Bioaccumulation of heavy metals in oysters from the southern coast of Korea: assessment of potential risk to human health.

From 2009 to 2013, 80 oyster and 16 seawater samples were collected from the southern coast of Korea, including designated shellfish growing areas for export. The concentrations and bioaccumulation of heavy metals were determined, and a potential risk assessment was conducted to evaluate their hazards towards human consumption. The cadmium (Cd) concentration in oysters was the highest of three hazardous metals, including Cd, lead (Pb), and mercury (Hg), however, below the standards set by various countries. The metal bioaccumulation ratio in oysters was relatively high for zinc and Cd but low for Hg, Pb, arsenic, and chromium. The estimated dietary intakes of all heavy metals for oysters accounted for 0.02%-17.75% of provisional tolerable daily intake. The hazard index for all samples was far <1.0, which indicates that the oysters do not pose an appreciable hazard to humans for the metal pollutants of study.

Dioxinodehydroeckol inhibits melanin synthesis through PI3K/Akt signalling pathway in α-melanocyte-stimulating hormone-treated B16F10 cells.

Antimelanogenic activity has previously been reported in ethyl acetate fraction of Ecklonia stolonifera. In this study, using the isolated dioxinodehydroeckol from the fraction, we sought to investigate an antimelanogenic signalling pathway in α-melanocyte-stimulating hormone (α-MSH)-stimulated B16F10 melanoma cells. Treatment with dioxinodehydroeckol inhibited the cellular melanin contents and expression of melanogenesis-related proteins, including microphthalmia-associated transcription factor (MITF), tyrosinase and tyrosinase-related proteins TRP-1 and TRP-2. Moreover, dioxinodehydroeckol stimulated phosphorylation of Akt in a dose-dependent manner without affecting phosphorylation of ERK. These data suggest that dioxinodehydroeckol reduces melanin synthesis through the MITF regulation dependent upon PI3K/Akt signalling pathway.

Triple inhibitory activity of Cliona celata against TNF-α-induced matrix metalloproteinase-9 production via downregulated NF-κB and AP-1, enzyme activity, and migration potential.

Extracellular matrix-degrading protease, matrix metalloproteinase-9 (MMP-9), is known to be involved in vascular smooth muscle cell (SMC)'s aberrant proliferation and movement in atherosclerotic lesions. During screening of the MMP-9-inhibitory compounds from marine animal resources, we have found that the ethyl acetate extract from Cliona celata (ECC) effectively inhibits the SMC-derived MMP-9 enzyme activity and gene expression. In addition, the ECC effectively repressed the migration potential of the tumor necrosis factor-α (TNF-α)-stimulated human aortic smooth muscle cell (HASMC). As assessed by Western blot analysis, the produced MMP-9 protein levels in the TNF-α-induced HASMC were significantly decreased by the concomitant treatment of ECC at the 50- to 300-µg/mL concentration ranges. In addition, in the RT-PCR experiment, the expressed MMP-9 mRNA levels in the TNF-α-induced HASMC were seemingly decreased by ECC treatment at the same concentration ranges (50-300 µg/mL). For the action mechanism(s) of ECC to the phenotype changes in HASMC, we have further evaluated the ECC's pharmacological activities on the signal molecules which are importantly linked in the MMP-9 expression and cell migration potential of HASMC. We have found that extracellular signal-regulated kinase 1 and 2 (ERK1/2) phosphorylation as a target point is suppressed by the ECC treatment in the TNF-α-treated HASMC. Using electrophoretic mobility shift assay, the nuclear extracts purified from ECC-treated HASMCs were shown to decrease the binding potentials on the labeled nuclear factor-kappaB (NF-κB) and activator protein 1 probes. NF-κB p65 and phosphorylated c-Jun contents were also decreased in the purified nuclear extracts from the ECC-treated HASMC, as confirmed by Western blot analysis. Finally, it was shown that the ECC-treated HASMCs were less migrated when compared to the TNF-α-treated cells, as confirmed by HASMC migration assays using the 8-µm pore transwell membranes. From these results, it was proposed that ECC has a potentially applicable anti-atherosclerotic activity.

A novel function of benzyl isothiocyanate in vascular smooth muscle cells: the role of ERK1/2, cell cycle regulation, and matrix metalloproteinase-9.

Dietary isothiocyanates (ITCs) have shown protective effects against certain chemically induced cancers in animal models. These inhibitory effects are associated with reduced levels of extracellular signal-regulated kinase (ERK) 1/2 activity and the arrest of the G(1) cell cycle. Benzyl isothiocyanate (BITC) treatment down-regulates cyclins and CDKs and up-regulates the expression of the CDK inhibitor p21, but up-regulation of p27 or p53 was not detected. Since antiatherogenic effects are not needed for antiproliferation, we determined whether BITC exerted inhibitory effects on matrix metalloproteinase-9 (MMP-9) activity in TNF-alpha-induced vascular smooth muscle cells (VSMCs). BITC inhibited TNF-alpha-induced MMP-9 secretion in VSMC in a dose dependent manner. This inhibition was characterized by the down-regulation of MMP-9, which is transcriptionally regulated at the NF-kappaB site, and the activation protein-1 (AP-1) site in the MMP-9 promoter. These findings indicate that BITC is an effective agent for inhibiting cell proliferation, the G1 to S phase cell cycle progress, and MMP-9 expression through the transcription factors NF-kappaB and AP-1 in TNF-alpha-induced VSMC.