Acute temperature elevation in tap and Rhine water affects skin and gill epithelia, hydromineral balance, and gill Na+/K+-ATPase activity of brown trout (Salmo trutta) smolts

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Effects of water pH on chromium toxicity to early life stages of the common carp (Cyprinus carpio)

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Effects of low water pH on lead toxicity to early life stages of the common carp (Cyprinus carpio)

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Inhibition of Ca2+ uptake in freshwater carp, Cyprinus carpio, during short-term exposure to aluminum

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Early life stages of carp (Cyprinus carpio L.) depend on ambient magnesium for their development

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PTHrP potentiating estradiol-induced vitellogenesis in sea bream (Sparus auratus, L.)

Contains fulltext : 35553.pdf ( ) (Open Access)In fish, vitellogenin is an important nutritional precursor protein produced solely in the liver and released into the blood where it binds calcium. In the gilthead sea bream (Sparus auratus) 17beta-Estradiol (E2) plays an important role in the synthesis of vitellogenin, but also the pituitary hormones prolactin (PRL) and growth hormone (GH) can stimulate vitellogenin induction in fish. Considering the emerging involvement of PTHrP in fish calcium metabolism and the importance of calcium regulation in reproduction, we investigated the possible role of PTHrP in vitellogenesis. E2-naive and E2-primed sea bream hepatocytes were used in an in vitro primary hepatocyte culture and stimulated with a recombinant sea bream PTHrP (sbPTHrP) to establish the contribution of sbPTHrP alone or in combination with E2 to the regulation of hepatic vitellogenin synthesis. Hepatocytes stimulated solely with sbPTHrP were not affected in their vitellogenesis. However, in hepatocytes stimulated with E2 in combination with sbPTHrP a higher vitellogenin production was seen than with E2 alone. It is concluded that sbPTHrP has a potentiating effect on estradiol stimulation of vitellogenin production by sea bream hepatocytes. The sea bream provides a unique model where vitellogenesis regulation can be studied on E2-naive liver cells, both in vivo and in vitro

CYP27A1 expression in gilthead sea bream (Sparus auratus, L.): effects of calcitriol and parathyroid hormone-related protein

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Dietary supplementation with arachidonic acid in tilapia (Oreochromis mossambicus) reveals physiological effects not mediated by prostaglandins.

Contains fulltext : 60326.pdf (publisher's version ) (Closed access)This study aims to clarify the role of the polyunsaturated fatty acid arachidonic acid (ArA, 20:4n-6) in the stress response of Mozambique tilapia (Oreochromis mossambicus). ArA is converted into eicosanoids, including prostaglandins, which can influence the response to stressors. Tilapia, a species able to form ArA from its precursor, was supplemented with ArA for 18 days, after which they were confined for 5 min. Acetylsalicylic acid (ASA, COX-inhibitor) was subsequently administered to distinguish ArA-mediated effects from enhanced prostaglandin E(2) (PGE(2)) synthesis. ArA supplemented fish had higher ArA levels in gills and kidneys, and these levels were further enhanced after ASA treatment. Levels of total monounsaturated and polyunsaturated fatty acids as well as docosahexaenoic acid (DHA), eicosapentaenoic acid (EPA), and ArA, were altered 24h after confinement, particularly in the kidneys. ArA supplementation had no effect on basal cortisol levels, while ArA + ASA reduced basal cortisol levels. ArA + ASA augmented the cortisol response to confinement. The combination of ArA + ASA also elevated plasma basal prolactin (tPRL)(177) and 3,5,3'-triiodothyronine (T(3)) levels. Neither ArA nor ASA affected the stress-associated increases in plasma glucose and lactate. Na(+), K(+)-ATPase activity in the gills was reduced after ArA supplementation and was even further suppressed by subsequent ASA treatment. In an additional feeding trial, ArA supplementation enhanced the renal Na(+), K(+)-ATPase activity. In vitro, ArA was a potent inhibitor of the Na(+), K(+)-ATPase activity of gill and kidney homogenates. In contrast, PGE(2) had no effect on branchial ATPase, whereas the effect on renal ATPase activity was concentration dependent. Modifying the dietary intake of ArA alters the response of tilapia to an acute stressor and influences osmoregulatory processes and it is unlikely that these effects are due to an enhanced production of prostaglandins

PTHrP regulation and calcium balance in sea bream (Sparus auratus L.) under calcium constraint

Contains fulltext : 35554.pdf ( ) (Open Access)Juvenile gilthead sea bream were exposed to diluted seawater (2.5 per thousand salinity; DSW) for 3 h or, in a second experiment, acclimated to DSW and fed a control or calcium-deficient diet for 30 days. Branchial Ca(2+) influx, drinking rate and plasma calcium levels were assessed. Sea bream plasma parathyroid hormone related protein (sPTHrP) was measured, and mRNAs of pthrp, its main receptor, pth1r, and the calcium-sensing receptor (casr) were quantified in osmoregulatory tissues and the pituitary gland. When calcium is limited in water or diet, sea bream maintain calcium balance; however, both plasma Ca(2+) and plasma sPTHrP concentrations were lower when calcium was restricted in both water and diet. Positive correlations between plasma sPTHrP and plasma Ca(2+) (R(2)=0.30, N=39, P<0.05), and plasma sPTHrP and body mass of the fish (R(2)=0.37, N=148, P<0.001) were found. Immunoreactive sPTHrP was demonstrated in pituitary gland pars intermedia cells that border the pars nervosa and co-localises with somatolactin. In the pituitary gland, pthrp, pth1r and casr mRNAs were downregulated after both short- and long-term exposure to DSW. A correlation between pituitary gland pthrp mRNA expression and plasma Ca(2+) (R(2)=0.71, N=7, P<0.01) was observed. In gill tissue, pthrp and pth1r mRNAs were significantly upregulated after 30 days exposure to DSW, whereas no effect was found for casr mRNA expression. We conclude that in water of low salinity, declining pituitary gland pthrp mRNA expression accompanied by constant plasma sPTHrP levels points to a reduced sPTHrP turnover and that sPTHrP, through paracrine interaction, is involved in the regulation of branchial calcium handling, independently of endocrine pituitary gland sPTHrP

Plasma α-MSH and acetylated β-endorphin levels following stress vary according to CRH sensitivity of the pituitary melanotropes in common carp, Cyprinus carpio

Pituitary melanotropes release alpha-melanocyte-stimulating hormone (alpha-MSH) and acetylated beta-endorphin (NAc beta-end) during stress responses. However, effects of stressors on plasma concentrations of these hormones are highly inconsistent among fish species. Here, we show that also within a species, the common carp (Cyprinus carpio), fish sometimes respond with elevated alpha-MSH and NAc beta-end plasma levels, and at other times not. The origin of this variable response was investigated by (1) studying the effects of corticotropin-releasing hormone (CRH) on alpha-MSH and NAc beta-end release in vitro, (2) establishing where in the second messenger pathway coupled to CRH receptors melanotrope responsiveness is determined, and (3) testing modulatory actions of other hypothalamic factors (here opioid beta-endorphin). Melanotropes were in a high or low responsive state to CRH in vitro, which was especially evident when tissue was tested from fish kept at higher ambient water temperatures, and this correlates with the variability in alpha-MSH and NAc beta-end responses in vivo. Relative rates of alpha-MSH and NAc beta-end release following stimulation with CRH in vitro match plasma level changes in vivo, and this indicates that the CRH pathway does act in vivo. cAMP did not stimulate melanotropes in the low responsive state to release hormones in vitro. Thus, the mechanism that determines the cell status, occurs downstream of cAMP accumulation. Opioid beta-endorphin differentially modulated the actions of CRH, as NAc beta-end, but not alpha-MSH, release was inhibited. This response was not observed in the stress paradigms studied. We conclude that the variation in alpha-MSH and NAc beta-end stress responses in vivo correlates with many CRH responses in vitro; whether a cell is in a high or low responsive state to CRH is determined downstream of accumulation of the second messenger. We propose that melanotropes have to be in the high responsive state to be activated by CRH during stress in carp and other teleosts