A Ca2+ chelator ameliorates chromium (VI)-induced hepatocyte L-02 injury via down-regulation of voltage-Dependent anion channel 1 (VDAC1) expression |
| |
| Affiliation: | 1. Department of Health Toxicology, School of Public Health, Central South University, Changsha 410078, PR China;2. Hunan Provincial Centers for Disease Control and Prevention, Changsha 410005, PR China;1. Department of Chemistry, Federal University of Agriculture, Abeokuta, Nigeria;2. Department of Biochemistry, Federal University of Agriculture, Abeokuta, Nigeria;3. Department of Statistics, Federal University of Agriculture, Abeokuta, Nigeria;1. Department of Medical Physiology, Cukurova University Medical Faculty, Adana, Turkey;2. Department of Biophysics, Cukurova University Medical Faculty, Adana, Turkey;3. Department of Biostatistics, Cukurova University Medical Faculty, Adana, Turkey;4. Department of Medical Biology, Cukurova University Medical Faculty, Adana, Turkey;1. Department of Nephrology and Rheumatology, Göttingen University Medical Center, Georg August University, Göttingen, Germany;4. Department of Cardiology and Pneumology, Göttingen University Medical Center, Georg August University, Göttingen, Germany;2. Division of Matrix Biology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts;3. Department of Cancer Biology and the Metastasis Research Center, University of Texas MD Anderson Cancer Center, Houston, Texas;5. German Center for Cardiovascular Research (DZHK), Göttingen, Germany;1. Department of Colorectal and General Surgery, Binzhou Medical University Hospital, Binzhou, 256603, China;2. The First Department of Liver Surgery, Eastern Hepatobiliary Surgery Hospital, Second Military Medical University, Shanghai, 200438, China;3. Department of Pathology, Binzhou Medical University Hospital, Binzhou, 256603, China |
| |
| Abstract: | Hexavalent chromium could result in cell malfunctions. Intracellular Ca2+ ([Ca2+]i) content and VDAC1 expression are both important features related to cell survial. This study aimed to explore the mechanism of cell injury induced by Cr(VI) and tentatively offer clues to repairing this cell damage using [Ca2+]i and VDAC1. L-02 hepatocytes were treated with Cr(VI)/BAPTA, and the levels of [Ca2+]i and cell injury associated with Cr(VI) were determined in addition to the effect of BAPTA. The expression of VDAC1 in Cr(VI)-induced cells was evaluated. The results showed a dose-dependent elevation of the level of VDAC1 and the mRNA level of the VDAC1 biogenesis-related gene Sam50. BAPTA could ameliorate less severe damage induced by 4 μM Cr(VI) via reducing VDAC1 and Sam50. Additionally, cell injury caused by less than 4 μM Cr(VI) could be ameliorated by VDAC1 knockdown. Taken together, the findings of this study suggest that inhibition of intracellular Ca2± overload could protect cells from damage and that VDAC1 plays a considerable role in Cr(VI)-induced liver injury. |
| |
| Keywords: | Hexavalent chromium [Cr(VI)] Voltage-dependent anion channel 1 (VDAC1) 1,2-bis(2-aminophenoxy)ethane-N,N,N’,N’-tetraacetic acid tetrakis(acetoxymethyl ester) (BAPTA-AM) Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) L-02 hepatocytes |
| 本文献已被 ScienceDirect 等数据库收录！ |
|
