Analysis and remediation of phthalates in aquatic matrices: current perspectives.

Phthalic acid esters (PAEs) are high production volume chemicals used extensively as plasticizers, to increase the flexibility of the main polymer. They are reported to leach into their surroundings from plastic products and are now a ubiquitous environmental contaminant. Phthalate levels have been determined in several environmental matrices, especially in water. These levels serve as an indicator of plasticizer abuse and plastic pollution, and also serve as a route of exposure to different species including humans. Reports published on effects of different PAEs on experimental models demonstrate their carcinogenic, teratogenic, reproductive, and endocrine disruptive effects. Therefore, regular monitoring and remediation of environmental water samples is essential to ascertain their hazard quotient and daily exposure levels. This review summarises the extraction and detection techniques available for phthalate analysis in water samples such as chromatography, biosensors, immunoassays, and spectroscopy. Current remediation strategies for phthalate removal such as adsorption, advanced oxidation, and microbial degradation have also been highlighted.

Calotropis procera extract inhibits prostate cancer through regulation of autophagy.

Current treatment options available for prostate cancer (PCa) patients have many adverse side effects and hence, new alternative therapies need to be explored. Anticancer potential of various phytochemicals derived from Calotropis procera has been studied in many cancers but no study has investigated the effect of leaf extract of C. procera on PCa cells. Hence, we investigated the effect of C. procera leaf extract (CPE) on cellular properties of androgen-independent PC-3 and androgen-sensitive 22Rv1 cells. A hydroalcoholic extract of C. procera was prepared and MTT assay was performed to study the effect of CPE on viability of PCa cells. The effect of CPE on cell division ability, migration capability and reactive oxygen species (ROS) production was studied using colony formation assay, wound-healing assay and 2',7'-dichlorodihydrofluorescein diacetate assay, respectively. Caspase activity assay and LDH assay were performed to study the involvement of apoptosis and necrosis in CPE-mediated cell death. Protein levels of cell cycle, antioxidant, autophagy and apoptosis markers were measured by western blot. The composition of CPE was identified using untargeted LC-MS analysis. Results showed that CPE decreased the viability of both the PCa cells, PC-3 and 22Rv1, in a dose- and time-dependent manner. Also, CPE significantly inhibited the colony-forming ability, migration and endogenous ROS production in both the cell lines. Furthermore, CPE significantly decreased NF-κB protein levels and increased the protein levels of the cell cycle inhibitor p27. A significant increase in expression of autophagy markers was observed in CPE-treated PC-3 cells while autophagy markers were downregulated in 22Rv1 cells after CPE exposure. Hence, it can be concluded that CPE inhibits PCa cell viability possibly by regulating the autophagy pathway and/or altering the ROS levels. Thus, CPE can be explored as a possible alternative therapeutic agent for PCa.