Bilirubin sulfate

W5. Watson, C. J., Color reaction of bilirubin with sulfuric acid a direct diazo-reacting bilirubin sulfate. Science 128, 142 (1958). 

Bilirubin is nonpolar and would persist in cells (eg, bound to lipids) if not rendered water-soluble. Hepatocytes convert bilirubin to a polar form, which is readily excreted in the bile, by adding glucuronic acid molecules to it. This process is called conjugation and can employ polar molecules other than glucuronic acid (eg, sulfate). Many steroid hormones and drugs are also... 

Hepatic Effects. A transient increase in serum bilirubin was observed in 3 of 10 workers who were hospitalized after drinking water during one work shift from a water fountain contaminated with nickel sulfate, nickel chloride, and boric acid (Sunderman et al. 1988). The workers who reported symptoms (20 of 35) or were hospitalized (10 of 35) were exposed to an estimated dose of 7.1-35.7 mg nickel/kg. The contribution of boric acid to these effects is not known. 

Bilirubin A false negative may occur when the sample contains ascorbic acid concentrations of 25 mg/dl or more. The yellow/orange-to-red color produced by the presence of indican (indoxyl sulfate) is also problematic. 

Another sinusoidal transporter catalyzes Na+-independent uptake of organic anions and is instrumental for biliary clearance of glucuronidated and sulfated steroids, the diagnostic chemical bromosulfophthalein (BSP) and possibly bilirubin. Canalicular transport of glucuronidate and GSH conjugates is coupled to ATP... 

Figure 28.3. Transport of bile acids and other constituents across the hepatocyte. The Na+ dependent bile salt (taurocholate) transporter (BA-) is shown on the sinusoidal membrane that utihzes the Na+ gradient maintained by the NAK pump, shown here on the lateral aspect of the plasmalemma. Bile salt transcellular transport involves microtubules, which then dehver substrate to the canahcular bile salt transporter (1). Bilary excretion of GSH, gluc-uronate (GluA), and sulfate conjugates of compounds such as 17P-estradiol (E2), bilirubin, and bromosulfothalein (BSP) is catalyzed by the multispecific organic anion transporter (MOAT 2). Both 1 and 2 are members of the ABC family of ATP-dependent transporters that also includes P-glycoprotein (3), another canalicular transporter catalyzing excretion of hpophihc compounds such as the chemotherapeutic drug, daunorubicin.

Levy G, Khanna NN, Soda DM, etal. (1975) Pharmacokinetics of acetaminophen in the human neonate formation of acetaminophen glucuronide and sulfate in relation to plasma bilirubin concentration and D-gJucaric acid excretion. Pediatrics 55 818-825. 

A 3.5-year-old girl was admitted after accidental ingestion of 50-60 tablets of ferrous sulfate 200 mg. She was unresponsive and her serum iron concentration was 138 pmol/l. She required resuscitation and ventilation and an intravenous infusion of deferoxamine was started at a rate of 15 mg/kg/hour, reducing to 5 mg/kg/hour 20 hours later, when the iron concentration was 27 pmol/l. At that time, her liver function deteriorated, with raised alanine transaminase activity (57 IU/1), raised bilirubin (56 pmol/l), and a coagulopathy with an INR of 2.7. She was given an infusion of A-acetylcysteine 12.5 mg/kg/hour and her hepatic function stabilized. After about 40 hours she had acute respiratory deterioration with tachypnea and hypoxemia. A chest X-ray showed widespread bilateral infiltrates. A diagnosis of acute respiratory distress syndrome was made. 

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