RESUMEN
Crassostrea virginica was exposed to different light crude oil levels to assess the effect on transcriptomic response and metabolic rate. The exposure time was 21 days, and levels of 100 and 200 µg/L were used, including a control. The most significant difference among treatments was the overexpression of several genes associated with energy production, reactive oxygen species (ROS) regulation, immune system response, and inflammatory response. Also, a hydrocarbon concentration-related pattern was identified in ROS regulation, with a gene expression ratio near 1.8:1 between 200 and 100 µg/L treatments. Statistical analysis showed no interaction effect for metabolic rate; however, significant differences were found for oil concentration and time factors, with a higher oxygen consumption at 200 µg/L. Our findings provide novel information about the metabolic response of C. virginica during hydrocarbons exposure. In addition, our results point out which biological processes should be investigated as targets for searching bioindicators.
Asunto(s)
Crassostrea , Contaminantes Químicos del Agua , Animales , Crassostrea/metabolismo , Hidrocarburos/metabolismo , Hidrocarburos/toxicidad , Inmunidad , Especies Reactivas de Oxígeno/metabolismo , Contaminantes Químicos del Agua/análisisRESUMEN
Artificial inducers have been used to study signal-transduction pathways involved in metamorphosis of some marine invertebrates. However, the transduction mechanisms for echinoderms have been less explored. In the present study, participation of protein kinase C (PKC), G-protein-coupled receptors (GPCRs), and calcium has been investigated during metamorphosis of the sea urchin Stronglylocentrotus purpuratus. Competent larvae were induced with different drugs that activate (PKC and GP activators, Ca2+ ionophores, and inhibitors of Ca2+ ATPase) or inhibit (PKC, G-protein, and Ca2+ flux inhibitors) metamorphosis. Six of the compounds were effective: the PKC activators TPA and indolactam; the G-protein inhibitors suramin and guanosine; the calcium ionophore A23187, and the calcium ATPase inhibitor thapsigargin. TPA was effective at 0.001 microM; indolactam was effective at 0.001 microM. In the presence of KCl as inducer, the G-protein inhibitor suramin was effective at 10 microM and guanosine at 0.001 microM. In the presence of a bacterial film as inducer, suramin was effective at 50 microM, and guanosine inhibited metamorphosis at 1 microM. A23187 was effective at 5 and 10 microM and thapsigargin at 50 and 100 microM. Our results indicate that GPCRs, protein kinase C, and calcium participate in the metamorphosis of S. purpuratus. These elements of the transduction pathways triggered during metamorphosis may be part of a cascade of signal transduction routes that interact from induction to the end of the morphogenetic events that shape the postlarval form. In addition, according to the results obtained with G-protein inhibitors, the GPCRs may be shared between the artificial (KCl) and natural (biofilm) inducers.