Next Article in Journal / Special Issue
Influence of Humic Acid on 1-Aminopyrene Ecotoxicity During Solar Photolysis Process
Previous Article in Journal / Special Issue
Neurotoxic Activity of the HIV-1 Envelope Glycoprotein: Activation of Protein Kinase C in Rat Astrocytes
Int. J. Mol. Sci. 2002, 3(11), 1117-1132; doi:10.3390/i3111117
Article

Differential Cytotoxicity and Gene Expression in Human Liver Carcinoma (HepG2) Cells Exposed to Arsenic Trioxide, and Monosodium Acid Methanearsonate (MSMA)

1,* , 1, 2, 1 and 1
Received: 7 June 2002; Accepted: 30 October 2002 / Published: 30 November 2002
Download PDF [210 KB, uploaded 19 June 2014]
Abstract: Research in our laboratory has demonstrated that a trivalent form of arsenic such as arsenic trioxide (AT) has the ability to cause significant cytotoxicity, and induction of a significant number of stress genes in human liver carcinoma cells (HepG2). However, the literature also indicates that the toxicity of arsenic depends on its chemical form. To test this hypothesis, we further evaluated the cellular and molecular responses of HepG2 cells following exposure to monosodium acid methanearsonate (MSMA), a pentavalent and organic form of arsenic. Cytotoxicity was evaluated using the MTT-assay for cell viability, while the gene profile assay was performed to measure the degree of gene induction in 13 different recombinant cell lines generated from a parental HepG2 cell line. Cytotoxicity experiments yielded LC50 values of 11.9 + 2.6 μg/mL for AT, and 257.3 + 51.4μg/mL for MSMA; indicating that AT was about 20 times more toxic than MSMA. Exposure of HepG2 cells to MSMA also resulted in a significant reduction (p < 0.05) in the number of stress genes induced, compared to AT. Upon MSMA exposure, only 2 (HMTIIA and HSP70) out of the 13 constructs evaluated yielded inductions to statistically significant levels (p < 0.05), compared to 11 (GSTYa, XRE, HMTIIA, c-fos, NF-kBRE, HSP70, p53RE, GADD153, GADD45, and GRP78) for AT. These results greatly support the hypothesis that the toxicity of arsenic compounds highly depends on their chemical forms; with the inorganic forms being more potent than the organic ones.
Keywords: Arsenic; chemical species; differential toxicity; gene expression; HepG2 cells Arsenic; chemical species; differential toxicity; gene expression; HepG2 cells
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Export to BibTeX |
EndNote


MDPI and ACS Style

Tchounwou, P.B.; Wilson, B.A.; Abdelghani, A.A.; Ishaque, A.B.; Patlolla, A.K. Differential Cytotoxicity and Gene Expression in Human Liver Carcinoma (HepG2) Cells Exposed to Arsenic Trioxide, and Monosodium Acid Methanearsonate (MSMA). Int. J. Mol. Sci. 2002, 3, 1117-1132.

AMA Style

Tchounwou PB, Wilson BA, Abdelghani AA, Ishaque AB, Patlolla AK. Differential Cytotoxicity and Gene Expression in Human Liver Carcinoma (HepG2) Cells Exposed to Arsenic Trioxide, and Monosodium Acid Methanearsonate (MSMA). International Journal of Molecular Sciences. 2002; 3(11):1117-1132.

Chicago/Turabian Style

Tchounwou, P. B.; Wilson, B. A.; Abdelghani, A. A.; Ishaque, A. B.; Patlolla, A. K. 2002. "Differential Cytotoxicity and Gene Expression in Human Liver Carcinoma (HepG2) Cells Exposed to Arsenic Trioxide, and Monosodium Acid Methanearsonate (MSMA)." Int. J. Mol. Sci. 3, no. 11: 1117-1132.


Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert