Ocean sunfish as indicators for the 'rise of slime'.

Overfishing and ocean warming are drastically altering the community composition and size structure of marine ecosystems, eliminating large bodied species [1]. Against a backdrop of such environmental change, the heaviest of all bony fish, the ocean sunfish (Mola mola), seems an improbable survivor. Indeed this indolent giant is killed globally as bycatch, and is listed as 'Vulnerable'[2]. We undertook the most extensive aerial surveys of sunfish ever conducted and found surprisingly high abundances off the Atlantic and Mediterranean coasts of Western Europe. With up to 475 individuals per 100 km2, these figures are one order of magnitude higher than abundance estimates for other areas [3-5]. Using bioenergetic modelling, we estimate that each sunfish requires 71 kg day-1 of jellyfish, a biomass intake more than an order of magnitude greater than predicted for a similarly sized teleost. Scaled up to the population level, this equates to a remarkable 20,774 tonnes day-1 of predated jellyfish across our study area in summer. Sunfish abundance may be facilitated by overfishing and ocean warming, which together cause reduced predation of sunfish by sharks and elevated jellyfish biomass. Our combined survey and bioenergetic data provide the first-ever estimate of spatialized ocean sunfish daily food requirements, and stress the importance of this species as a global indicator for the 'rise of slime'. This hypothesis posits that, in an overfished world ocean exposed to global warming, gelatinous zooplankton should flourish, to the detriment of other mesotrophic species such as small pelagic fish, causing irreversible trophic cascades as well as a series of other environmental and economic issues.

Fish Balistes capriscus skin extract-induced relaxation in mesenteric arterial bed of rat.

The vasorelaxing activity of the aqueous extract of fish Balistes capriscus skin (AEBc) on mesenteric arterial bed (MAB) of rats was studied. The bolus injections of AEBc (bolus of 5.1, 10.2, 20.5, and 41.1mg) significantly inhibited, in a concentration-dependent manner, the maximal contractile response induced by methoxamine (30 microM) in MAB. The vasodilatation action of AEBc is not mediated through beta-adrenoceptors or cyclo-oxigenase, since it was not affected by propranolol (20 microM) or diclofenac sodium (3 microM). The vasodilator response induced by subsequent addition of AEBc Balistes capriscus in bolus was significantly reduced in water infusion for endothelium removal. Treatment with an inhibitor of NO synthase (L-NAME, 10 microM) decreased AEBc effect. The guanylate cyclase inhibitor methylene blue (MB, 100 microM) had no significant effect on AEBc-induced vasodilatation. These results suggest that the vasorelaxing effect of AEBc is mediated by endothelium-dependent (NO/EDRF) and endothelium-independent neurally induced vasorelaxation from nonadrenergic and noncholinergic nerves (NO).