Calcium alleviates fluoride-induced kidney damage via FAS/FASL, TNFR/TNF, DR5/TRAIL pathways in rats
| Autor: | Xiaofang Cheng, Ram Kumar Manthari, Jinming Wang, Huimiao Xu, Yangfei Zhao, Jiarong Yang, Junjiang Fan, Haojie Li, Jundong Wang |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2021 |
| Předmět: |
medicine.medical_specialty
Fas Ligand Protein Health Toxicology and Mutagenesis chemistry.chemical_element Renal function Caspase 3 Apoptosis Calcium Caspase 8 Kidney Fas ligand Environmental pollution Rats Sprague-Dawley Fluorides chemistry.chemical_compound Internal medicine Sodium fluoride medicine Animals Death receptor-mediated pathway GE1-350 Fluoride Tumor Necrosis Factor-alpha Public Health Environmental and Occupational Health General Medicine Pollution Rats Calcium Dietary Environmental sciences medicine.anatomical_structure Endocrinology chemistry TD172-193.5 |
| Zdroj: | Ecotoxicology and Environmental Safety, Vol 226, Iss, Pp 112851-(2021) |
| ISSN: | 0147-6513 |
| Popis: | Long-term excessive intake of fluoride (F) can cause osseous and non-osseous damage. The kidney is the main fluoride excretion organ of the body. This study aimed to explore whether dietary calcium (Ca) supplementation can alleviate kidney damage caused by fluorosis and to further investigate the effects of Ca on the mitigation mechanism of renal cell apoptosis triggered by F. We evaluated the histopathological structure, renal function indicators, and gene and protein expression levels of death receptor-mediated apoptosis pathways in Sprague Dawley (SD) rats treated with sodium fluoride (NaF) and/or calcium carbonate (CaCO3) for 120 days. The results showed that 100 mg/L NaF induced kidney histopathological injury and apoptosis, increased the concentrations of Creatinine (CRE), uric acid (UA), blood urea nitrogen (BUN), potassium (K), phosphorus (P) and F (p |
| Databáze: | OpenAIRE |
| Externí odkaz: |
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