Bile salt transport after selective damage to acinar zone 3 hepatocytes by bromobenzene in the rat

Gumucio, Jorge J.; Katz, Michael E.; Miller, Deborah L.; Balabaud, Charles; Greenfield, Jeremy M.; Wagner, Renate M.

doi:10.1016/0041-008x(79)90494-0

Cited by 24 publications

(8 citation statements)

References 15 publications

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“…The authors concluded that in each zone the hepatocytes are able to take up TCA with ease, but that their recruitment following a TCA load depends on the acinar bile acid distribution. The conclusion confirmed early studies of Gumucio et al (1979) who selectively damaged zone 3 hepatocytes. The effect of zone 3 necrosis by bromobenzene was recently used again to measure the hepatic transport of CA and CDCA in the rat (Dionne et al 1990).…”

Section: Zonal Distribution Of Hepatic Bile Acid Transportsupporting

confidence: 79%

Transport of organic anions in the liver. An update on bile acid, fatty acid, monocarboxylate, anionic amino acid, cholephilic organic anion, and anionic drug transport

Petzinger¹

1994

Reviews of Physiology, Biochemistry and Pharmacology

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Section: Zonal Distribution Of Hepatic Bile Acid Transportsupporting

confidence: 79%

Transport of organic anions in the liver. An update on bile acid, fatty acid, monocarboxylate, anionic amino acid, cholephilic organic anion, and anionic drug transport

Petzinger¹

1994

Reviews of Physiology, Biochemistry and Pharmacology

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“…As previously described, re-absorption of bile salts from the portal circulation to hepatocellular parenchyma is an energy-dependent event that occurs homogeneously among the liver lobules. 37,38 However, when the ''first pass'' effects are taken into accounts, hepatocytes in periportal regions are likely to participate in uptake of the reabsorbed bile salts to greater extents than those of pericentral regions. 37,39 In this context, the current study raised a possibility that loss of functional integrity in periportal hepatocytes, a primary site of oxidant generation, appears to be a critical event that could dictate the severity of biliary dysfunction, and these cells serve as a potentially important target that needs to be treated with antioxidants presumably before the start of reperfusion.…”

Section: Discussionmentioning

confidence: 99%

“…37,38 However, when the ''first pass'' effects are taken into accounts, hepatocytes in periportal regions are likely to participate in uptake of the reabsorbed bile salts to greater extents than those of pericentral regions. 37,39 In this context, the current study raised a possibility that loss of functional integrity in periportal hepatocytes, a primary site of oxidant generation, appears to be a critical event that could dictate the severity of biliary dysfunction, and these cells serve as a potentially important target that needs to be treated with antioxidants presumably before the start of reperfusion. The present study sheds light on a possible importance of development and refinement of preservation methods to control early oxidative changes in hepatocytes as a potential strategem to diminish the risk of suboptimal graft function.…”

Section: Discussionmentioning

confidence: 99%

Kupffer cell-independent acute hepatocellular oxidative stress and decreased bile formation in post-cold-ischemic rat liver

et al. 1999

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The purpose of this study was to examine distribution and time history of oxidative stress during the hyperacute period of reperfusion in the liver grafts undergoing cold ischemia and to investigate roles of Kupffer cells as a potential oxidant source. Rat livers were harvested at 4ЊC in University of Wisconsin solution and followed by reperfusion with Krebs-Henseleit buffer under monitoring bile excretion. To investigate oxidative changes, laser-confocal microfluorography was performed in reperfused livers preloaded with dichlorodihydrofluorescein diacetate succinimidyl ester, a fluorescence precursor sensing intracellular hydroperoxide generation. Livers undergoing the 16-hour cold storage displayed an impaired recovery of bile aciddependent bile output concurrent with a marked increase in hydroperoxide generation in hepatocytes, which occurred as early as 5 minutes after the onset of reperfusion, whereas the status of lobular perfusion was well maintained. Pretreatment with liposome-encapsulated dichloromethylene diphosphonate, a Kupffer cell-depleting reagent, did neither alter the reperfusion-induced periportal oxidative changes nor improve the recovery of bile output in the graft. On the other hand, EPCK, a hepatotropic antioxidant composed of vitamin E phosphate ester bound to vitamin C, not only diminished the oxidative changes but also improved the reduction of bile acid-dependent bile output. Furthermore, the reagent was capable of inhibiting H 2 O 2 -induced oxidative stress in cultured hepatocytes. These results suggest that hepatocytes constitute a major site of the oxidative insult triggered through Kupffer cell-independent mechanisms and serve as an important cellular component to be protected by antioxidant therapeutics.

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“…Some previous methods to isolate hepatocytes originating from different acinar zones relied on the zonespecific damage of liver cells by toxins (10,19) or modifications in zonal specific cell density by application of phenobarbital prior to cell isolation (27,29). Other methods use various centrifugation methods (1,5,7,(23)(24)(25)28) and affinity chromatography with lectins (21) but have revealed preparations of variable purity.…”

mentioning

confidence: 99%

Separation of hepatocytes of different acinar zones by flow cytometry

et al. 1989

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Hepatocytes in the proximal (zone 1) and distal (zone 3) regions of the liver acinus are selectively stained by perfusion of the isolated rat liver with 0.2–20 μM acridine orange (AO). After 10–60 min of anterograde perfusion, AO fluorescence is visible in zone 1 cells, whereas retrograde perfusion stains cells of zone 3. In this paper, we describe a technique to isolate a mixed population of fluorescent and nonfluorescent hepatocytes (cells from all acinar zones, which do not loose the zone specific AO labeling) and to separate these cells according to their zonal origin by fluorescence activated cell sorting. The zonal populations obtained were either fluorescent or non‐fluorescent (purity >95%). Separated cell fractions differed in their enzyme content (5' nucleotidase, succinate‐dehydrogenase, β‐glucuronidase). An unidentified AO metabolite, which is not found in bile after retrograde perfusion (not formed in zone 3 cells), is also absent after retrograde perfusion in sorted fluorescent cells (zone 3 cells), indicating zonal purity of sorted cells.

show abstract

Bile salt transport after selective damage to acinar zone 3 hepatocytes by bromobenzene in the rat

Cited by 24 publications

References 15 publications

Transport of organic anions in the liver. An update on bile acid, fatty acid, monocarboxylate, anionic amino acid, cholephilic organic anion, and anionic drug transport

Transport of organic anions in the liver. An update on bile acid, fatty acid, monocarboxylate, anionic amino acid, cholephilic organic anion, and anionic drug transport

Kupffer cell-independent acute hepatocellular oxidative stress and decreased bile formation in post-cold-ischemic rat liver

Separation of hepatocytes of different acinar zones by flow cytometry

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