Comparaison des échanges branchiaux de Cl− en eau douce chez Salmo gairdneri in vivo et in vitro sur la tête isolée perfusée

1978 ◽  
Vol 35 (4) ◽  
pp. 477-479 ◽  
Author(s):  
P. Payan ◽  
P. Pic ◽  
G. De Renzis
Keyword(s):  

The Cl− influxes are identical in vivo and in vitro providing that the gills are externally irrigated during the preparation of the isolated head. A net uptake of Cl− is observed. When no irrigation is used the Cl− influx is reduced by 66% and Cl− is lost by the preparation.

1985 ◽  
Vol 114 (1) ◽  
pp. 151-179 ◽  
Author(s):  
Chris M. Wood ◽  
James N. Cameron

The 14C-DMO/3H-inulin method for pHi was critically assessed in intact Callinectes and found to be reliable provided adequate equilibration time and significant radiolabel excretion were taken into account. An unusually high ‘mean whole body pHi’ (7.54 at 20°C compared with a pHa of 7.80) was due to a highly alkaline fluid compartment (pHi = 8.23) in the carapace. At 20°C the pHi of the heart was 7.35 and skeletal muscle pHi was 7.30, and there were small but consistent differences in the pHi of different muscle types. The change in pHa with temperature was −0.0151 u°C−1 between 10 and 30°C, slightly less than the slope for the neutral pH of water (ΔpN/ΔT ≃ −0.0175 u °C−1). With data corrected to constant PiCoCo2 this was associated with a change in [HCO3−]a between 10 and 20°C (−0.13 mequivl−1°C−1, constant PaCoCo2) and a change in PaCoCo2 between 20 and 30°C (+0.13Torr°C−1, constant [HCO3−]a). The disturbing effect of relatively small PiCOCO2 changes on this pattern was demonstrated. ΔpHi/ΔT slopes for all tissues except carapace were not significantly different from pHa/ΔT but generally lower than ΔpN/ΔT. The slope for the. carapace was very flat and greatly influenced the ‘mean whole body pHi’ slope (−0.0062u°C−1). In haemolymph in vitro at constant Picoco2 ‘passive’ Δ[HCO3−]/ΔT (−0.17mequivI −1°C−1) was comparable to that in vivo between 10 and 20°C, independent of absolute PCOCO2. and directly related to total protein concentration. Haemolymph non-bicarbonate buffer value (β) was similarly related to protein, but increased with temperature. Crabs subjected to an acute 20→10°C shift showed initial overshoots of pHa and pHi associated with undershoot of PaCOCO2, all of which were corrected over 24 h as [HCO3−]a rose. During this period there was a significant net uptake


1968 ◽  
Vol 46 (5) ◽  
pp. 423-432 ◽  
Author(s):  
M. Yamamoto

Glycogen phosphorylase b was purified 70- to 90-fold from skeletal muscle of rainbow trout (Salmo gairdneri). The purified enzyme exhibited maximal activity near pH 6.8 at 37°. Of several 5′-nucleotides tested, only 5′-AMP caused stimulation of phosphorylase b. The Km value for glucose-1-phosphate was 10–15 mM, and for 5′-AMP, 0.2–0.4 mM. Glucose (25 mM) and ATP (5 mM) were both inhibitory, but glucose-6-phosphate (5 mM) had no effect. Inactive trout muscle phosphorylase was converted to the active form in vivo by subjecting a fish to physical exercise. The conversion of fish muscle phosphorylase b to a was also catalyzed in vitro with purified rabbit muscle phosphorylase b kinase in the presence of ATP and Mg++. Evidence is presented to indicate the presence of phosphorylase b kinase and phosphorylase phosphatase in trout skeletal muscle.


2017 ◽  
Vol 61 (5) ◽  
Author(s):  
M. Masud Parvez ◽  
Ho Jung Shin ◽  
Jin Ah Jung ◽  
Jae-Gook Shin

ABSTRACT para-Aminosalicylic acid (PAS) is a second-line antituberculosis drug that has been used to treat multidrug-resistant and extensively drug-resistant tuberculosis for more than 60 years. Renal secretion and glomerular filtration are the major pathways for the elimination of PAS. We comprehensively studied PAS transport by using cell lines that overexpressed various transporters and found that PAS acts as a novel substrate of an organic anionic polypeptide (OATP1B1), organic cationic transporters (OCT1 and OCT2), and organic anion transporters (OAT1 and OAT3) but is not a substrate of any ATP-binding cassette (ABC) transporters. Net PAS uptake was measured, and the transport affinities (Km values) for OATP1B1, OCT1, OCT2, OAT1, and OAT3 were found to be 50.0, 20.3, 28.7, 78.1, and 100.1 μM, respectively. The net uptake rates suggested that renal OAT1 and OAT3 play relatively major roles in PAS elimination. The representative inhibitors rifampin for OATP1B1, probenecid for OAT1 and OAT3, and verapamil for OCT1 and OCT2 greatly inhibited PAS uptake, suggesting that PAS is dependent on multiple transporters for uptake. We also evaluated nonsteroidal anti-inflammatory drugs (NSAIDs), proton pump inhibitors (PPIs), and metformin for the inhibition of PAS uptake via these transporters. Half-maximal (50%) inhibitory concentrations (IC50s) were kinetically determined and used to predict the drug-drug interactions (DDIs) affecting these transporters' activity toward PAS. We found that rifampin, probenecid, ibuprofen, naproxen, cimetidine, and quinidine each exhibited a significant potential for in vivo DDIs with PAS. In this study, PAS was found to be a novel substrate of several transporters, and drugs that inhibit these transporters can reduce PAS elimination.


1984 ◽  
Vol 62 (8) ◽  
pp. 1495-1501 ◽  
Author(s):  
J. G. Eales ◽  
Shirley Shostak ◽  
Catherine G. Flood

The effects of the thiols DTT (dithiothreitol) and GSH (reduced glutathione) on hepatic in vitro and in vivo T4 (L-thyroxine) deiodination by rainbow trout held at 11 °C were studied. Hepatic deiodination increased progressively over the DTT range of 0.02–20 mM. GSH was less potent than DTT at low concentrations and strongly inhibited deiodination at high concentrations (> 1 mM). Hepatic deiodination was not increased by 1 mM NADPH or anaerobic conditions and was enhanced and not inhibited by the GSH inhibitor, diamide (2.5 mM), indicating that the low T4 deiodination in the absence of DTT is not due to endogenous GSH deficiency. Intraperitoneally injected GSH consistently increased plasma levels of 125I and [125I]-3,5,3′-triiodo-L-thyronine (T3) in fed or starved [125I]T4-injected trout, suggesting a GSH stimulation of extrahepatic T4 deiodination. However, injected GSH did not elevate plasma T3 concentrations. This was probably due to a demonstrated GSH stimulation of plasma T4 and T3 clearance. Force-fed GSH did not increase [125I]T4 deiodination. It is concluded that exogenous thiols can enhance T4 deiodination both in vitro and in vivo. However, availability of neither endogenous nor dietary GSH appears to regulate T4 deiodination under physiological conditions, including altered nutritional state.


2008 ◽  
Vol 417 (1) ◽  
pp. 305-312 ◽  
Author(s):  
Lucia Corich ◽  
Alejandro Aranda ◽  
Laura Carrassa ◽  
Cristina Bellarosa ◽  
J. Donald Ostrow ◽  
...  

In vitro and in vivo studies have demonstrated that UCB (unconjugated bilirubin) is neurotoxic. Although previous studies suggested that both MRP1 (multidrug resistance-associated protein 1) and MDR1 (multidrug resistance protein 1) may protect cells against accumulation of UCB, direct comparison of their role in UCB transport was never performed. To this end, we used an inducible siRNA (small interfering RNA) expression system to silence the expression of MRP1 and MDR1 in human neuroblastoma SH-SY5Y cells. The effects of in vitro exposure to clinically-relevant levels of unbound UCB were compared between unsilenced (control) cells and cells with similar reductions in the expression of MRP1 or MDR1, documented by RT–PCR (reverse transcription–PCR) (mRNA), immunoblotting (protein), and for MDR1, the enhanced net uptake of a specific fluorescent substrate. Cytotoxicity was assessed by the MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide] test. MRP1-deficient cells accumulated significantly more UCB and suffered greater cytotoxicity than controls. By contrast, MDR1-deficient cells exhibited UCB uptake and cytotoxicity comparable with controls. At intermediate levels of silencing, the increased susceptibility to UCB toxicity closely correlated with the decrease in the expression of MRP1, but not of MDR1. These data support the concept that limitation of cellular UCB accumulation, due to UCB export mediated by MRP1, but not MDR1, plays an important role in preventing bilirubin encephalopathy in the newborn.


1988 ◽  
Vol 134 (1) ◽  
pp. 267-280 ◽  
Author(s):  
V. Tetens ◽  
G. Lykkeboe ◽  
N. J. Christensen

The red cell adrenoceptor affinity for the unspecific agonists adrenaline and noradrenaline and the specific beta-agonist isoprenaline was studied in vitro on whole blood of rainbow trout, Salmo gairdneri at 15 degrees C. The erythrocytic adrenoceptors could be pharmacologically characterized as beta-receptors of the ‘noradrenaline’-type (beta 1-type), with an order of potency of isoprenaline greater than noradrenaline much greater than adrenaline. The adrenoceptor affinities, expressed as agonist concentrations for 50% response (EC50), were 1.3 X 10(−8) and 7.6 X 10(−7) mol l-1 for noradrenaline and adrenaline, respectively. Winter fish showed a red cell adrenergic response identical to that of summer-acclimated fish. It is concluded that most red cell beta-adrenergic responses in vivo are exclusively elicited by noradrenaline.


Sign in / Sign up

Export Citation Format

Share Document