Molecular Characterization and Expression of α-Globin and β-Globin Genes in the Euryhaline Flounder (Platichthys flesus)

In order to understand the possible role of globin genes in fish salinity adaptation, we report the molecular characterization and expression of all four subunits of haemoglobin, and their response to salinity challenge in flounder. The entire open reading frames of α1-globin and α2-globin genes were 432 and 435 bp long, respectively, whereas the β1-globin and β2-globin genes were both 447 bp. Although the head kidney (pronephros) is the predicted major site of haematopoiesis, real-time PCR revealed that expression of α-globin and β-globin in kidney (mesonephros) was 1.5 times higher than in head kidney. Notably, the α1-globin and β1-globin mRNA expression was higher than α2-globin and β2-globin in kidney. Expression levels of all four globin subunits were higher in freshwater- (FW-) than in seawater- (SW-)adapted fish kidney. If globins do play a role in salinity adaptation, this is likely to be more important in combating the hemodilution faced by fish in FW than the dehydration and salt loading which occur in SW

Conopressin-T from Conus tulipa reveals an antagonist switch in vasopressin-like peptide

We report the discovery of conopressing-T, a novel bioactive peptide isolated from Conus tulipa venom. Conopressin-T belongs to the vasopressin-like peptide family and displays high sequence homology to the mammalian hormone oxytocin (OT) and to vasotocin, the endogenerous vasopressin analogue found in the teleost fish, the cone snail's prey

Renal Action of Acute Chloroquine and Paracetamol Administration in the Anesthetized, Fluid-Balanced Rat

ABSTRACT Chloroquine induces diuresis, natriuresis, and an increase in glomerular filtration rate (GFR) in the rat. These responses are modified in rats with analgesic nephropathy induced by longterm paracetamol (acetaminophen) administration. Here, the effects of acute paracetamol treatment on renal function and the response to chloroquine are reported. Under intraval anesthesia (100 mg kg Ϫ1 ) male Sprague-Dawley rats (n ϭ 6/group) were infused with 2.5% dextrose for 3 h. After a control hour, they received either vehicle, chloroquine (0.04 mg h Ϫ1 ), paracetamol (priming dose of 210 mg kg Ϫ1 followed by 110 mg kg Ϫ1 h Ϫ1 ) or chloroquine and paracetamol over the next hour. Compared with vehicle, chloroquine infusion resulted in increases in GFR (2.4 Ϯ 0.3 versus 4.8 Ϯ 0.6 ml min Ϫ1 ), urine flow (4.2 Ϯ 0.3 versus 10.4 Ϯ 0.7 ml h Ϫ1 ), and sodium excretion (47.7 Ϯ 4.1 versus 171.2 Ϯ 18.6 mol h Ϫ1 ) and a reduction in urine osmolality (223.2 Ϯ 5.9 versus 121.7 Ϯ 23.9 mOsM kg Ϫ1 ). Paracetamol reduced sodium excretion but had no effect on urine flow, GFR, or urine osmolality. When combined, paracetamol blocked the chloroquine-induced diuresis (3.9 Ϯ 0.7 ml h Ϫ1 ) and natriuresis (22.6 Ϯ 8.5 mol h Ϫ1 ), attenuated the increase in glomerular filtration rate (3.5 Ϯ 0.2 ml min Ϫ1 ), and raised urine osmolality (280.0 Ϯ 22.8 mOsM kg Ϫ1 ). The differing effects of acute and long-term paracetamol treatment on basal and chloroquine-mediated renal function suggest that the length of prior exposure to paracetamol, and thus the presence of analgesic nephropathy, is an important determinant of the renal response to chloroquine