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Open AccessArticle

Optimal Regimen of N-Acetylcysteine on Chromium-Induced Renal Cell Damage

1
Department of Emergency Medicine, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung 807, Taiwan
2
Family Medicine Department, Taoyuan Branch, Taipei Veterans General Hospital, Taipei 112, Taiwan
3
Department of Renal Care, College of Medicine, Kaohsiung Medical University, Kaohsiung 807, Taiwan
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Division of Gastroenterology, Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung 807, Taiwan
5
Graduate Institute of Clinical Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 807, Taiwan
6
Department of Public Health, College of Health Science, Kaohsiung Medical University, Kaohsiung 807, Taiwan
7
Research Center for Environmental Medicine, Kaohsiung Medical University, Kaohsiung 807, Taiwan
*
Author to whom correspondence should be addressed.
Metabolites 2019, 9(9), 172; https://doi.org/10.3390/metabo9090172
Received: 24 July 2019 / Revised: 15 August 2019 / Accepted: 26 August 2019 / Published: 28 August 2019
Chromium (Cr) is a well-known heavy metal that can cause renal damage. The production of reactive oxygen species (ROS) due to chromium-induced toxicity induces cell dysfunction, apoptosis, and death. N-acetylcysteine (NAC) is an antioxidant used as an antidote for chromium-induced toxicity. However, the optimal regimen and protective mechanisms of NAC are not fully understood in human renal cells. Our results showed that exposure to 10 μM K2Cr2O7, a toxic Cr(VI) compound, induced apoptosis and production of intracellular ROS in the human proximal tubular epithelial cell line HK-2. Supplements of 600 or 1000 µg/mL NAC inhibited intracellular ROS in HK-2 cells exposed to Cr(VI) and significantly increased cell viability within 2 h of Cr(VI)-induced cytotoxicity. Moreover, Cr(VI) induced the expression of apoptosis markers, including cleaved-caspase-3, cleaved-poly (ADP-ribose) polymerase, cleaved-caspase 8, and cleaved-caspase 9, and altered the expression ratio of Bax/Bcl-xL. Expression of apoptosis markers within 2 h of Cr(VI)-induced cytotoxicity in cells treated with 600 µg/mL NAC was significantly suppressed. However, delayed treatment with NAC at 4 h and 8 h after exposure to Cr did not suppress the activation of apoptotic pathways. In summary, our study reports the optimum timing and dose of NAC for the protection of human renal proximal tubular cells from Cr(VI)-induced cell death. The NAC treatment strategy described could be applied in clinical practice to suppress renal cell apoptosis, which in turn could rescue renal function. View Full-Text
Keywords: apoptosis; hexavalent chromium; human proximal tubular epithelial cell; N-acetylcysteine (NAC), reactive oxygen species apoptosis; hexavalent chromium; human proximal tubular epithelial cell; N-acetylcysteine (NAC), reactive oxygen species
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Yeh, I.-J.; Wang, T.-Y.; Lin, J.-C.; Lin, T.-J.; Chang, J.-S.; Yen, M.-C.; Liu, Y.-H.; Wu, P.-L.; Chen, F.-W.; Shih, Y.-L.; Peng, C.-Y. Optimal Regimen of N-Acetylcysteine on Chromium-Induced Renal Cell Damage. Metabolites 2019, 9, 172.

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