Levels of PCDDs and PCDFs in Korean river sediments and their detection by biomarkers

Polychlorinated dibenzo-p-dioxins (PCDDs) and dibenzofurans (PCDFs) are a group of toxic halogenated aryl hydrocarbons inducing various physiological disorders against biological organisms. Here, we investigated their levels in sediment samples taken from 12 different rivers in Korea. The levels of PCDD/PCDFs in sediment samples were expressed as concentrations and international TEQ values. Among 17 PCDD/PCDFs selected as target compounds in this study, the 1,2,3,4,7,8-HxCDD and OCDD were found in all river sediments with significant variation in various congener profiles of PCDD/PCDFs in sediments. PCDD/PCDFs could be monitored by sensitive biomarkers using insect immune system. Out of 12 river sediment samples, the biomarkers reported four spots (up, middle, and down Singil sites and Ansan) as putative contamination areas. When comparing both chemical and biological monitoring results, two methods agreed three spots of Singil as contamination areas (above 10ppt levels) as well as six river sediment samples as relatively less-contaminated areas, but differed in the results in Ansan and Miho, probably due to relative non-specificity of biomarkers. Despite some disparity between bio- and chemical monitoring results, the biomarkers can be recommended as a device warning the contamination of dioxins in the environment because of a fast and inexpensive detection method.     

In vivo evaluation and comparison of developmental toxicity and teratogenicity of perfluoroalkyl compounds using Xenopus embryos

Perfluoroalkyl compounds (PFCs) are environmental toxicants that persistently accumulate in human blood. Their widespread detection and accumulation in the environment raise concerns about whether these chemicals might be developmental toxicants and teratogens in ecosystem. We evaluated and compared the toxicity of PFCs of containing various numbers of carbon atoms (C8–11 carbons) on vertebrate embryogenesis. We assessed the developmental toxicity and teratogenicity of various PFCs. The toxic effects on Xenopus embryos were evaluated using different methods. We measured teratogenic indices (TIs), and investigated the mechanisms underlying developmental toxicity and teratogenicity by measuring the expression of organ-specific biomarkers such as xPTB (liver), Nkx2.5 (heart), and Cyl18 (intestine). All PFCs that we tested were found to be developmental toxicants and teratogens. Their toxic effects were strengthened with increasing length of the fluorinated carbon chain. Furthermore, we produced evidence showing that perfluorodecanoic acid (PFDA) and perfluoroundecanoic acid (PFuDA) are more potent developmental toxicants and teratogens in an animal model compared to the other PFCs we evaluated [perfluorooctanoic acid (PFOA) and perfluorononanoic acid (PFNA)]. In particular, severe defects resulting from PFDA and PFuDA exposure were observed in the liver and heart, respectively, using whole mount in situ hybridization, real-time PCR, pathologic analysis of the heart, and dissection of the liver. Our studies suggest that most PFCs are developmental toxicants and teratogens, however, compounds that have higher numbers of carbons (i.e., PFDA and PFuDA) exert more potent effects.     

Isoperoxidases show differing sensitivity to salicylic acid

The effects of salicylic acid (SA) on the activity of total peroxidase and the patterns of isoperoxidases of cultured tobacco cells were investigated. The total peroxidase activity of tobacco cells was inhibited by 70% when the cells were treated with 5 mM SA for one week. The peroxidase activity of tobacco cells is declined by 90% in the presence of 30 mM SA. Moreover, the activity of isoperoxidases C3, A1, and A3 decreased dramatically with increasing SA concentration, while, one of the anodic isoperoxidases, A2, was somewhat resistant to SA treatment. When isoperoxidase C3 was isolated, SA inhibited the activity of purified C3 in a concentration-dependent manner. The IC50 of isoperoxidase C3 was approximately 0.45 mM. However, the inhibition of isoperoxidase C3 activity was removed by the addition of Fe2+ ion. The possible mechanism of inhibition of peroxidase by SA is discussed.