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Adsorption of Miscellaneous Organic Compounds from Nonaqueous Solutions
Published in Alexander Samokhvalov, Adsorption on Mesoporous Metal-Organic Frameworks in Solution for Clean Energy, Environment, and Healthcare, 2017
Chlorinated aromatic compounds are widely used as herbicides; many of them have an offensive odor and are toxic or even carcinogenic (Alavanja et al. 2004). Chloroaromatic pesticides can easily accumulate in soil and water, which represents a global environmental concern (e.g., Pereira et al. 1996, Muller et al. 2008). Among the chlorinated aromatic compounds, polychlorinated dibenzodioxins (PCDDs) are most well known for their acute toxicity. The defoliant Agent Orange (Stellman et al. 2003) sprayed over vegetation during the Vietnam War contained PCDDs, which caused multiple birth defects and cancer. Brominated aromatic compounds produced by burning chemical waste (Schafer and Ballschmiter 1986) are also very toxic (Behnisch et al. 2003). Therefore, it is essential to find active and selective sorbents that can effectively remove chlorinated and brominated aromatic compounds.
Targeting gap junctional intercellular communication by hepatocarcinogenic compounds
Published in Journal of Toxicology and Environmental Health, Part B, 2020
Kaat Leroy, Alanah Pieters, Andrés Tabernilla, Axelle Cooreman, Raf Van Campenhout, Bruno Cogliati, Mathieu Vinken
Polychlorinated dibenzodioxins (PCDDs), also known as dioxins, are organic byproducts of combustion and industrial processes, which are released in the environment through air and contaminated soil and water. Eventually, PCDDs accumulate in human fatty tissues through food contamination (Patrizi and Siciliani de Cumis 2018). Dioxins might induce cancer (Lin et al. 2012), damage the immune system (Mrema et al. 2013), disrupt the endocrine system (Maqbool et al. 2016), and produce developmental (Maqbool et al. 2016) and reproductive problems (Lin et al. 2012), mediated by the AhR (Patrizi and Siciliani de Cumis 2018). The most toxic and most frequently used dioxin in research is 2,3,7,8-tetrachlorodibenzo-p-dioxin (Patrizi and Siciliani de Cumis 2018). This compound disrupts contact inhibition in rat liver epithelial cells, reduces gap junction plaques and inhibits GJIC (Andrysik et al. 2013). The latter occurs in a time-dependent and concentration-dependent manner (Baker et al. 1995), yet multiple studies indicated that it takes 48 hr prior to changes in GJIC becoming manifested (Bager et al. 1997; Warngard et al. 1996). Further, protein levels of Cx43 are reduced, possibly because of increased proteasomal activity (Andrysik et al. 2013) and decreased Cx43 mRNA quantities (Bager et al. 1997). Cx32 mRNA levels and plasma membrane localization are also adversely affected (Herrmann et al. 2002).