oxidative stress (17,18). The rVSMCs were then trypsinized and resuspended in Hank's balanced salt solution. Induction of HO-1, MCP-1, and IL-6 gene expression in iAs-treated hVSMCs. Control of distal lysine coordination in a monomeric hemoglobin: A role for heme peripheral interactions. Thus, different pro-oxidants are probably involved in the enhancement of HO-1, MCP-1, and IL-6 expression seen in iAs-treated VSMCs. Some conventional metal chelators are available to treat arsenic-mediated … 2A). (, Funakoshi, Y., Ichiki, T., Shimokawa, H., Egashira, K., Takeda, K., Kaibuchi, K., Takeya, M., Yoshimura, T., and Takeshita, A. Colonized extremophile Deinococcus radiodurans alleviates toxicity of cadmium and lead by suppressing heavy metal accumulation and improving antioxidant system in rice. protects against sodium arsenite-induced oxidative stress and genotoxicity in Wistar rats. 1 © The Author 2005. *p < 0.05 compared to the untreated control; #p < 0.05 compared to iAs treatment alone. The 20S proteasome activity (. Resting hVSMCs were treated with 5 μM iAs for various time periods. The data are presented as the mean ± SD of three to four independent experiments. When indicated, antibody against MCP-1 was added to the conditioned medium 10 min before adding the cells to the upper chamber to block MCP-1 activity. Oxidative stress is involved in the regulation of mammalian reproduction. Toxicokinetic and Genotoxicity Study of NNK in Male Sprague-Dawley Rats Following Nose-Only Inhalation Exposure, Intraperitoneal Injection, and Oral Gavage, Firsthand and secondhand exposure levels of maltol-flavored electronic nicotine delivery system (ENDS) vapors disrupt amino acid metabolism, Converging Roles of the Aryl Hydrocarbon Receptor in Early Embryonic Development, Maintenance of Stemness and Tissue Repair, Implications of Species Differences in Function and Localization of Transporters at the Blood–Testis Barrier, Effects of the Hedgehog signalling inhibitor itraconazole on developing rat ovaries, Receive exclusive offers and updates from Oxford Academic, Statin-Induced Heme Oxygenase-1 Increases NF-κB Activation and Oxygen Radical Production in Cultured Neuronal Cells Exposed to Lipopolysaccharide, Heme and Heme Biosynthesis Intermediates Induce Heme Oxygenase-1 and Cytochrome P450 2A5, Enzymes With Putative Sequential Roles in Heme and Bilirubin Metabolism: Different Requirement for Transcription Factor Nuclear Factor Erythroid- Derived 2-like 2, Tienilic Acid Enhances Hyperbilirubinemia in Eisai Hyperbilirubinuria Rats through Hepatic Multidrug Resistance–Associated Protein 3 and Heme Oxygenase-1 Induction. 8600 Rockville Pike We measured the protein levels of HO-1, c-Myc and β-actin with the aim of assessing the effects of arsenite on a typical oxidative stress-responsive protein and on an essential activator of cell proliferation. Since the concentrations of secreted IL-6 in medium of iAs-treated cultures were ranged at pg/ml levels, anti-IL-6 antibody was unable to inhibit the proliferation or migration ability in iAs-treated rVSMCs (data not shown). The relative mRNA levels for the genes of interest were calculated from the difference between the Ct value (number of cycles required to reach the detection threshold for the double-strand DNA product) for the gene of interest and that for an internal control gene, glyceraldehyde-3-phosphate dehydrogenase as described previously (Wu et al., 2003). Would you like email updates of new search results? Epidemiological evidence has shown that long-term chronic arsenic exposure is associated with increased risks of skin, bladder, lung, and liver cancers (Chen et al., 1992; IARC, 1987). In the present study, iAs treatment of HFW resulted in increased HO-1 gene expression, but suppression of MCP-1 and IL-6 expression. Keywords: The findings presented here suggest a possible mechanism for atherogenesis in arsenic-exposed humans. All rights reserved. Recently, HO-1 was further reported to play an important role in angiogenesis (Bussolati et al., 2004). Furthermore, the expression of these three genes has been detected in atherosclerotic lesion (Nelken et al., 1991; Seino et al., 1994; Wang et al., 1998). The data are presented as the mean ± SD of at least four independent experiments. The human monocyte cell line, THP-1 (ATCC, TIB-202), was cultured in RPMI 1640 medium containing 10% FBS. Methods: Rats were orally exposed to sodium arsenite at 10, 20 and 40 mg/kg daily for 4 weeks followed by 4 weeks of withdrawal. N-acetyl-cysteine inhibited the effect of DISC1, suggesting that DISC1 affects translation in response to oxidative stress. In this study, we demonstrated that iAs-treatment resulted in increasing intracellular ROS production in VSMCs. 7). For full access to this pdf, sign in to an existing account, or purchase an annual subscription. Objective: The present study evaluates the protective effect of PLo against sodium arsenite-induced hepatic dysfunction and oxidative stress in experimental Wistar rats. After further cultivating for 72 h, the cells were trypsinized and counted with a cell counter (hematology analyzer, EXCELL 300, Metertech). To confirm the observed chemotaxis was due to secreted MCP-1, anti-human MCP-1 antibody (R&D Systems, Inc., Minneapolis, MN) at a final concentration of 0.83 μg/ml was added to the conditioned medium in the lower chamber 10 min before loading the cells into the upper chamber. The appearance of large amounts of HO-1, an intracellular protein, in iAs-treated hVSMCs was confirmed by Western blotting (Fig. Sodium arsenite suppresses the expression of uterine estrogen receptor-α at both proteomic and genomic levels via limiting the functions of the cell cycle regulating proteins CDK4 and cyclin D1 at G1 phase [, ]. Our results demonstrated that alpha-MnO(2) has important potential in arsenic transformation and … As shown in Figure 6, conditioned medium from iAs-treated (5 μM, 9 h) resting hVSMCs showed significantly higher chemotactic activity than conditioned medium from untreated cells supplemented with 5 μM iAs prior to assay. As shown in Figure 3B, the fluorescence intensity of the oxidized product, DCF, was increased 1.6-fold in proliferating rVSMCs treated with 5 μM iAs for 4 h. Enhanced expression of the HO-1, MCP-1, and IL-6 genes by H2O2 and enhanced intracellular oxidant production by iAs in rVSMCs. Oxidative stress-related liver dysfunction by sodium arsenite: Alleviation by Pistacia lentiscus oil. Increased levels of adhesion molecules and increased ECs permeability could promote the attachment and penetration of circulating immune cells, such as monocytes. *p < 0.05 compared to the untreated control. 2D). The data are presented as the mean ± SD of five independent experiments. In the present study, the iAs-induced increase in MCP-1 expression was suppressed by AP, but enhanced by SOD. READ PAPER. 1B). Superoxide dismutase (SOD) was added to the culture medium 4 h before iAs treatment, while allopurinol (AP), dimethylsulfoxide (DMSO), and L-ω-nitro-L-arginine (L-NNA) were added 30 min before iAs treatment; these reagents were then left in the medium during the subsequent iAs treatment (5 μM for 4 h). 2005 Nov;279(1-2):123-31. doi: 10.1007/s11010-005-8284-2. However, HO-1 protein became remarkable even when iAs at the concentration of 1 μM (Fig. In this study, twenty four adult female rats were divided in to four groups of 6 animals each. (, Huang, H.-S., Chang, W. C., and Chen, C. J. Biochem Biophys Res Commun. MCP-1-induced monocyte chemotaxis was measured using 12-well Transwell polystyrene trays (Corning Costar Corp., Cambridge, MA) and a 5 μm pore polycarbonate membrane (McQuibban et al., 2002). The data are…, Effects of NaAsO 2 on levels of oxidative stress indicators, 20S proteasome, and…, Effects of MG132 on levels of 20S proteasome and gene expression of PSMB5,…, Effects of PSMB5-siRNA on levels of 20S proteasome and gene expression of PSMB5,…, National Library of Medicine IL-6, a proinflammatory cytokine and a major inducer of C-reactive protein (CRP) (Heinrich et al., 1990), is also present in atherosclerotic lesions (Seino et al., 1994). 2′,7′-dichlorofluorescein diacetate (DCF-DA) was used to measure ROS production in VSMCs (Huang et al., 1993). (, Wenzel, U. O., Fouqueray, B., Grandaliano, G., Kim, Y. S., Karamitsos, C., Valente, A. J., and Abboud, H. E. (, Wu, M. M., Chiou, H. Y., Ho, I. C., Chen, C. J., and Lee, T. C. (, Wu, M.-M., Chiou, H.-Y., Wang, T.-W., Hsueh, Y.-M., Wang, I.-H., Chen, C.-J., and Lee, T.-C. (, *Institute of Biopharmaceutical Science, National Yang-Ming University, Taipei, Taiwan, ROC, and †Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan, ROC, Oxford University Press is a department of the University of Oxford. Arsenic-induced oxidative stress or redox disturbance (17,19–21) contributes to DNA damage (22–24), chromosomal aberrations (25), and protein expression alterations (22,26). These results indicated that superoxide anions play a role in the effect of iAs on IL-6 mRNA levels, but are less important in the effect on HO-1 mRNA levels and play a complicated role in MCP-1 induction. (, Stocker, R., Yamamoto, Y., McDonagh, A. F., Glazer, A. N., and Ames, B. N. (, Sundaresan, M., Yu, Z.-X., Ferrans, V. J., Irani, K., and Finkel, T. (, Taketani, S., Kohno, H., Yoshinaga, T., and Tokunaga, R. (, Tokunou, T., Ichiki, T., Takeda, K., Funakoshi, Y., Iino, N., Shimokawa, H., Egashira, K., and Takeshita, A. oxidative stress is involved in regulating the expression of genes related to atherogenesis, we investigated its involvement in the en-hanced expression of three atherosclerosis-related genes coding for heme oxygenase-1 (HO-1), monocyte chemoattractant protein-1 (MCP-1), and interleukin-6 (IL-6) in VSMCs treated with in-organic sodium arsenite (iAs). Recent epidemiological studies have established a relationship between chronic arsenic exposure and increased levels of reactive oxidants in the blood of human populations drinking arsenic-contaminated water (Pi et al., 2002; Wu et al., 2001). In iAs-treated rVSMCs, catalase, dimethylsulfoxide, and L-ω-nitro-L-arginine significantly inhibited the increase in expression of all three genes, allopurinol inhibited the increase in MCP-1 and IL-6 expression, but had no effect on HO-1 expression, while superoxide dismutase had no significant effect on HO-1 expression, but had an inhibitory effect on IL-6 expression and a stimulatory effect on MCP-1 expression. These results indicated that although HO-1, MCP-1, and IL-6 are oxidative response genes, their response to iAs-enhanced oxidative stress is cell type dependent. Modulation of the iAs-induced increase in HO-1, MCP-1, and IL-6 mRNA levels by AP and SOD. Therefore, iAs may enhance the expression of HO-1, MCP-1, and IL-6 in VSMCs via different reactive oxygen molecules. These results indicate that H2O2, hydroxyl radicals, and NO are probably involved in the induction of HO-1, MCP-1, and IL-6 expression in iAs-treated VSMCs. 4A), and a similar effect was seen in iAs-treated resting hVSMCs (data not shown). Both IL-6 and CRP are considered as strong risk markers of cardiovascular diseases (Blake and Ridker, 2001). These results are consistent to several other reports (Foresti et al., 2001; Morse and Choi, 2002) showing that increased HO-1 expression is a general response of cells to iAs insult, whereas regulation of MCP-1 and IL-6 expression by iAs differs in different cell types. The etiology is clear, but the mechanisms involved remain unknown. (A) Proliferating rVSMCs were treated with 200 μM H2O2 for the indicated time periods, then relative levels of HO-1, MCP-1, and IL-6 mRNA were determined by quantitative RT-PCR as described in the Materials and Methods. 1A). Numerous reports have shown that MCP-1 is induced in VSMCs by a variety of stimuli, including Ang II (Funakoshi et al., 2001), thrombin (Wenzel et al., 1995), uric acid (Kanellis et al., 2003), Fas ligand plus cycloheximide (Schaub et al., 2000), and activated platelets (Massberg et al., 2003). Similarly, iAs-induced Nrf2 nuclear accumulation is enhanced by copper (II) 3,5-diisopropyl salicylate hydrate, a cell-permeable SOD (Pi et al., 2003). Lipopolysaccharide-induced hepatic oxidative injury is not potentiated by knockout of GPX1 and SOD1 in mice. Free Radic Biol Med. (, Tseng, C. H., Tai, T. Y., Chong, C. K., Tseng, C. P., Lai, M. S., Lin, B. J., Chiou, H. Y., Hsueh, Y. M., Hsu, K. H., and Chen, C. J. Catalase (CAT) was added to the culture medium for 4 h. To avoid the interference with iAs, the medium was replaced with fresh medium before treatment with iAs (5 μM for 4 h). Therefore, the roles of HO-1 on atherogenesis require further clarification. Usoh , E.J. CAT catalyzes the degradation of H2O2 to H2O and O2. Our results showed that the enhanced chemotactic activity for human monocytes seen in conditioned medium from iAs-treated VSMCs could be suppressed by antibody against MCP-1. However, the mechanism by which arsenic induces COX-2 in bladder cells remains unclear. Results showed that activities of antioxidant enzymes decreased significantly due to oxidative stress generated by sodium arsenite. (, Chiou, H.-Y., Huang, W.-I., Su, C.-L., Chang, S.-F., Hsu, Y.-H., and Chen, C.-J. Published by Oxford University Press on behalf of the Society of Toxicology. (, Rahman, M., Tondel, M., Ahmad, S. A., Chowdhury, I. In each treatment, the average cell number of three randomly selected fields (using 10× eyepieces and 40× objective) was scored under a fluorescence microscopy. CONCLUSION: Both sodium arsenite and arsenic trioxide could induce oxidative stress in human hepatocyte L02 and result in chromosomal damage, apoptosis, cell cycle arrest and cellular proliferation inhibition, suggesting that oxidative stress induction might be the common molecular mechanism of malignant transformation induced by sodium arsenite and therapeutic effects exhibited by arsenic … Allowing for the lag in protein synthesis, the levels of HO-1, MCP-1, and IL-6 protein correlated well with the mRNA levels determined by quantitative RT-PCR. Results: Exposure to arsenic caused a significant increase in malondialdehyde, H2O2 generation but decrease total thiol and reduced glutathione levels in both cardiac and renal tissues. The fluorescence of the DCF formed by oxidation of DCF-DA by cellular oxidants was measured using a flow cytometer with an excitation wavelength of 488 nm and an emission wavelength of 525 nm. 37 Full PDFs related to this paper . The data are presented as the mean ± SD of three to five independent experiments. 6A). The involvement of reactive oxidants in iAs-induced DNA and chromosomal damage (Ho et al., 2000; Lynn et al., 2000), DNA repair inhibition (Mei et al., 2002), and apoptosis (Nakagawa et al., 2002) is well documented. Privacy, Help Several reports have shown that iAs treatment results in increased ROS and NO production in a variety of cells in culture (Barchowsky et al., 1999; Lee and Ho, 1995; Lynn et al., 2000), and in the blood of human populations drinking arsenic-contaminated water (Pi et al., 2002; Wu et al., 2001). Il-6 requires further study ) AP ; ( B ) HO-1 protein remarkable! Increasing the attachment, penetration, and Chau, L.-Y acid acted as antioxidant and caused mostly all the parameters... Ias-Treated HFW ( Ho et al., 2004 ), but enhanced by SOD by this author on: Sciences... % FBS of Toxicology THP-1 cells on skin wound of horses due to Amblyomma tick. 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Grants from the National Science Council, Republic of China ( NSC91-2320-B010-055 and NSC92-2320-B-010-017 ) arsenic induces the processes... Time periods in this study, suggesting that ROS/NO were involved … sodium arsenite Alleviation. Results are expressed as the mean ± SD of three to four independent.... # p < 0.05 compared to the untreated control Dokki, Giza 12311, Egypt expressed the. We demonstrated that iAs-treatment resulted in increasing intracellular ROS production in VSMCs for arsenic and fluoride toxicity. Psmb5-Sirna on levels of HO-1, MCP-1, and IL-6 mRNA levels by AP and SOD toxicity cadmium... Be delineated expression seen in iAs-treated hVSMCs was determined using the Transwell migration.! The initiation of atherosclerosis ( Ross, 1999 ) phosphatases ABSTRACT arsenic has been reviewed blotting antibody... As described previously ( Yih et al., 2001, 2003 ) to 140 migrating were... 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