Therapeutic Effect of Taurine Administration on Carbon Tetrachlor1de-Induced Hepatic Injury

Nakashima, Tomoki; TANIKO, Tatsuro; Kuriyama, Kinya

doi:10.1016/s0021-5198(19)52635-x

Cited by 9 publications

(3 citation statements)

References 14 publications

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“…In addition, the remarkable decreases of hepatic CSAD, CDO expressions and taurine level are closely related to the progression of hepatopathy, including the increased serum ALT, AST, ALP levels and hepatic α-SMA expression, which are in accordance with the reported studies. 29,35,36 Therefore, the inhibiting effects of CCl 4 on CDO, CSAD expressions and taurine synthesis are important mechanism causing liver injury and occurrence of liver fibrosis. This is supported by the results of the present study that taurine supplement reduced the loss of hepatic taurine concentration concomitant with reduced liver injury observed both histologically and biochemically, although the rescuing effects of the taurine supplement on CSAD, CDO expressions were not detected in this study.…”

Section: Discussionmentioning

confidence: 99%

CCl₄ inhibits the expressions of hepatic taurine biosynthetic enzymes and taurine synthesis in the progression of mouse liver fibrosis

et al. 2022

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Carbon tetrachloride (CCl4) is a widely used hepatotoxin for the studies of liver fibrosis and cirrhosis, and taurine has function to abate liver fibrosis induced by CCl4. But the interacting mechanisms between taurine and CCl4 in liver are still largely unknown. These made us to hypothesize that CCl4 may induce liver fibrosis by affecting the expressions of taurine biosynthetic enzymes and taurine synthesis. We thus assayed the expressions of hepatic cysteine dioxygenase (CDO), cysteine sulfonate acid decarboxylase (CSAD) and taurine transporter (TauT) in the progression of mouse liver fibrosis induced by CCl4. The results demonstrated that CCl4 treatment markedly decreased hepatic CSAD, CDO expressions, and taurine levels in hepatic tissue, although TauT expression did not exhibit significant decline. It was contrasting that hepatic α-SMA, serum AST, ALT, ALP kept increasing, which were accompanied by the pathological characters of liver, whereas taurine supplement attenuated the progression of liver fibrosis induced by CCl4. These results demonstrate that CCl4 may induce liver fibrosis by inhibiting hepatic CSAD and CDO expressions and taurine synthesis, which are crucial for our understanding the mechanisms of liver fibrosis induced by CCl4, and also potential for establishing therapeutic strategies of liver fibrosis and related diseases.

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Section: Discussionmentioning

confidence: 99%

CCl₄ inhibits the expressions of hepatic taurine biosynthetic enzymes and taurine synthesis in the progression of mouse liver fibrosis

et al. 2022

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“…In 1982, it was suggested that hepatic Tau could play a protective role in hepatocytes against hepatotoxicants such as CCl 4 , and that dietary Tau may be a useful treatment in hepatotoxin-induced liver injury [ 228 ]. However, subsequently, in a paper from the same department, it was shown that pre-treatment with Tau facilitated hepatic lipid peroxide formation associated with CCl 4 intoxication in rats [ 229 ].…”

Section: Antioxidant Properties Of Taumentioning

confidence: 99%

Taurine as a Natural Antioxidant: From Direct Antioxidant Effects to Protective Action in Various Toxicological Models

2021

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Natural antioxidants have received tremendous attention over the last 3 decades. At the same time, the attitude to free radicals is slowly changing, and their signalling role in adaptation to stress has recently received a lot of attention. Among many different antioxidants in the body, taurine (Tau), a sulphur-containing non-proteinogenic β-amino acid, is shown to have a special place as an important natural modulator of the antioxidant defence networks. Indeed, Tau is synthesised in most mammals and birds, and the Tau requirement is met by both synthesis and food/feed supply. From the analysis of recent data, it could be concluded that the direct antioxidant effect of Tau due to scavenging free radicals is limited and could be expected only in a few mammalian/avian tissues (e.g., heart and eye) with comparatively high (>15–20 mM) Tau concentrations. The stabilising effects of Tau on mitochondria, a prime site of free radical formation, are characterised and deserve more attention. Tau deficiency has been shown to compromise the electron transport chain in mitochondria and significantly increase free radical production. It seems likely that by maintaining the optimal Tau status of mitochondria, it is possible to control free radical production. Tau’s antioxidant protective action is of great importance in various stress conditions in human life, and is related to commercial animal and poultry production. In various in vitro and in vivo toxicological models, Tau showed AO protective effects. The membrane-stabilizing effects, inhibiting effects on ROS-producing enzymes, as well as the indirect AO effects of Tau via redox balance maintenance associated with the modulation of various transcription factors (e.g., Nrf2 and NF-κB) and vitagenes could also contribute to its protective action in stress conditions, and thus deserve more attention.

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“…Taurine has many important and beneficial effects on the human body, It has been implicated in many physiological functions, pharmacological actions, and pathological conditions. Among the physiological roles attributed to taurine are membrane stabilisation (23), antioxidation (24), osmoregulaion, neuromodulation (25), detoxification (26), and regulation of calcium homeostasis (27). Clinically, taurine has been used in the protection and also in treatment of a wide Effect of taurine in treatment of IDA variety of conditions, including cardiomyopathy, hepatic disorders, cystic fibrosis (28), alcoholism, growth retardation, retinal degeneration (29), and diabetes mellitus (30).…”

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Possible ameliorative effect of taurine in the treatment of iron‐deficiency anaemia in female university students of Gaza, Palestine

Sirdah

El-Agouza

Shahla

2002

European J of Haematology

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The aim of the study was to evaluate the haematological effects of adding the antioxidant taurine to iron sulfate in the treatment of iron-deficiency anaemia (IDA). A sample of 730 students from Al-Azhar University, Gaza, in Palestine underwent screening with complete blood counts and serum samples. In subjects with microcytosis/hypochromasia, Alpha2 delta2 (HbA2) and serum concentrations of iron, total iron binding capacity (TIBC), ferritin and taurine were determined. Samples from 17 normocytic, normochromic, and non-anaemic subjects were used as baseline controls. At base-line, 81 of the 730 subjects (11.1%) had microcytosis/hypochromasia, 26 (3.6%) were diagnosed as beta-thalassemia carriers, none of which was iron deficient. Four subjects had microcytosis of unknown cause. Fifty-one subjects (all females) had iron-deficiency anaemia and were included in the therapeutic study, which lasted for 20 wk. They were matched for Hb into pairs and were treated with oral iron (325 mg of slow-release iron sulfate). In addition, they were, in a double-blind procedure, randomised to additional oral taurine (1000 mg d(-1) at a cost comparable to that of adding ascorbic acid) or placebo. Mean S-taurine was significantly lower in the IDA subjects than in the controls. After 20 wk of iron supplementation, both the taurine and placebo group significantly improved their Hb concentrations and normalised the markers of iron deficiency. Apart from the expected, albeit in this study mild side-effects of oral iron, no significant side-effects were noted. In the taurine group, there was a statistically significant additive positive change from the baseline values on Hb (2.67 +/- 1.24 g dL(-1)), red blood cell (RBC) count [(0.57 +/- 0.25) x 1012 L(-1)] and serum ferritin (30.33 +/- 17.99 microg L(-1)) as compared to placebo group values, which were 1.80 +/- 1.10 g dL-1, (0.39 +/- 0.36) x 1012 L(-1), and 20.11 +/- 7.34 microg L(-1), respectively. Oral taurine appears to increase the effectiveness of oral iron in the treatment of IDA, and has no significant side-effects. This merits further cost-benefit and clinical analyses.

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Therapeutic Effect of Taurine Administration on Carbon Tetrachlor1de-Induced Hepatic Injury

Cited by 9 publications

References 14 publications

CCl₄ inhibits the expressions of hepatic taurine biosynthetic enzymes and taurine synthesis in the progression of mouse liver fibrosis

CCl₄ inhibits the expressions of hepatic taurine biosynthetic enzymes and taurine synthesis in the progression of mouse liver fibrosis

Taurine as a Natural Antioxidant: From Direct Antioxidant Effects to Protective Action in Various Toxicological Models

Possible ameliorative effect of taurine in the treatment of iron‐deficiency anaemia in female university students of Gaza, Palestine

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Therapeutic Effect of Taurine Administration on Carbon Tetrachlor1de-Induced Hepatic Injury

Cited by 9 publications

References 14 publications

CCl4 inhibits the expressions of hepatic taurine biosynthetic enzymes and taurine synthesis in the progression of mouse liver fibrosis

CCl4 inhibits the expressions of hepatic taurine biosynthetic enzymes and taurine synthesis in the progression of mouse liver fibrosis

Taurine as a Natural Antioxidant: From Direct Antioxidant Effects to Protective Action in Various Toxicological Models

Possible ameliorative effect of taurine in the treatment of iron‐deficiency anaemia in female university students of Gaza, Palestine

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CCl₄ inhibits the expressions of hepatic taurine biosynthetic enzymes and taurine synthesis in the progression of mouse liver fibrosis

CCl₄ inhibits the expressions of hepatic taurine biosynthetic enzymes and taurine synthesis in the progression of mouse liver fibrosis