Despite the reports of widespread occurrence of perfluorinated compounds (PFCs) in estuarine and coastal waters and open seas, little is known on the effect of salinity on bioaccumulation. In this study, effects of salinity on bioaccumulation of PFCs in Pacific oysters (Crassostrea gigas) were investigated. Furthermore, partitioning of PFCs between water and particles (oysters' food) was examined at different salinities. The distribution coefficients (K(d); partitioning between water and particles) for selected PFCs, that is, PFOS, PFOA, PFDA, and PFUnDA, increased by 2.1- to 2.7-fold with the increase in water salinity from 10 to 34 psu, suggesting "salting-out" effect, and the salting constant (delta) was estimated to range from 0.80 to 1.11. The nonlinear regression analysis of bioaccumulation suggested increase in aqueous and dietary uptake rates (K(w) and K(f)), with the increase in salinity, which resulted in elevated bioaccumulation, although the depuration rates (K(e)) also increased. The relative abundance of long carbon chain length PFCs (i.e., PFDA and PFUnDA) increased as salinity increased, while the proportion of PFOS and PFOA decreased, which is explained by the positive relationship between delta and carbon chain length. The contribution of diet to bioaccumulation in oysters ranged from 18 to 92%. Overall, salinity not only affected the chemistry of PFCs, but also the physiology of oysters, contributing to sorption and bioaccumulation of perfluorochemicals in oysters.

Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase is upregulated in a variety of tissues in obesity. It is still unclear as to whether NADPH oxidase upregulation in a specific tissue is part of a systemic response. Here we analyzed the expression pattern of NADPH oxidase in vascular, adipose, and kidney tissues in a rat model of diet-induced obesity. After weaning, rats were fed either a normal or high-fat diet for 12 weeks. The high-fat diet resulted in 20% increased body weight. In the aorta, Nox4 expression was increased by three-fold in obese rats. Upregulations of p22phox and p47phox in adipose, and Nox4, p22phox, and p47phox in kidney were observed in obesity. Marked increases in plasma leptin and insulin were observed, with more modest changes in adiponectin in obese rats. The average systolic blood pressure in the obese group was 11 mmHg higher than that of lean rats (P < 0.005). There was a significant correlation between blood pressure and aortic Nox4 expression (P < 0.01). In cultured vascular smooth muscle cells, adiponectin reduced the expression of Nox4 in a protein kinase A-dependent manner. Our results suggest that upregulation of NADPH oxidase in multiple tissues during obesity appears to be a systemic response. At least in vitro, adiponectin may have a protective antioxidant role by suppressing vascular NADPH oxidase expression. The association between NADPH oxidase Nox4 expression in the vasculature and the elevated blood pressure in obesity requires further investigation.