New evidence on the nephrotoxicity of fine particulate matter: Potential toxic components from different emission sources
Associations exist between fine particulate matter (PM2.5) exposure and impaired kidney function. However, the specific mechanisms and components causing renal damage remain unclear. PM2.5 was collected from an industrial and a rural area. Mice were categorized according to exposure, and biochemical...
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Elsevier
2025-02-01
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| Series: | Ecotoxicology and Environmental Safety |
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| Online Access: | http://www.sciencedirect.com/science/article/pii/S0147651325001447 |
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| author | Fu-Jen Cheng Chien-Er Huang Pei-Shih Chen Yu-Lun Tseng Chung-Shin Yuan Ching-Shu Lai |
| author_facet | Fu-Jen Cheng Chien-Er Huang Pei-Shih Chen Yu-Lun Tseng Chung-Shin Yuan Ching-Shu Lai |
| author_sort | Fu-Jen Cheng |
| collection | DOAJ |
| description | Associations exist between fine particulate matter (PM2.5) exposure and impaired kidney function. However, the specific mechanisms and components causing renal damage remain unclear. PM2.5 was collected from an industrial and a rural area. Mice were categorized according to exposure, and biochemical, western blotting, histological, and immunohistochemical analyses were performed to evaluate the impact of PM2.5 constituents on their kidneys. To assess the impact of different PM2.5 components on inflammatory responses, a study was conducted by exposing the murine macrophage cell line (RAW 264.7). The study used a chelating resin to remove the influence of heavy metals from the water extract and employed a Toll-like receptor 4 (TLR4) antagonist to eliminate the effects of endotoxin, thereby evaluating the cellular inflammatory responses induced by various PM2.5 components. The major metallic elements at the industrial site were Fe, Mg, Zn, and Ca, whereas those at site Rural were Ca, K, and Mg. PM2.5 water extracts from both sites induced inflammatory cytokine upregulation in the lungs and kidneys, and inflammatory cell infiltration, antioxidant activity downregulation, and elevated levels of kidney injury molecule 1 in the kidneys. Exposure to PM2.5 water extract increased the mRNA levels of tumor necrosis factor-α, interleukin-6, and nitrite production in RAW264.7 macrophages. The inflammatory response and nitrite production induced by the industrial-site PM2.5 water extract were significantly suppressed after treatment with a chelating resin, whereas those from the rural area were suppressed by the Toll-like receptor 4 (TLR4) antagonist. These results suggest that heavy metals are crucial factors in PM2.5-induced cellular inflammatory responses in industrial areas, whereas endotoxin receptor--TLR4 mediated inflammatory pathways are the primary factor responsible for this response in rural areas. Furthermore, at equivalent dosages, the renal toxicity induced by the water-soluble components of rural-site PM2.5 may exceed that from industrial areas. |
| format | Article |
| id | doaj-art-db0c7691b3d94cf599981d22ec857f86 |
| institution | Kabale University |
| issn | 0147-6513 |
| language | English |
| publishDate | 2025-02-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Ecotoxicology and Environmental Safety |
| spelling | doaj-art-db0c7691b3d94cf599981d22ec857f862025-02-05T04:31:02ZengElsevierEcotoxicology and Environmental Safety0147-65132025-02-01291117808New evidence on the nephrotoxicity of fine particulate matter: Potential toxic components from different emission sourcesFu-Jen Cheng0Chien-Er Huang1Pei-Shih Chen2Yu-Lun Tseng3Chung-Shin Yuan4Ching-Shu Lai5Department of Emergency Medicine, Kaohsiung Chang Gung Memorial Hospital, 123, Ta-Pei Road, Niao-Sung, Kaohsiung City 833, Taiwan, ROC; Chang Gung University College of Medicine, 259, Wenhua 1st Road, Guishan District, Taoyuan City 333, Taiwan, ROCDepartment of Chemical and Materials Engineering, Cheng Shiu University, No. 840 Chengcing Rd., Kaohsiung City 833, Taiwan, ROC; Super Micro Mass Research and Technology Center, Cheng Shiu University, No. 840 Chengcing Rd., Kaohsiung City 833, Taiwan, ROCDepartment of Public Health, College of Health Sciences, Kaohsiung Medical University, Kaohsiung City 807, Taiwan, ROCInstitute of Environmental Engineering, National Sun Yat-Sen University, 70, Lian-Hai Road, Kaohsiung City 804, Taiwan, ROCInstitute of Environmental Engineering, National Sun Yat-Sen University, 70, Lian-Hai Road, Kaohsiung City 804, Taiwan, ROC; Aerosol Science Research Center, National Sun Yat-sen University, 70, Lian-Hai Road, Kaohsiung City 804, Taiwan, ROC; Corresponding author at: Institute of Environmental Engineering, National Sun Yat-Sen University, 70, Lian-Hai Road, Kaohsiung City 804, Taiwan, ROC.Department of Seafood Science, National Kaohsiung University of Science and Technology, Kaohsiung City 811, Taiwan, ROC; Corresponding author.Associations exist between fine particulate matter (PM2.5) exposure and impaired kidney function. However, the specific mechanisms and components causing renal damage remain unclear. PM2.5 was collected from an industrial and a rural area. Mice were categorized according to exposure, and biochemical, western blotting, histological, and immunohistochemical analyses were performed to evaluate the impact of PM2.5 constituents on their kidneys. To assess the impact of different PM2.5 components on inflammatory responses, a study was conducted by exposing the murine macrophage cell line (RAW 264.7). The study used a chelating resin to remove the influence of heavy metals from the water extract and employed a Toll-like receptor 4 (TLR4) antagonist to eliminate the effects of endotoxin, thereby evaluating the cellular inflammatory responses induced by various PM2.5 components. The major metallic elements at the industrial site were Fe, Mg, Zn, and Ca, whereas those at site Rural were Ca, K, and Mg. PM2.5 water extracts from both sites induced inflammatory cytokine upregulation in the lungs and kidneys, and inflammatory cell infiltration, antioxidant activity downregulation, and elevated levels of kidney injury molecule 1 in the kidneys. Exposure to PM2.5 water extract increased the mRNA levels of tumor necrosis factor-α, interleukin-6, and nitrite production in RAW264.7 macrophages. The inflammatory response and nitrite production induced by the industrial-site PM2.5 water extract were significantly suppressed after treatment with a chelating resin, whereas those from the rural area were suppressed by the Toll-like receptor 4 (TLR4) antagonist. These results suggest that heavy metals are crucial factors in PM2.5-induced cellular inflammatory responses in industrial areas, whereas endotoxin receptor--TLR4 mediated inflammatory pathways are the primary factor responsible for this response in rural areas. Furthermore, at equivalent dosages, the renal toxicity induced by the water-soluble components of rural-site PM2.5 may exceed that from industrial areas.http://www.sciencedirect.com/science/article/pii/S0147651325001447PM2.5constituentsheavy metalsendotoxinmice kidneyangiotensin converter enzyme |
| spellingShingle | Fu-Jen Cheng Chien-Er Huang Pei-Shih Chen Yu-Lun Tseng Chung-Shin Yuan Ching-Shu Lai New evidence on the nephrotoxicity of fine particulate matter: Potential toxic components from different emission sources Ecotoxicology and Environmental Safety PM2.5 constituents heavy metals endotoxin mice kidney angiotensin converter enzyme |
| title | New evidence on the nephrotoxicity of fine particulate matter: Potential toxic components from different emission sources |
| title_full | New evidence on the nephrotoxicity of fine particulate matter: Potential toxic components from different emission sources |
| title_fullStr | New evidence on the nephrotoxicity of fine particulate matter: Potential toxic components from different emission sources |
| title_full_unstemmed | New evidence on the nephrotoxicity of fine particulate matter: Potential toxic components from different emission sources |
| title_short | New evidence on the nephrotoxicity of fine particulate matter: Potential toxic components from different emission sources |
| title_sort | new evidence on the nephrotoxicity of fine particulate matter potential toxic components from different emission sources |
| topic | PM2.5 constituents heavy metals endotoxin mice kidney angiotensin converter enzyme |
| url | http://www.sciencedirect.com/science/article/pii/S0147651325001447 |
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