Occurrence of potentially toxic microalgae and diarrhetic shellfish toxins in the digestive tracts of green sea turtles (Chelonia mydas) from southern Brazil.

Algal toxins are involved in the mortality and/or illness of marine organisms via consumption of contaminated prey, or upon direct exposure to toxic cells. In this study, the presence of potentially toxic microalgal cells was investigated within the digestive tract contents of a threatened species of green turtle (Chelonia mydas). Additionally, lipophilic toxins were determined by LC-MS/MS in tissue samples (liver, stomach and/or intestine) of selected animals (n = 39 individuals) found dead-stranded in southern Brazil, from winter/2015 to autumn/2016. Thirteen potentially toxic species of microalgae (both benthic and planktonic), including seven dinoflagellates, six cyanobacteria and one diatom, were found in the digestive tract contents of green turtles. Among them, dinoflagellates belonging to the Dinophysis acuminata species complex were the most frequent (36%) and abundant (maximum average abundance of 566 cells g-1 in spring/2015). Moreover, 23% of the examined sea turtles exhibited detectable levels of the diarrhetic shellfish toxin okadaic acid (OA) in washed digestive tissues. Seven individuals accumulated OA in their intestines (max. 24.1 ng g-1) and two in the stomachs (max. 7.4 ng g-1). Toxin levels in the tissues were directly and significantly (r = 0.70, p < 0.025) associated with the cell abundance of OA-producing D. acuminata and Prorocentrum lima species complexes within the digestive contents of green turtles. Although OA concentrations were relatively low, possible chronic exposure might deteriorate general health conditions of exposed sea turtles, increasing the risk for diseases. Okadaic acid has been regarded as a tumor-promoting compound and an environmental co-factor in the incidence of fibropapillomatosis, a frequent disease in juvenile green turtles inhabiting this geographic region. Even though, only one green turtle containing OA in the digestive tissues (out of six examined) also presented fibropapillomatosis in this study. Notwithstanding, sea turtles are sentinels of ocean health. Monitoring the accumulation of algal toxins and their negative effects on these organisms contributes to conserving biodiversity and marine habitats.

Summer bloom of Vulcanodinium rugosum in Cienfuegos Bay (Cuba) associated to dermatitis in swimmers.

The marine dinoflagellate Vulcanodinium rugosum produces powerful paralyzing and cytotoxic compounds named pinnatoxins (PnTX) and portimines. Even though, no related human intoxication episodes following direct exposure in seawater or the ingestion of contaminated seafood have been documented so far. This study aimed at investigating a dinoflagellate bloom linked to acute dermatitis cases in two recreational beaches in Cienfuegos Bay, Cuba. We used epidemiological and clinical data from 60 dermatitis cases consisting of individuals in close contact with the bloom. Seawater physical-chemical properties were described, and the microorganism causing the bloom was identified by means of light and scanning electron microscopy. Morphological identification was confirmed genetically by sequencing the internal transcribed spacers ITS1 and ITS2, and the 5.8S rDNA region. Toxic compounds were identified from a bloom extract using liquid chromatography (LC) coupled to high-resolution mass spectrometry (HRMS), and their concentrations were estimated based on low-resolution tandem mass spectrometry (LC-MS/MS). Sixty people who had prolonged contact with the dinoflagellate bloom suffered acute dermal irritation. Most patients (79.2%) were children and had to be treated with antibiotics; some required >5-day hospitalization. Combined morphological and genetic characters indicated V. rugosum as the causative agent of the bloom. rDNA sequences of the V. rugosum genotype found in the bloom aligned with others from Asia, including material found in the ballast tank of a ship in Florida. The predominant toxins in the bloom were portimine, PnTX-F and PnTX-E, similar to strains originating from the Pacific Ocean. This bloom was associated with unusual weather conditions such as frequent and prolonged droughts. Our findings indicate a close link between the V. rugosum bloom and a dermatitis outbreak among swimmers in Cienfuegos Bay. Phylogenetic evidence suggests a recent introduction of V. rugosum from the Pacific Ocean into Caribbean waters, possibly via ballast water.

Alcohol worsens acute lung injury by inhibiting alveolar sodium transport through the adenosine A1 receptor.

OBJECTIVE: Alcohol intake increases the risk of acute lung injury (ALI) and the acute respiratory distress syndrome (ARDS) and is associated with poor outcomes in patients who develop these syndromes. No specific therapies are currently available to treat or decrease the risk of ARDS in patients with alcoholism. We have recently shown increased levels of lung adenosine inhibit alveolar fluid clearance, an important predictor of outcome in patients with ARDS. We hypothesized that alcohol might worsen lung injury by increasing lung adenosine levels, resulting in impaired active Na(+) transport in the lung. METHODS: We treated wild-type mice with alcohol administered i.p. to achieve blood alcohol levels associated with moderate to severe intoxication and measured the rate of alveolar fluid clearance and Na,K-ATPase expression in peripheral lung tissue and assessed the effect of alcohol on survival during exposure to hyperoxia. We used primary rat alveolar type II cells to investigate the mechanisms by which alcohol regulates alveolar Na(+) transport. RESULTS: Exposure to alcohol reduced alveolar fluid clearance, downregulated Na,K-ATPase in the lung tissue and worsened hyperoxia-induced lung injury. Alcohol caused an increase in BAL fluid adenosine levels. A similar increase in lung adenosine levels was observed after exposure to hyperoxia. In primary rat alveolar type II cells alcohol and adenosine decreased the abundance of the Na,K-ATPase at the basolateral membrane via a mechanism that required activation of the AMPK. CONCLUSIONS: Alcohol decreases alveolar fluid clearance and impairs survival from acute lung injury. Alcohol induced increases in lung adenosine levels may be responsible for reduction in alveolar fluid clearance and associated worsening of lung injury.