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ISSN: 2392-1099
Clinical and Experimental Hepatology
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3/2022
vol. 8
 
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abstract:
Original paper

Cellular and mitochondrial taurine depletion in bile duct ligated rats: a justification for taurine supplementation in cholestasis/cirrhosis

Asma Najibi
1
,
Heresh Rezaei
2
,
Ram Kumar Manthari
3
,
Hossein Niknahad
1, 2
,
Akram Jamshidzadeh
1, 2
,
Omid Farshad
1
,
Feng Yan
4
,
Yanqin Ma
4
,
Dongmei Xu
4
,
Zhongwei Tang
4
,
Mohammad Mehdi Ommati
5
,
Reza Heidari
1

1.
Pharmaceutical Sciences Research Center, Shiraz University of Medical Sciences, Shiraz, Iran
2.
Department of Pharmacology and Toxicology, School of Pharmacy, Shiraz University of Medical Sciences, Shiraz, Iran
3.
Department of Biotechnology, GITAM Institute of Science, Gandhi Institute of Technology and Management, Visakhapatnam, Andhra Pradesh, India
4.
Department of Life Sciences, Shanxi Agricultural University, Shanxi, Taigu, China
5.
College of Veterinary Medicine, Shanxi Agricultural University, Jinzhong, China
Clin Exp HEPATOL 2022; 8, 3: 195-210
DOI: https://doi.org/10.5114/ceh.2022.119216
Online publish date: 2022/09/21
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Taurine (TAU) is a free amino acid abundant in the human body. Various physiological roles have been attributed to TAU. At the subcellular level, mitochondria are the primary targets for TAU function. Meanwhile, it has been found that TAU depletion is associated with severe pathologies. Cholestasis is a severe clinical complication that can progress to liver fibrosis, cirrhosis, and hepatic failure. Bile duct ligation (BDL) is a reliable model for assessing cholestasis/cirrhosis and related complications. The current study was designed to investigate the effects of cholestasis/cirrhosis on tissue and mitochondrial TAU reservoirs. Cholestatic rats were monitored (14 and 42 days after BDL surgery), and TAU levels were assessed in various tissues and isolated mitochondria. There was a significant decrease in TAU in the brain, heart, liver, kidney, skeletal muscle, intestine, lung, testis, and ovary of the BDL animals (14 and 42 days after surgery). Mitochondrial levels of TAU were also significantly depleted in BDL animals. Tissue and mitochondrial TAU levels in cirrhotic animals (42 days after the BDL operation) were substantially lower than those in the cholestatic rats (14 days after BDL surgery). These data indicate an essential role for tissue and mitochondrial TAU in preventing organ injury induced by cholestasis/cirrhosis and could justify TAU supplementation for therapeutic purposes.
keywords:

amino acid, bile acids, cirrhosis, mitochondrial impairment, oxidative stress
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