Venlafaxine and atenolol disrupt epinephrine-stimulated glucose production in rainbow trout hepatocytes.

The beta-blocker atenolol (ATEN), and the selective serotonin and norepinephrine reuptake inhibitor, venlafaxine (VEN) are found in municipal wastewater effluents, but little is known about the effect of these pharmaceuticals on aquatic animals. We tested the hypothesis that VEN and ATEN disrupt acute stress mediated glucose production in fish liver. To this end, rainbow trout (Oncorhynchus mykiss) hepatocytes were exposed in vitro to different concentrations (0, 0.1, 10, 1000 nM) of VEN or ATEN and glucose production in response to either cortisol or epinephrine (two key stress hormones) was ascertained. Both VEN and ATEN did not affect either the unstimulated or cortisol (100 ng/mL)-stimulated glucose release over a 24 h period. The acute (3 h) unstimulated glucose production by isolated hepatocytes in suspension was also not modified by ATEN, while VEN (100 and 1000 nM) reduced basal glucose release. However, ATEN, even at concentration as low as 0.01 nM completely abolished epinephrine (1 µM)-induced glucose production in trout hepatocytes. Interestingly, VEN also suppressed epinephrine-induced glucose production but only at higher concentrations (100 and 1000 nM). Neither VEN nor ATEN significantly impacted the glucose production in response to either 8-bromo-cAMP (cAMP analogue) or glucagon (a metabolic hormone that increases glucose production) stimulation. ATEN but not VEN attenuated the epinephrine-induced increase in glucose transporter 2 (GLUT2) mRNA abundance in trout hepatocytes. Taken together, our results suggest that the impact of ATEN and VEN on glucose production involves inhibition of ß-adrenoceptor signaling in trout hepatocytes. Overall, VEN and ATEN are beta-blockers and may disrupt the adaptive acute glucose response to a secondary stressor in rainbow trout.

Handling of ferric iron by branchial and intestinal epithelia of climbing perch (Anabas testudineus Bloch).

With a view to test how the branchial and intestinal tissues of fish, the two sites of metal acquisition, utilize the water-borne ferric [Fe(III)] iron and whether the accumulation of this form of iron influences cellular Na/K gradient in these tissues, the gills and intestines of climbing perch adapted to freshwater (FW) and acclimated to dilute seawater (20 ppt; SW) were analyzed for ouabain-sensitive Na+, K+-ATPase activity, Fe and electrolyte contents after loading a low (8.95 microM) or high dose (89.5 microM) of Fe(III) iron in the water. The SW gills showed higher levels of total Fe after treating with 8.95 microM of Fe(III) iron which was not seen in the FW gills. Na+, K+-ATPase activity, reflecting Na/K pump activity, showed an increase in the FW gills and not in the SW gills. Substantial increase in the branchial Na and K content was observed in the SW gills, but the FW gills failed to show such effects after Fe(III) loading. The total Fe content was declined in the FW intestine but not in the SW intestine. Water-borne Fe(III) iron decreased the activity of Na+, K+-ATPase in the SW intestine while not changing its activity in the FW intestine. The Na and K content in the FW intestine did not respond to Fe(III) iron exposure but showed a reduction in its Na levels in the SW intestine. The moisture content in the gills and intestines of both the FW and SW perch remained unaffected after Fe(III) loading. In FW fish, the plasma Na levels were decreased by a low dose of Fe(III) iron, though a high dose of Fe(III) iron was required in the SW fish for such an effect. Overall, the results for the first time provide evidence that gills act as a major site for Fe(III) iron absorption and accumulation during salinity acclimation which depends on a high cellular Na/K gradient.