Heme catabolism in fish. Bile pigments in gallbladder bile of the electric torpedo, Torpedo californicus

McDonagh, Antony F.; Palma, Lucita A.

doi:10.1016/0305-0491(82)90066-9

Cited by 6 publications

(6 citation statements)

References 17 publications

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“…Cornelius (1991) verified that the concentration of biliverdin and conjugated bilirubin increases with time and fasting. Grossbard and collaborators (1987) found that Raja erinacea excreted approximately equal amounts of bilirubin and biliverdin and McDonagh and Palma (1982) found that biliverdin (unconjugated) was the predominant pigment in the gallbladder of Torpedo californicus . This does not support Qin's hypothesis that the feeding habits of carnivorous fish would result in the development of a higher bilirubin liver secretion than biliverdin, a pigment essentially associated with herbivorous diets (Qin, 2007).…”

Section: Discussionmentioning

confidence: 99%

The Gallbladder of the Electric Ray Torpedo Marmorata Risso Displays Excrescent Cholecystocytes with Merocrine and Apocrine‐Like Secretions

Gilloteaux

Ott

Oldham-Ott

2012

The Anatomical Record

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The gallbladder of Torpedo marmorata exhibits a mucosal surface layer of simple columnar epithelium with very tall cholecystocytes. The apical domain of each cell has few microvilli, but many mucous vesicles that are secreted by exocytosis at the cell apices. The apical regions may also elongate and undergo self-excision while shedding mucus and cell debris into the gallbladder lumen in a manner similar to that described in mammals as a result of sex steroid treatment to induce gallstones and to that found in the cholecystitis associated with cholelithiasis. Numerous small mitochondria, spherical to elongated, are distributed throughout the cells, while the nuclei are often located in the lower third of each cell. In the lower part of the cholecystocytes, large and very densely contrasted lysosomes can be found. All cells are tightly joined by junctional complexes, including long, highly contrasted desmosomes. The fibromuscular layer is made of a loose stroma with a limited muscular component and a poor blood supply. Large diameter blood vessels can only be found in the subserosal layer. It is hypothesized that the obligatorily carnivorous diet of this ureotelic fish has resulted in the evolution of a gallbladder ultrastructure resembling that found in cholecystitis but without the associated cholelithiasis. Anat Rec,

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Section: Discussionmentioning

confidence: 99%

The Gallbladder of the Electric Ray Torpedo Marmorata Risso Displays Excrescent Cholecystocytes with Merocrine and Apocrine‐Like Secretions

Gilloteaux

Ott

Oldham-Ott

2012

The Anatomical Record

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“…Abbreviations used in this paper: BDG, bilirubin #-I-O-acyl diglucuronide; BMG, bilirubin, -1-O-acyl monoglucuronides; HPLC, high-diazo method (14) and by high-performance liquid chromatography (HPLC) (12).…”

Section: Methodsmentioning

confidence: 99%

“…Received for publication 28 December 1983 and in revised form 14 May 1984. free or reversibly associated with albumin. Measurement of these in body fluids is useful clinically, particularly in the detection and diagnosis of hepatobiliary disease (1).…”

Section: Introductionmentioning

confidence: 99%

Origin of mammalian biliprotein and rearrangement of bilirubin glucuronides in vivo in the rat.

McDonagh¹,

Palma²,

Lauff³

et al. 1984

J. Clin. Invest.

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Abstract. In hepatobiliary disease bilirubin becomes bound covalently to serum albumin, producing a nondissociable bile pigment-protein complex (biliprotein). To elucidate the mechanism of biliprotein formation we studied the bile pigment composition of blood from animals with experimental cholestasis and carried out comparative studies on the rate of biliprotein formation in vivo and in vitro during incubation of bilirubin glucuronides with albumin. Bile duct ligation in the rat and guinea pig led to rapid accumulation in the circulation of bilirubin, heterogeneous bilirubin esters of glucuronic acid, and a biliprotein that migrated along with albumin on high performance liquid chromatography. When the obstruction was removed, biliprotein remained longer in the circulation than did the other bile pigment species. Biliprotein and heterogeneous bilirubin esters of glucuronic acid were not formed in bile duct-ligated homozygous Gunn rats but they were formed when bilirubin glucuronides were incubated with Sprague-Dawley rat serum or human serum albumin at 370C in vitro. Bilirubin glucuronide rearrangement in vitro was accompanied by nonenzymic hydrolysis. We conclude that the formation of biliprotein in vivo is probably nonenzymic and suggest that mammalian biliprotein is formed by acyl migration of bilirubin from a bilirubin-glucuronic acid ester to a nucleophilic site on albumin.

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“…The resultant bilirubin monoand diglucuronides are actively secreted across the canalicular membrane of the hepatocyte into the bile by MRP2. In some nonmammalian vertebrates (e.g., birds, reptiles, amphibians), heme degradation terminates at the heme oxygenase step, 1 with the biliverdin end product efficiently eliminated in the bile and urine. 2,3 The evolutionary development of the energetically costly process of bilirubin production and elimination suggests that this bile pigment may serve an important physiologic function.…”

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confidence: 99%

Unconjugated bilirubin induces apoptosis in colon cancer cells by triggering mitochondrial depolarization

Keshavan¹,

Schwemberger²,

Smith³

et al. 2004

Intl Journal of Cancer

112

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Bilirubin is the principal end product of heme degradation. Prompted by epidemiologic analyses demonstrating an inverse correlation between serum bilirubin levels and cancer mortality, we examined the effect(s) of bilirubin on the growth and survival of colon adenocarcinoma cells. Adenocarcinoma cell monolayers were treated with bilirubin over a range of bilirubin:BSA molar ratios (0 -0.6), and viability was assessed colorimetrically. Apoptosis was characterized by TUNEL assay, annexin V staining and caspase-3 activation. The mechanism(s) by which bilirubin induces apoptosis was investigated by Western blotting for cytochrome c release, assaying for caspase-8 and caspase-9 activation and for mitochondrial depolarization by JC-1 staining. The direct effect of bilirubin on the membrane potential of isolated mitochondria was evaluated using light-scattering and fluorescence techniques. Bilirubin decreased the viability of all colon cancer cell lines tested in a dose-dependent manner. Cells exhibited substantial apoptosis when exposed to bilirubin concentrations ranging 0 -50 M, as demonstrated by an 8-to 10-fold increase in TUNEL and annexin V staining and in caspase-3 activity. Bilirubin treatment evokes specific activation of caspase-9, enhances cytochrome c release into the cytoplasm and triggers the mitochondrial permeability transition in colon cancer monolayers. Additionally, bilirubin directly induces the depolarization of isolated rat liver mitochondria, an effect that is not inhibited by cyclosporin A. Bilirubin stimulates apoptosis of colon adenocarcinoma cells in vitro through activation of the mitochondrial pathway, apparently by directly dissipating mitochondrial membrane potential. As this effect is triggered at concentrations normally present in the intestinal lumen, we postulate a physiologic role for bilirubin in modulating colon tumorigenesis.

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Heme catabolism in fish. Bile pigments in gallbladder bile of the electric torpedo, Torpedo californicus

Cited by 6 publications

References 17 publications

The Gallbladder of the Electric Ray Torpedo Marmorata Risso Displays Excrescent Cholecystocytes with Merocrine and Apocrine‐Like Secretions

The Gallbladder of the Electric Ray Torpedo Marmorata Risso Displays Excrescent Cholecystocytes with Merocrine and Apocrine‐Like Secretions

Origin of mammalian biliprotein and rearrangement of bilirubin glucuronides in vivo in the rat.

Unconjugated bilirubin induces apoptosis in colon cancer cells by triggering mitochondrial depolarization

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