Disease relevance of Sulfobromophthalein

• Administration of galactosamine to control rats resulted in hypoglycemia and increased serum bilirubin concentration, elevated serum glutamic oxalacetic transaminase, lactic dehydrogenase and glutamic pyruvic transaminase activities, and retention of sodium sulfobromophthalein [1].
• To determine whether phenobarbital affects hepatocellular bilirubin/sulfobromophthalein uptake mechanism, we administered it to male Sprague-Dawley rats, body weight 175 +/- 25 gm, at doses of 1 to 75 mg/kg body wt/day for 7 days [2].
• Effects of morphine and respiratory depression on sulfobromophthalein disposition in rats [3].
• Functional changes of the biliary tree associated with experimentally induced cholestasis: sulfobromophthalein on manganese-bilirubin combinations [4].
• Male urethane-anesthetized Wistar rats with biliary fistulas were infused for 60 min i.v. with sulfobromophthalein (BSP) or BSP-glutathione conjugate (BSP-GSH) at 594 nmol/100 g/min [5].

High impact information on Sulfobromophthalein

• Abnormal sulfobromophthalein metabolism in Rotor's syndrome and obligate heterozygotes [6].
• Previous studies in cultured rat hepatocytes revealed that initial uptake of sulfobromophthalein (BSP) was markedly reduced upon removal of Cl- from the medium [7].
• Transport of 35S-labeled sulfobromophthalein [35S]BSP was studied in short-term cultured rat hepatocytes incubated in bovine serum albumin [8].
• Hepatic functional deterioration after portacaval shunt in the rat. Effects on sulfobromophthalein transport-maximum, indocyanine green clearance and galactose elimination capacity [9].
• Three distinct proteins [bilitranslocase (BTL), sulfobromophthalein (BSP)/bilirubin-binding protein (BBBP), and organic anion-binding protein] have been isolated from the basolateral plasma-membrane domain of the hepatocyte [10].

Biological context of Sulfobromophthalein

• The Gilbert's syndrome patients studied included all three subtypes, as determined from studies of the plasma disappearance kinetics of sulfobromophthalein and indocyanine green [11].
• Plasma ALDO concentration was positively correlated with plasma renin (p less than 0.001) but not with serum sodium, potassium or albumin concentration, inferior vena cava pressure, corrected hepatic venous wedge pressure, plasma volume or sulfobromophthalein storage or transport [12].
• In the presence of cholecystographic agents or sulfobromophthalein (BSP), the amount of labeled hormone bound to adsorbent increased in a dose-dependent fashion, reflecting displacement from protein-binding sites [13].
• METHODS: Parameters of hepatic function (liver biochemistry, indocyanine green and sulfobromophthalein clearances, histology) were analyzed in 170 consecutive adult recipients, who were followed prospectively on the basis of repeat annual work-up [14].
• Unbound sulfobromophthalein concentration was estimated according to a three binding site model [15].

Anatomical context of Sulfobromophthalein

• In previous studies, we purified a 55,000-mol wt organic anion-binding protein (OABP) by affinity chromatography on sulfobromophthalein (BSP)-Sepharose of deoxycholate solubilized liver cell plasma membrane preparations [16].
• Naltrexone injected in a cerebral ventricle also reversed analgesia and sulfobromophthalein elevation but not intestinal slowing [17].
• After spinal cord transection, intravenous morphine did not retard the tail-flick response or affect sulfobromophthalein disposition, but peripherally mediated intestinal transit was slowed as it was in intact mice [17].
• Unlike liver cytosol, testicular cytosol does not contain protein components that bind bilirubin or sulfobromophthalein with high affinity [18].
• The MTX influx properties of the transfectant cell line were identical to those of the well characterized reduced folate carrier from parental L1210 cells in terms of: 1) patterns of sensitivity to competing folates, 2) sensitivity to the organic anion sulfobromophthalein, 3) lack of energy dependence, and 4) capacity for trans-stimulation [19].

Associations of Sulfobromophthalein with other chemical compounds

• Induction of a dose-related increase in sulfobromophthalein uptake velocity in freshly isolated rat hepatocytes by phenobarbital [2].
• This was accompanied by an inhibition of hepatocellular uptake of taurocholate by 16.8% +/- 1.8% and of sulfobromophthalein (BSP) by 32.9% +/- 3.0% compared with controls [20].
• These studies showed that cultured rat hepatocytes transported bilirubin with kinetics virtually identical to the transport of sulfobromophthalein [21].
• In contrast, ATP-dependent DNP-SG uptake was unaffected by GSH, GSH ester, S-methyl glutathione, or S-carbamidomethyl glutathione, but was strongly inhibited by sulfobromophthalein, DIDS, and by high molecular weight and relatively hydrophobic glutathione S-conjugates [22].
• Organic anions transported by human OATP8 included sulfobromophthalein, with a K(m) of 3.3 microm, and 17beta-glucuronosyl estradiol, with a K(m) of 5.4 microm [23].

Gene context of Sulfobromophthalein

• Our results indicate that OATP2 is important for the uptake of organic anions, including bilirubin conjugates and sulfobromophthalein, in human liver [24].
• The selective ABC1 inhibitors 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid and sulfobromophthalein mimicked the suppressive effect of glibenclamide on IL-12 p40 production [25].
• Induction of ornithine decarboxylase and S-adenosylmethionine decarboxylase by sulfobromophthalein in rats [26].
• OAT4 interacted with chemically heterogeneous anionic compounds, such as nonsteroidal anti-inflammatory drugs, diuretics, sulfobromophthalein, penicillin G, and bile salts, whereas tetraethylammonium, an organic cation, did not [27].
• Probenecid and sulfobromophthalein inhibit methotrexate influx in both L1210 and MTXrA-TF1 cell lines; however, inhibition in MTXrA-TF1 could be accounted for on the basis of inhibition of methotrexate binding to FR-alpha [28].

Analytical, diagnostic and therapeutic context of Sulfobromophthalein

• The biliary transport maximum for sulfobromophthalein, on the other hand, decreased by almost 70% from 153 to 52 nmoles per min per min per 100 g after portacaval anastomosis [9].
• An intravenous dose of naloxone that reversed morphine analgesia also prevented sulfobromophthalein elevation but did not prevent gut slowing [17].
• The initial uptake rate of sulfobromophthalein was determined at sulfobromophthalein concentrations of 1 to 50 mumol/L with a rapid filtration technique [2].
• The plasma disappearance rate of sulfobromophthalein (VBSP; mumol/kg/min) was measured in 15 Gilbert's syndrome patients and 12 control subjects after intravenous injection of two different doses (0.59 and 5.90 mumol/kg) of the dye [29].
• A simultaneous intravenous infusion of sulfobromophthalein (BSP) (0.3 mg.min-1.100 g-1) and ursodeoxycholate (UDC) or tauroursodeoxycholate (TUDC) (1.2 mumol.min-1.100 g-1) caused a significantly higher excretion rate of BSP than in the control value without bile salt infusion [30].

References