Morphologic changes in livers of hamsters treated with high doses of ursodeoxycholic acid: Correlation with bile acids in bile

Mamianetti, A; Konopka, H.; Lago, Noemí; Vescina, Cristina; Scarlato, Eduardo; Carducci, C. N.

doi:10.1016/1043-6618(94)80043-x

Cited by 2 publications

(2 citation statements)

References 33 publications

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“…However, in spite of many scientific studies confirming the similarities between hamsters and human metabolism, the main BA studied are chenodeoxycholic acid (CDCA) and ursodeoxycholic acid (UDCA) due to their therapeutic utilization [24,26,27].…”

Section: Discussionmentioning

confidence: 99%

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Hepatobiliary effects of cholic and lithocholic acids: experimental study in hamsters

et al. 2007

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Etiopathogenesis of biliary atresia remains unknown. Among several theories, one proposes that the disorder may be caused by the toxic effect of monohydroxy bile acids on fetal and neonatal hepatobiliary system. In this paper we evaluated toxic effects produced by ingestion of cholic acid, a trihydroxy bile acid, and lithocholic acid, a monohydroxy bile acid in the hepatobiliary system of a hamster during gestational and perinatal periods. A diet composed by 0.5% cholic acid and 0.25% lithocholic acid was administrated to pregnant hamsters. Liver and bile ducts of the adult and newborn animals were analyzed to point out the changes induced by these acids after birth. Because hamsters and humans have a similar bile metabolism, these animals were eligible for the study. The ingestion of 0.5% lithocholic acid, during hamster's gestation, caused maternal intense ductal/ductular proliferation, inflammatory signs, hepatic cells degeneration and regeneration, hyperplasia of extra hepatic ducts epithelium, and abortion. Both 0.5% cholic acid and 0.25% lithocholic acid ingested by pregnant hamsters, caused ductal/ductular proliferation and hepatobiliary inflammatory damage in a different degree of intensity in adult animals and mild intensity in the young; and also the number of the young was reduced in the litter. We found that the ingestion of these bile acids by hamsters, during gestational period caused different degrees of toxicity on maternal and neonatal hepatobiliary systems. The histopathologic findings observed in biliary atresia patients could not be found in newborn hamsters. New experimental models are needed in the attempt to establish a correlation of these acids with neonatal cholestatic diseases.

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Section: Discussionmentioning

confidence: 99%

“…Even when these BA, CDCA and UDCA were tested, the toxicity produced was assigned to LCA [27,28,29,30]. On the other hand, despite monohydroxy bile acids being responsible as probable agents in the etiopathogenesis of biliary atresia and/or neonatal cholestasis, there are few studies about hepatic morphologic changes provoked by them.…”

Section: Discussionmentioning

confidence: 99%

Hepatobiliary effects of cholic and lithocholic acids: experimental study in hamsters

et al. 2007

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Hepatic bile formation: bile acid transport and water flow into the canalicular conduit

Javitt

2020

American Journal of Physiology-Gastrointestinal and Liver Physi

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Advances in molecular biology that identified the many carrier-mediated organic anion transporters and advances in microscopy that have provided a more detailed anatomy of the canalicular conduit provide for an updating of the concept of osmotically determined canalicular flow. For the most part water flow is not trans-membrane but via specific pore proteins in both the hepatocyte and the tight junction. These pores independently regulate the rate at which water flows in response to and osmotic gradient and therefore are determinants of canalicular bile acid concentration. Review of the literature indicates that the initial effect on hepatic bile flow of cholestatic agents such as Thorazine and estradiol 17b-glucuronide are on water flow and not BSEP- mediated bile acid transport provides new approaches to the pathogenesis of drug-induced liver injury. Attaining a micellar concentration of bile acids in the canaliculus is essential to the formation of cholesterol-lecithin vesicles, which mostly occur in the peri-portal region of the canalicular conduit. The other regions, mid- and peri-central, may transport lesser amounts of bile acid but augment water flow. By broadening the concept of how hepatic bile flow is initiated, a better understanding of the pathogenesis of canalicular cholestasis is obtained.

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Morphologic changes in livers of hamsters treated with high doses of ursodeoxycholic acid: Correlation with bile acids in bile

Cited by 2 publications

References 33 publications

Hepatobiliary effects of cholic and lithocholic acids: experimental study in hamsters

Hepatobiliary effects of cholic and lithocholic acids: experimental study in hamsters

Hepatic bile formation: bile acid transport and water flow into the canalicular conduit

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