopropyl phosphate in hepatocyte |
| topic | (2 3-dibromopropyl) phosphate Mitochondria dynamics Mitochondria dysfunction Lipid accumulation |
| url | http://www.sciencedirect.com/science/article/pii/S0147651321005376 |
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