1. Academic Validation
  2. Therapeutic properties of dihydroxy-dibutylether on sub-acute liver damage induced by several hepatotoxic agents in rats

Therapeutic properties of dihydroxy-dibutylether on sub-acute liver damage induced by several hepatotoxic agents in rats

  • Int J Tissue React. 1982;4(4):309-18.
G B Fregnan L Frigerio R Porta M Prada F Ruggieri
PMID: 7169302
Abstract

The data presently reported show that repeated exposure of rats to allyl alcohol, ethionine or alpha-naphthyl isothiocyanate (ANIT) impaired some plasmatic parameters mainly by means of different mechanisms which involve the liver function. In particular, four administrations of allyl alcohol, given every other day, increased glutamate oxaloacetate transaminase (GOT) for at least 48 hours from the last dose; ethionine reduced the bromsulphthalein (BSP) clearance even after 48 hours from the 1st, 2nd, or 3rd administration given on the 1st, 5th, or 12th day; ANIT, administered daily for seven days, increased glutamate pyruvate transaminase (GPT), Alkaline Phosphatase (AP), bilirubin, triglycerides (TG) and Cholesterol (CH) while it decreased the body-weight and retarded growth for at least six to seven days after intoxication. Twice daily administrations of dihydroxy-dibutylether (DHBE), a strong choleretic agent, brought to normality the parameters impaired by the three hepatointoxicating agents even when the intoxication was already established. In fact, DHBE reduced the plasma GOT levels increased by allyl alcohol, improved the BSP clearance impaired by ethionine and tended to normalize the parameters modified by ANIT by lowering GPT, AP, CH, TG and bilirubin plasma levels and by enhancing body growth. The curative activity of DHBE does not seem to be related only to a membrane stabilizing action since silymarin, a known cell membrane stabilizer, does not significantly influence the parameters described above in all the experimental conditions. Even the choleretic activity of DHBE alone might not be sufficient to explain its hepatoprotective action since fenipentol (a known choleretic agent) is inactive at least after ANIT intoxication.

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