Purpose: To investigate the anti-cancer potential of astaxanthin from Litopenaeus vannamei encapsulated in liposomes (ASX) to treat lung cancer A549 cells.Methods: Lung adenocarcinoma A549 cells were cultured and treated with ASX, following which cell viability and nuclear staining were performed. Generation of ROS was identified by the DCFH-DA assay while tetramethylrhodamine ethyl ester was used to determine the mitochondrial membrane potential. Flow cytometry was applied to investigate caspase-3/7 activity and cell cycle distribution.Results: ASX inhibited growth of A549 in a concentration- and time- dependent manner. The IC50 values at 24, 48 and 72 h were 53.73, 22.85, 17.46 μg/mL, respectively (p < 0.05). After incubation with ASX, the morphological changes were observed in A549 cells following Hoechst 33342/PI fluorescent staining. ASX increased ROS generation and was associated with the collapse of mitochondrial membrane potential, which subsequently triggered the activation of caspase-3/7 activity leading to apoptosis (p < 0.05). In addition, A549 cells accumulated in the G0/G1 phase.Conclusion: The results suggest that ASX is a valuable nutraceutical agent to target A549 lung cancer cells via ROS-dependent pathway as well as blockage of cell cycle progression. Keywords: Astaxanthin, Litopenaeus vannamei, Lung cancer, A549, Apoptosis

Purpose: To investigate the capacity of aqueous Pseuderanthemum paltiferum leaf extracts (PPA) to induce apoptosis in A549 human lung cancer cells and the possible mechanisms of action. Methods: Human lung cancer A549 cells were cultured in the presence of PPA (0-1000 µg/mL). Cell viability was assessed by MTT assay while morphological alterations in the cells were observed by Hoechst 33342/PI double staining. Intracellular reactive oxygen species (ROS) levels and subsequent changes of mitochondrial membrane potential were also investigated. Involvement of caspase-3 activation in the apoptotic pathway was determined. Results: PPA inhibited the growth of A549 cells in a concentration-and time-dependent manner. Major phenotypic apoptotic cell death was evidenced in microscopic images. Furthermore, treatment of A549 cells with PPA resulted in a significant increase in the production of ROS accompanied by attenuation of mitochondrial membrane potential, thus inducing the activation of caspase-3 activity (p < 0.05). Conclusion: PPA exerts anti-cancer activity by suppression of cell viability and induction of ROSmediated mitochondrial dependent apoptosis in A549 cells, and may be a potential candidate for the development of a therapeutic agent for lung cancer.

Lead is an environmental toxicant of great concern for humans and animals. Lead-induced liver damage and malfunction are partly due to a disturbance of the cellular antioxidant balance. Paraoxonase 1 (PON1) and PON2 are highly expressed in the liver and have been proposed as antioxidative enzymes. In this study, the effects of lead on PON1 and PON2 activities were investigated in human hepatoma HepG2 cells by exposing the cells to various concentrations of lead acetate for 24, 48, or 72 h. The results show that a significant increase in reactive oxygen species was observed even at the lowest concentration of lead treatment. However, only the highest concentration of lead significantly influenced cell viability. Lead had no influence on cell-associated PON1 activity, but it significantly decreased cytoplasmic PON2 activity in a concentration- and time-dependent manner. This reduction was rescued by the addition of calcium. A significant increase of PON2 transcript was observed by real-time polymerase chain reaction, while PON2 protein expression did not change in the western blot analysis. Taken together, these results indicate that lead reduces PON2, but not PON1, activity and that this reduction is reversed by calcium. Lead-induced oxidative stress and decreased PON2 activity lead to the upregulation of PON2 transcript.

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