| | Study | Model | LOEL | Concentrations tested | Summary |
| | Ahn et al., 2008 | BG1-ERE; H4L1.1c4-DRE; T47D-ARE; mMyoblasts | 1 × 10−7 M | 1 × 10−9, 1 × 10−8, 1 × 10−7, 1 × 10−6 M | TCC enhances the ER- and AR-mediated activity of E2 and T, respectively. |
| | Blake et al., 2010 | MDA-kb2 | 1000 nM | Cells dosed from 125 to 2,000 nM | TCC induced AR-activated luciferase activity alone and in conjunction with 17β-trenbolone. Activity was significantly higher than control at a range from 1000 to 2000 nM TCC. |
| | Chen et al., 2007 | 2933Y; JK293; MDA-kb2 | 0.5 µM | 0.1, 0.5, 1.0 µM | TCC did not induce cell proliferation in the MTT assay. TCC enhanced T-mediated AR activity over T-treatment alone. |
| | Christen et al., 2010 | MDA-kb2 | NA | 0.05, 0.5, 5 µM | TCC showed no in vitro androgenic activity. |
| | Duleba et al., 2011 | C4-2B; LNCaP | 1.0 µMol/L | 1.0 µMol/L | TCC induced androgen receptor activity only when administered with DHT or T. |
| | Gao et al., 2015 | Tetrahymena thermophila | 1 µg/L | 1, 10, 100, 250, 500, 750, 1000, 2000, 4000 µg/L | TCC inhibited the growth of Tetrahymena thermophile and was more potent than TCS. At environmentally relevant levels, TCC caused DNA damage and at higher levels TCC impaired the plasma membrane resulting in decreased cell viability. TCC inhibited efflux transporter activities by downregulating the expression of the membrane efflux protein Abcb15. |
| | Hinther et al., 2011 | GH3 | 10 nM | 10, 100, 1000 nM | In the C-fin assay, TCC reduced Rana larval keratin I (RLKI, a TH-repressed gene) but not TRβ expression (a TH-induced gene). T3 + TCC exposure showed no differences in these genes. TCC also induced HSP30 and CAT expression (measures of cellular stress response). T3 + TCC exposure induced HSP30 but not CAT. In the GH3 assay, TCC alone decreased GH, Dio1, PRL, and HSP70 expression, but TCC + T3 increased GH, Dio1, and HSP70; PRL levels were still decreased (nonmonotonically). |
| | Huang et al., 2014 | CV-1; MCF-7 | 1 × 10−7 M | 1 × 10−9, 5 × 10−9, 1 × 10−8, 5 × 10−8, 1 × 10−7, 5 × 10−7, 1 × 10−6 M | TCC was shown to be a weak estrogen agonist. TCC induced a dose-dependent response in the ERα reporter gene assay and MCF7 proliferation assay (E-Screen). Cell proliferation was mediated by ERα as cotreatment with ICI 182,780 blocked cell growth. Protein and mRNA expression of pS2 were increased, while those of ERα were decreased. The expression of several miRNAs (miR-22, -206, and -193b) that regulate ER-α was upregulated with TCC exposure. |
| | Kolšek et al., 2014 | MDA-kb2 | 2 µM | 2 µM | TCC produced amplification of the T and GR response in the assays assessing antagonism by an unknown mechanism. TCC showed cytotoxicity at concentrations higher than 2 µM. TCC did not appear to be an AR or GR agonist or antagonist in reporter gene assays. |
| | Simon et al., 2014 | H295R; RTL-W1; T47D | 125 µg/L | 31.25, 62.50, 125, 250, 500 µg/L; ~0.01–10 mg/L | Antiestrogenic activity of TCC was shown at 125 µg/L and higher. The addition of CNT ameliorated the effects of TCC. Production of E2 was not impacted by TCC exposure in H295R cells and the compound did not induce ROS in any of the tested cell lines. |
| | Tarnow et al., 2013 | HeLa9903; MCF-7; MDA-kb2 | 1 µM | | TCC enhanced estrogen and androgen activity mediated through ER and AR, respectively. TCC did not enhance the expression of DHT-induced AR target genes. TCC did not enhance E2-induced proliferation in the E-Screen assay. TCC enhanced estrogen (E2, butyl paraben, BPA, genistein)-induced expression of CYP1A1 and CYP1B1 in MCF-7 cells, mediated through the AhR pathway. |
| | Tonoli et al., 2015 | H295R | 0.5 µM | .5, 1, 2.5, 10 µM | TCC exposure caused altered adrenal steroidogenesis by affecting an early step in steroid biosynthesis. Pregnenolone, progesterone, 11-DOC, 17α-hydroxyprogesterone, and DHEA were the most sensitive to increasing TCC concentrations. 11-Dehydrocorticosterone, androstenedione, and DHEAS were markedly decreased and aldosterone and cortisone were slightly decreased. |
| | Wu et al., 2016 | FRTL-5 | 0.3 µM | 0.03, 0.1, 0.3, 1, 3, 10, 30, 100, 300 µM; 20, 40, 80 µM | TCC disrupts thyroid hormone homeostasis. TCC decreased NIS-mediated iodide uptake in a noncompetitive manner. The expression of three genes involved in TH synthesis (Slc5a5, TPO, and Tg) or thyroid transcription factors (Pax8, FoxE1, and Nkx2-1) was not altered by TCC exposure. TCC was a weak inhibitor of TPO activity, indicating that TPO may not be a primary target of TCC. |
| | Yueh et al., 2012 | CV-1; MCF-7; MDA-MB-231 | 1 µM | 10 µM | TCC activated ERα and CAR in vitro, in luciferase reporter gene transfected cell lines, but not ERβ, PXR, LXR, FXR, PPARs, and GR. TCC induced expression of CYP genes in cells that contained ERα (MCF-7) but not in MDA-MB-231 cells which do not contain ERα. |
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