scholarly journals Hepatic expression of sodium-dependent vitamin C transporters: ontogeny, subtissular distribution and effect of chronic liver diseases

2011 ◽  
Vol 106 (12) ◽  
pp. 1814-1825 ◽  
Author(s):  
Rocio I. R. Macias ◽  
Carlos Hierro ◽  
Susana Cuesta de Juan ◽  
Felipe Jimenez ◽  
Francisco Gonzalez-San Martin ◽  
...  

Ascorbic acid uptake is a key step in determining the overall bioactivity of this vitamin. Expression of Na-dependent vitamin C transporters (SVCT; SLC23A1 and SLC23A2) during long-term oxidative stress occurring in several chronic liver diseases may determine the antioxidant defence in this organ. In patients with hepatocellular cholestasis, primary biliary cirrhosis, haemochromatosis and non-alcoholic steatohepatitis, using real-time RT-PCR, an enhanced hepatic expression of both SLC23A1 and SLC23A2, but not other organic anions transporters, such as OATP1A2, OATP1B1 and OATP1B3, was found. To further investigate these findings, we used secondary biliary cirrhosis induced in rats by long-term biliary obstruction as a model of chronic liver disease accompanied by oxidative stress because of bile acid accumulation. In control rat liver, expression of Slc23a1 was low at birth, increased progressively up to adulthood and decreased in senescence, whereas expression of Slc23a2 did not change significantly after birth. In 8-week-old rats, immunohistochemistry and confocal microscopy studies revealed the expression in hepatocytes and bile duct cells of mainly Slc23a1, whereas both Slc23a1 and Slc23a2 were expressed in endothelial, stellate and Kupffer cells. In adult rats, when obstructive cholestasis was maintained for 8 weeks, a significant up-regulation of Slc23a2 accompanied by a down-regulation of Slc23a1 was found. In sum, there is a selective cell-type distribution of SVCT in the liver tissue, which, in addition to differential control in the expression of both isoforms, may play a role in the ability of different liver cell types to take up vitamin C under physiological and pathological conditions.

Author(s):  
Devaraj Ezhilarasan ◽  
Shanmugam Rajeshkumar ◽  
Thangavelu Lakshmi

1983 ◽  
Vol 33 (6) ◽  
pp. 1095-1104
Author(s):  
Yasuni Nakanuma ◽  
Goroku Ohta ◽  
Haruo Takeshita ◽  
Yoshikiyo Yamazaki ◽  
Kenji Doishita ◽  
...  

2002 ◽  
Vol 34 ◽  
pp. A137
Author(s):  
F. Terraciano ◽  
A. Federico ◽  
T. De Simone ◽  
C. Tuccillo ◽  
E. Finamore ◽  
...  

2001 ◽  
Vol 21 (5) ◽  
pp. 295-299 ◽  
Author(s):  
Yoshio Sumida ◽  
Toshiaki Nakashima ◽  
Takaharu Yoh ◽  
Yuko Kakisaka ◽  
Yoshiki Nakajima ◽  
...  

Author(s):  
Sangale Mukta

Abstract: Ursodeoxycholic acid is a dihy- droxy bile acid with a rapidly expanding spectrum of usage in acute and chronic liver diseases. The various mechanisms of action of this hydrophilic bile acid include direct cytoprotection, detergent action on dysfunctional microtubules, immunomodulation and induction of hypercholer- esis. Its efficacy in primary biliary cirrhosis and primary sclerosing cholangitis as an adjunct to medical therapy has been well established.Ursodeoxycholic acid prolongs survival in primary biliary cirrhosis and it improves biochemical parameters of cholestasis in various other cholestatic disorders including primary sclerosing cholangitis, intrahepatic cholestasis of pregnancy, cystic fibrosis and total parenteral nutritioninduced cholestasis. However, a positive effect on survival remains to be established in these diseases. Ursodeoxycholic acid is of unproven efficacy in non- cholestatic disorders such as acute rejection after liver transplantation, non-alcoholic steatohepatitis, alcoholic liver disease and chronic viral hepatitis. This review outlines the present knowledge of the Pharmacology of ursodeoxycholic acid, and presents data from clinical trials on its use in chronic liver diseases. Keywords: Liver cirrhosis, Urisodeoxycholic acid


1979 ◽  
Vol 76 (6) ◽  
pp. 1333-1340 ◽  
Author(s):  
Ian G. McFarlane ◽  
Barbara M. Wojcicka ◽  
Demetrios C. Tsantoulas ◽  
Bernard C. Portmann ◽  
Adrian L.W.F. Eddleston ◽  
...  

Nutrients ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 1576 ◽  
Author(s):  
Daisuke Uchida ◽  
Akinobu Takaki ◽  
Atsushi Oyama ◽  
Takuya Adachi ◽  
Nozomu Wada ◽  
...  

Chronic viral hepatitis B and C and non-alcoholic fatty liver disease (NAFLD) have been widely acknowledged to be the leading causes of liver cirrhosis and hepatocellular carcinoma. As anti-viral treatment progresses, the impact of NAFLD is increasing. NAFLD can coexist with chronic viral hepatitis and exacerbate its progression. Oxidative stress has been recognized as a chronic liver disease progression-related and cancer-initiating stress response. However, there are still many unresolved issues concerning oxidative stress, such as the correlation between the natural history of the disease and promising treatment protocols. Recent findings indicate that oxidative stress is also an anti-cancer response that is necessary to kill cancer cells. Oxidative stress might therefore be a cancer-initiating response that should be down regulated in the pre-cancerous stage in patients with risk factors for cancer, while it is an anti-cancer cell response that should not be down regulated in the post-cancerous stage, especially in patients using anti-cancer agents. Antioxidant nutrients should be administered carefully according to the patients’ disease status. In this review, we will highlight these paradoxical effects of oxidative stress in chronic liver diseases, pre- and post-carcinogenesis.


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