Disease relevance of Sulfobromophthalein

• Since spironolactone treatment was not associated with improvement in the fractional clearance of bromosulfophthalein, nor in serum albumin, prothrombin time, and factor V, the data are compatible with the idea that even in cirrhosis the hepatic drug-oxidizing enzymes were induced by spironolactone [1].
• In contrast, bromosulfophthalein, a MOAT substrate, had no effect on either E(2)17G-mediated cholestasis or its biliary excretion [2].
• The kinetics of plasma clearance of indocyanine green and bromosulfophthalein were studied in 49 consecutive patients with chronic unconjugated hyperbilirubinemia [3].
• These patients were older (p less than 0.02) and, 3 months following bypass, had greater cumulative per cent weight loss (p less than 0.05), higher levels of serum aspartate aminotransferase (p less than 0.005), and greater 45-min bromosulfophthalein retention (p less than 0.02) [4].
• The other sister (L.R.) had never had symptomatic liver disease and only a slight increase in serum transaminase and bromsulfalein retention [5].

High impact information on Sulfobromophthalein

• Administration of BSP or probenecid simultaneously with [C14] penicillin resulted in increased plasma retention and reduced kidney and urinary bladder content of [14C] penicillin and a correlation coefficient of -0.8 between total kidney/plasma radioactivity and percent of protein-bound radioactivity bound to ligandin in the kidney [6].
• ATP-dependent daunomycin transport by brush border vesicles was unidirectional (inside to outside) and temperature dependent and was blocked by Gp170 inhibitors but not by taurocholate or bromsulphalein glutathione [7].
• Routine tests of liver function and histology were normal, except for a slight increase in bromsulphalein retention (9% at 45 min) [8].
• Effects of phototherapy on bile acid turnover, biliary lipid concentration, liver function tests, and bromosulfophthalein (BSP) kinetics were studied in 8 alcoholic cirrhotics [9].
• EE decreased the secretory rate maximum (SRM) of tauroursodeoxycholate, (-71%) and bromosulfophthalein (BSP; -60%), as well as the expression of the BSP canalicular carrier, mrp2; SIL failed to increase mrp2 expression, and had only a marginal beneficial effect on both tauroursodeoxycholate and BSP SRM values [10].

Chemical compound and disease context of Sulfobromophthalein

• Dubin-Johnson syndrome (DJS), a congenital metabolic disorder of bilirubin excretion, was classically diagnosed by the bromsulfalein (BSP) curve and needle hepatic biopsy methods [11].
• Patients receiving full doses of doxorubicin with mild hepatic dysfunction as determined by bromsulphalein (BSP) retention and serum liver function studies had the same incidence of toxicity and complete response rate as those with normal hepatic function [12].
• 5. In summary, rats with arterial calcinosis showed an increase in total body clearance of both BSP and SA, probably associated with modifications in their metabolism and/or in organ extraction [13].

Biological context of Sulfobromophthalein

• Per cent recovery at 48-hr posthepatectomy was considerably greater for carbon phagocytosis than for bromosulfophthalein removal by regenerating livers [14].
• Other investigators identified another 55 kD bromosulfophthalein/bilirubin binding protein on the surface of rat hepatocytes and HepG2 cells and suggested that this protein served as a transporter for these ligands [15].
• Molecular aspects of the interaction of bromosulfophthalein with high-affinity binding sites of bovine serum albumin [16].
• Both latter amino acid substitutions abolished the transport of bile acids mediated by OATP1B3, whereas other substrates, like bromosulfophthalein, were transported by all polymorphic variants of the protein [17].
• GST activity and GTN biotransformation by rat aortic cytosol and affinity-purified GSTs were highly sensitive to inhibition by the class mu selective inhibitors Basilen Blue and bromosulfophthalein [18].

Anatomical context of Sulfobromophthalein

• Functional capacities were assessed by bromosulfophthalein uptake for hepatocytes and carbon phagocytosis for Kupffer cells [14].
• Vincristine did not increase methotrexate uptake in CCRF-CEM lymphoblasts, a human cell line which contains much lower levels of bromosulfophthalein-sensitive efflux route for methotrexate [19].
• As GSH loss was blocked by bromosulfophthalein and dibromosulfophthalein, known inhibitors of hepatocyte GSH transport, a specific export rather than nonspecific leakiness through plasma membranes is proposed to be responsible [20].
• The proximal jejunum was perfused with isotonic saline containing sodium-sulphobromophthalein as a non-absorbable marker [21].
• Bromosulfophthalein disposition in chronically bile duct obstructed rats [22].

Associations of Sulfobromophthalein with other chemical compounds

• Fluorescence studies showed the approximate association constants of this protein and bilirubin, bromosulfophthalein, and indocyanine green were 10(6) M-1, 10(5) M-1, and 10(6) M-1, respectively [23].
• Oatp1, the organic anion transport polypeptide, is an integral membrane protein cloned from rat liver that mediates the uptake of various organic anions such as bromosulfophthalein (BSP) and taurocholate (TCA) [24].
• Concentrations of vincristine which inhibited the bromosulfophthalein-sensitive efflux route of L1210 cells by 80-90% had little or no effect on the intracellular pH or on intracellular levels of ATP, GTP, cyclic AMP, K+, or oxidized glutathione [19].
• Uptake sensitive to inhibition by bromosulfophthalein or probenecid was observed for taurocholate, estrone sulfate, and para-aminohippurate in renal slices from wild-type mice, whereas in Oat3(-/-) animals transport of these substances was greatly reduced [25].
• Substrates less well transported by OATP-F include T(3), bromosulfophthalein, estrone-3-sulfate, and estradiol-17beta-glucuronide [26].

Gene context of Sulfobromophthalein

• Suramin is a more potent (IC50, 0.9 microM) inhibitor of FPGS partially purified from CCRF-CEM human leukemia cells than is bromosulfophthalein (IC50, 17 microM), the first reported nonsubstrate-analog inhibitor of FPGS (J. J. McGuire et al., Adv. Exptl. Med. Biol. 163, 199, 1983) [27].
• Bromosulfophthalein (BSP), a substrate not transported by the rat Oatp2, is transported very well by mouse Oatp2 [28].
• Similar to Oatp1 and Oatp2, Oatp4 is a multispecific transporter with high affinities for bromosulfophthalein, dehydroepiandrosterone sulfate, leukotriene C4, and anionic peptides [29].
• Bilirubin and bromosulfophthalein inhibited mucin-induced ANS fluorescence, but bile acids did not [30].
• Compared to detection methods involving prechromatographic addition of bromosulfophthalein or radiolabeled fatty acids to cytosolic proteins, the post-chromatographic binding assay offers the advantage of leaving the bulk of the FABP preparation free of these marker ligands [31].

Analytical, diagnostic and therapeutic context of Sulfobromophthalein

• No significant change in serum liver function tests or BSP plasma disappearance curves was seen [9].
• Evaluation immediately after partial hepatectomy revealed a 66% reduction of liver mass, a 63% decrease in hepatocyte bromosulfophthalein removal, and a 65% decline in Kupffer cell carbon phagocytosis [14].
• The entry and exit kinetic parameters obtained during the perfusion of Gd-BOPTA plus bromosulfophthalein were identical and comparable to those obtained during Gd-DTPA perfusion (P =.95) [32].
• Enzymes were measured in preservation and reperfusion solutions, and reperfused liver function was evaluated by O(2) consumption and bromsulphalein clearance [33].
• To investigate the role of sex steroids in the sex-related difference in the hepatic uptake of organic anions, sulphobromophthalein (bromsulphalein, BSP) transport was measured in hepatocytes isolated from rats either deprived of hormonal influence by castration at prepubertal age or after hormonal substitution [34].

References