Andrea Pace

Phthalic acid esters (PAEs) are a class of ubiquitous and dangerous lipophilic chemicals widely used as additives in various products to improve their physical and chemical properties. Although they have been banned in many countries, their persistence in all environmental compartments is of particular concern. The aquatic environment is especially affected by these compounds because it is strongly influenced both by contamination of anthropic origin and natural contaminants including those produced biosynthetically by some organisms such as algae. In this context, algal organisms can be a source and remedy for phthalate pollution. Both the increase and decrease in uptake and production depend on the physicochemical characteristics of the environment. The dynamics of the natural processes are aimed at achieving an optimal environmental state for their competitiveness and balance of the cellular homeostasis. This review summarizes the studies dealing with biosynthesis and bioaccumulation of phthalates in algae and investigates the source of their origin by suggesting strategies to identify the process leading to their presence.

Nonsense mutations cause several genetic diseases such as cystic fibrosis, Duchenne muscular dystrophy, β-thalassemia, and Shwachman–Diamond syndrome. These mutations induce the formation of a premature termination codon (PTC) inside the mRNA sequence, resulting in the synthesis of truncated polypeptides. Nonsense suppression therapy mediated by translational readthrough-inducing drugs (TRIDs) is a promising approach to correct these genetic defects. TRIDs generate a ribosome miscoding of the PTC named “translational readthrough” and restore the synthesis of full-length and potentially functional proteins. The new oxadiazole-core TRIDs NV848, NV914, and NV930 (NV) showed translational readthrough activity in nonsense-related in vitro systems. In this work, the possible off-target effect of NV molecules on natural termination codons (NTCs) was investigated. Two different in vitro approaches were used to assess if the NV molecule treatment induces NTC readthrough: (1) a study of the translational-induced p53 molecular weight and functionality; (2) the evaluation of two housekeeping proteins’ (Cys-C and β2M) molecular weights. Our results showed that the treatment with NV848, NV914, or NV930 did not induce any translation alterations in both experimental systems. The data suggested that NV molecules have a specific action for the PTCs and an undetectable effect on the NTCs.