Public willingness to pay for eradicating a harmful marine organism: the case of Aurelia aurita in South Korea.

Aurelia aurita (AA), a legally registered harmful marine organism in South Korea, is damaging marine human leisure activities, local residents' tourism income, fisheries, and cooling water intake at power plants. The government is therefore seeking to eradicate AA by removing AA-attached larvae (polyps). This article looks into the public willingness to pay (WTP) for the eradication, utilizing a contingent valuation. For the sake of eliciting the WTP response, the one-and-one-half-bounded (OB) model was adopted. For comparison, the single-bounded (SB) model, which uses only the response to the first question in the OB model, was also applied. A spike model with a considerable plausibility that could explicitly deal with zero WTP responses was employed. Consequently, the estimation results of the SB model were used for further policy analysis. The household average WTP was estimated as KRW 3,911 (USD 3.49) per year, securing statistical significance. The national value was KRW 80.46 billion (USD 71.71 million) per annum. This figure can be interpreted as public value of the AA eradication project and used as essential basic data to evaluate the economic feasibility of implementing the project. Some factors such as income and education level significantly positively affected the intention of paying a suggested bid.

Rhus javanica Linn protects against hydrogen peroxide­induced toxicity in human Chang liver cells via attenuation of oxidative stress and apoptosis signaling.

Rhus javanica Linn, a traditional medicinal herb from the family Anacardiaceae, has been used in the treatment of liver diseases, cancer, parasitic infections, malaria and respiratory diseases in China, Korea and other Asian countries for centuries. In the present study, the protective effects of R. javanica ethanolic extract (RJE) on hydrogen peroxide (H2O2)-induced oxidative stress in human Chang liver cells was investigated. The cell cytotoxicity and viability were assessed using a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The activities of superoxide dismutase (SOD) and catalase (CAT) were measured using respective enzymatic kits. Cell cycle analysis was performed using flow cytometric analysis. The protein expression levels of p53, B-cell lymphoma (Bcl)-2, Bcl-2-associated X protein (Bax) and caspase-3 were assessed by western blotting. Human Chang liver cells were treated with different concentrations (0.1, 0.3 or 0.5 mg/ml) of RJE, and were subsequently exposed to H2O2 (30 µM). Treatment with H2O2 (30 µM) significantly induced cytotoxicity (P<0.05) and reduced the viability of the Chang liver cells. However, pretreatment of the cells with RJE (0.1, 0.3 or 0.5 mg/ml) significantly increased the cell viability (P<0.001 at 0.5 mg/ml) in a concentration-dependent manner following H2O2 treatment. Furthermore, pretreatment with RJE increased the enzyme activities of SOD and CAT, and decreased the sub-G1 growth phase of the cell cycle in response to H2O2-induced oxidative stress (P<0.001 at 0.3 and 0.5 mg/ml H2O2). RJE also regulated the protein expression levels of p53, Bax, caspase-3 and Bcl-2. These results suggested that RJE may protect human Chang liver cells against oxidative damage by increasing the levels of antioxidant enzymes and regulating antiapoptotic oxidative stress mechanisms, thereby providing insights into the mechanism which underpins the traditional claims made for RJE in the treatment of liver diseases.