Elsevier

Biochemical Pharmacology

Volume 33, Issue 16, 15 August 1984, Pages 2599-2604
Biochemical Pharmacology

Effects of adenosine on liver cell damage induced by carbon tetrachloride

https://doi.org/10.1016/0006-2952(84)90631-2Get rights and content

Abstract

Adenosine administration delayed the fatty liver and cell necrosis induced by carbon tetrachloride without affecting the action of the hepatotoxin on protein synthesis and liver triacylglycerol release. Adenosine produced a drastic antilipolytic effect accompanied by a decrease in the incorporation of [1-14C]palmitic acid into triacylglycerols and free fatty acids of the liver. Furthermore, a decrease in the serum levels of ketone bodies was observed at early times. The nucleoside also avoided the release of intracellular enzymes and prevented the lipid peroxidation produced by carbon tetrachloride during the 4 hr of treatment. The protective action of adenosine was transient, lasting 3–4 hr, probably the time required to be metabolized. The results suggest that the antilipolytic effect of the nucleoside, the inhibition of hepatic fatty acid metabolism, and the decrease in carbon tetrachloride-induced lipoperoxidation that it produced are involved in the delayed acute hepatotoxicity induced by carbon tetrachloride.

References (43)

  • R. Hernández-Muñoz et al.

    Archs Biochem. Biophys.

    (1978)
  • J.A. García-Sáinz et al.

    Biochem. Pharmac.

    (1980)
  • J.A. García-Sáinz et al.

    Biochem. Pharmac.

    (1979)
  • W.M. Butler et al.

    J. Lipid. Res.

    (1961)
  • M. Novak

    J. Lipid Res.

    (1965)
  • V.P. Dole et al.

    J. biol. Chem.

    (1960)
  • D.H. Williamson et al.
  • J. Folch et al.

    J. biol. Chem.

    (1957)
  • J.A. García-Sáinz et al.

    Biochem. Pharmac.

    (1975)
  • J. Brown et al.

    J. Lipid Res.

    (1962)
  • B.N. Ames et al.

    J. biol. Chem.

    (1960)
  • E. Schmidt
  • A. Ottolenghi

    Archs Biochem. Biophys.

    (1959)
  • Y. Masuda et al.

    Biochem. Pharmac.

    (1978)
  • T.J. Player et al.

    Biochem. biophys. Res. Commun.

    (1977)
  • E.J. Jacobs

    J. biol. Chem.

    (1956)
  • V.P. Dole

    J. biol. Chem.

    (1961)
  • M. Poggi et al.

    Biochem. Pharmac.

    (1964)
  • M. Eliakim
  • B.D. Dinman et al.

    Archs. environ. Hlth

    (1963)
  • S.Z. Cagen et al.
  • Cited by (34)

    • Involvement of cell oxidant status and redox state in the increased non-enzymatic ethanol oxidation by the regenerating rat liver

      2019, Biochemical Pharmacology
      Citation Excerpt :

      In the same acid extracts, neutralized with 4 mol • L−1 K2CO3, the redox-pair metabolites: lactate, pyruvate, α-glycerophosphate, dihydroxyacetone phosphate, β-hydroxybutyrate, and acetoacetate, were enzymatically determined, as described before [29,30]. The amount of aldehydic products generated by lipid peroxidation was quantified in the cytosolic fraction through the technique using the thiobarbituric acid reaction (TBARS), as previously modified [31]. Cytoplasmic and mitochondrial NAD/NADH ratios were calculated as follows: NAD/NADH = [oxidized substrate]/[reduced substrate] × 1/Keq, taking into account equilibrium constants for lactate, α-glycerophosphate, and β-hydroxybutyrate dehydrogenases [32].

    • An Adenosine Derivative Compound as a Hepatoprotective Agent

      2017, Liver Pathophysiology: Therapies and Antioxidants
    • Neuroprotective effect of thalidomide on MPTP-induced toxicity

      2015, NeuroToxicology
      Citation Excerpt :

      MAO activity was expressed as μmol of 4-HOQ formed/1 h incubation per g of tissue wet weight. The amount of aldehydic products generated by lipoperoxidation was determined by the thiobarbituric acid reactive substances (TBARS) (Buege and Aust, 1978) in 10 brain ST and SN per group, modified as previously reported (Hernandez-Munoz et al., 1984). Briefly, homogenate preparation for the MAO-B determination, was taken 1 mg of protein per sample, was diluted in Tris–HCl (150 mM, pH 7.4) buffer.

    • α-Tocopherol administration blocks adaptive changes in cell NADH/NAD<sup>+</sup> redox state and mitochondrial function leading to inhibition of gastric mucosa cell proliferation in rats

      2013, Free Radical Biology and Medicine
      Citation Excerpt :

      In isolated mitochondria from our experimental groups, the following enzymatic activities were measured: cytochrome c oxidase (Cox; EC 1.9.3.1) was determined by the method described by Rafael [22] and succinate dehydrogenase (SDH; EC 1.2.1.16) according to the technique of King [23]. The activity of two mitochondrial matrix enzymes, malate dehydrogenase (MDH; EC 1.1.1.37) and isocitrate dehydrogenase (IDH; EC 1.1.1.42), was assessed by methods reported elsewhere [24,25]. Mitochondrial levels of ROS were estimated through the method described by Viarengo et al. [26], using the fluorescence signal generated by ROS reacting with 2′,7′-dichlorodihydrofluorescein diacetate (Molecular Probes).

    • Prevention of in vitro hepatic stellate cells activation by the adenosine derivative compound IFC305

      2010, Biochemical Pharmacology
      Citation Excerpt :

      We have determined that adenosine reverses experimental cirrhosis by enhancing liver collagenolytic activity, stimulating hepatocyte proliferative capacities, as well as accelerating normalization of parameters indicative of liver function and reducing levels of oxidative stress. Adenosine's beneficial effects have been associated with a cell redox state modulation, maintenance of liver energy availability, and an adequate mitochondrial function of hepatic cells [8–13]. Recently, we synthesized the aspartate salt of adenosine IFC305, which has a longer half-life in the liver and its beneficial effects on CCl4-induced cirrhosis in rats are achieved with a lower dose [14].

    • Food restricted schedules promote differential lipoperoxidative activity in rat hepatic subcellular fractions

      2007, Comparative Biochemistry and Physiology - A Molecular and Integrative Physiology
    View all citing articles on Scopus
    View full text