This study presents the behavior of novel anti-fouling nanomaterials in seawater and their toxicity towards target and non-target marine species.

Mutations in genes that encode tRNAs, aminoacyl-tRNA syntheases, tRNA modifying enzymes and other tRNA interacting partners are associated with neuropathies, cancer, type-II diabetes and hearing loss, but how these mutations cause disease is unclear. We have hypothesized that levels of tRNA decoding error (mistranslation) that do not fully impair embryonic development can accelerate cell degeneration through proteome instability and saturation of the proteostasis network. To test this hypothesis we have induced mistranslation in zebrafish embryos using mutant tRNAs that misincorporate Serine (Ser) at various non-cognate codon sites. Embryo viability was affected and malformations were observed, but a significant proportion of embryos survived by activating the unfolded protein response (UPR), the ubiquitin proteasome pathway (UPP) and downregulating protein biosynthesis. Accumulation of reactive oxygen species (ROS), mitochondrial and nuclear DNA damage and disruption of the mitochondrial network, were also observed, suggesting that mistranslation had a strong negative impact on protein synthesis rate, ER and mitochondrial homeostasis. We postulate that mistranslation promotes gradual cellular degeneration and disease through protein aggregation, mitochondrial dysfunction and genome instability.

Prenatal exposure to ethanol leads to a myriad of developmental disorders known as fetal alcohol spectrum disorder, often characterized by growth and mental retardation, central nervous system damage, and specific craniofacial dysmorphic features. The mechanisms of ethanol toxicity are not fully understood, but exposure during development affects the expression of several genes involved in cell cycle control, apoptosis, and transcriptional regulation. MicroRNAs (miRNAs) are implicated in some of these processes, however, it is not yet clear if they are involved in ethanol-induced toxicity. In order to clarify this question, we have exposed zebrafish embryos to ethanol and evaluated whether a miRNA deregulation signature could be obtained. Zebrafish embryos were exposed to 1 and 1.5% of ethanol from 4 h postfertilization (hpf) to 24 hpf. The miRNA expression profiles obtained reveal significant miRNA deregulation and show that both ethanol concentrations upregulate miR-153a, miR-725, miR-30d, let-7k, miR-100, miR-738, and miR-732. Putative gene targets of deregulated miRNAs are involved in cell cycle control, apoptosis, and transcription, which are the main processes affected by ethanol toxicity. The conservation of affected mechanisms among vertebrates leads us to postulate that similar miRNA deregulation occurs in humans, highlighting a relevant role of miRNAs in ethanol toxicology.

Metallic corrosion is an unsolved problem that has been minimized through the application of specialized coatings containing corrosion inhibitors, such as 2-mercaptobenzothiazole (MBT).

An array of anthropogenic pressures is affecting tropical ecosystems, posing major conservation challenges for scientists, stakeholders and populations. Illegal cyanide fishing is one of the major threats to Indo-Pacific coral reefs, targeting a multitude of colorful species for the marine aquarium trade as well as large-sized groupers and wrasses for the food fish trade. Ultimately, the continued use of this destructive practice as oceans warm may overload tropical ecosystems and result in irreversible ecological damage. Here we show that the impact of cyanide poisoning in an ornamental tropical marine fish is magnified under increased temperatures. A sole pulse exposure of 60 s to 50 mg L −1 of cyanide under current temperature (26 • C) caused substantial mortality (50-100%) in eight species of Pomacentridae. The clownfish Amphiprion ocellaris was the most resistant, especially medium-sized fish [average total length and weight of 38 mm and 1.12 g; LC 50 (95% CI) = 50.00 (46.76 − 53.24) mg L −1 ] that showed shorter recovery times and higher survival rates (%) when compared to small-sized ones [average total length and weight of 25 mm and 0.30 g; LC 50 (95% CI) = 28.45 (20.17 − 36.72) mg L −1 ]. However, when the most resistant size-class was concomitantly exposed to a sub-lethal dosage of cyanide (25 mg L −1 instead of 50 mg L −1 ) and ocean warming scenarios for 2100 (+3 • C and heat wave +6 • C), survival rates (%) decreased to 60 and 20%, respectively, and recovery times increased in the worst case scenario. Mortality outbreaks, as well as vulnerability to predation, will likely expand in fish inhabiting coral reefs exposed to cyanide fishing unless stronger conservation measures are taken in tropical reefs to limit this destructive practice now and in the oceans of tomorrow.