Abstract
Hexavalent chromium, Cr(VI), is an environmental toxicant and is associated with hepatotoxicity. However, very little is known about the intracellular antioxidant defense mechanism against Cr(VI)-induced cytotoxicity in hepatocytes. In the present study, we cultured human liver (HepG2) cells in the absence or presence of Cr(VI) and determined its effect on cellular oxidative stress, mitochondrial damage, apoptosis and the expression of the transcription factor Nrf2 and the Nrf2-dependent antioxidant enzymes. Cr(VI) intoxication at a dose of 0, 3.125, 6.25, 12.5, 25, or 50μM for 24h exhibited a dose dependent cytotoxic effects in hepatocytes. Besides, Cr(VI) induced oxidative stress and subsequent mitochondrial damage. Cr(VI) also induced caspase 3-dependent apoptosis in HepG2 cells. In addition, Cr(VI) induced the translocation of Nrf2 into the nucleus and up-regulated the expression of Nrf2-dependent antioxidant enzymes, including SOD2, GCLC, and HO1. Our present experimental data support the notion that Cr(VI) caused mitochondrial damage, apoptosis, oxidative stress, and subsequently lead to a strong induction of HO1, GCLC and SOD2 via the Nrf-2 signaling pathway in hepatocytes.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
