Toxicity of barakol: Hepatotoxicity and subacute toxicity

Barakol, an active principle of Cassia siamea (Caesalpiniaceae), exhibits an anxiolytic property. This study was undertaken to evaluate the acute hepatotoxicity and subacute toxicity of barakol in rats. The LD50of barakol after oral administration was 2.33 g/kg. In an acute hepatotoxicity study, sin...

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Main Authors: W. Pumpaisalchai, S. Kaewvichit, T. Taesothikul, K. Sanichwankul, S. Siriaunkgul, W. Niwatananun
Format: Book Series
Published: 2018
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spelling th-cmuir.6653943832-620462018-09-11T09:21:14Z Toxicity of barakol: Hepatotoxicity and subacute toxicity W. Pumpaisalchai S. Kaewvichit T. Taesothikul K. Sanichwankul S. Siriaunkgul W. Niwatananun Agricultural and Biological Sciences Barakol, an active principle of Cassia siamea (Caesalpiniaceae), exhibits an anxiolytic property. This study was undertaken to evaluate the acute hepatotoxicity and subacute toxicity of barakol in rats. The LD50of barakol after oral administration was 2.33 g/kg. In an acute hepatotoxicity study, single-oral administration of various doses of barakol (60, 100 and 200 mg/kg) were given to rats and the animals were sacrified at 24 hours after the administration. Results from a liver biopsy revealed no sign of liver damage when compared to those from a paracetamol treated positive control group. In a subacute toxicity test, barakol at doses of 60, 120 and 240 mg/kg were orally administered daily for a period of four weeks. A half of 240 mg/kg group, called a recovery group, was maintained for 2 further weeks without barakol administration. No mortality was observed in the controlled and barakol-treated animals. Body weight gain of the barakol-treated group significantly decreased (p < 0.05). From histological examination, the barakoltreated group showed only fatty changes in the liver, but hepatocellular necrosis was not identified. Barakol did not interfere with the hematological examination values. From blood chemistry determination, bilirubin was increased (p < 0.05) in a dosedependent manner and the value return to normal values within two weeks. Barakol in doses of 60-240 mg/kg also decreased triglycerides and the effect persisted for at least two weeks in the recovery group. In conclusion, barakol may disrupt liver function, especially lipid metabolism and bilirubin, in dose-dependent manner. These effects were reversible. The data indicated that barakol may be clinically used in short-term treatment. In repeated administration, serum bilirubin should be carefully monitored. © ISHS 2005. 2018-09-11T09:21:14Z 2018-09-11T09:21:14Z 2005-01-01 Book Series 05677572 2-s2.0-84879908923 10.17660/ActaHortic.2005.679.19 https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=84879908923&origin=inward http://cmuir.cmu.ac.th/jspui/handle/6653943832/62046
institution Chiang Mai University
building Chiang Mai University Library
country Thailand
collection CMU Intellectual Repository
topic Agricultural and Biological Sciences
spellingShingle Agricultural and Biological Sciences
W. Pumpaisalchai
S. Kaewvichit
T. Taesothikul
K. Sanichwankul
S. Siriaunkgul
W. Niwatananun
Toxicity of barakol: Hepatotoxicity and subacute toxicity
description Barakol, an active principle of Cassia siamea (Caesalpiniaceae), exhibits an anxiolytic property. This study was undertaken to evaluate the acute hepatotoxicity and subacute toxicity of barakol in rats. The LD50of barakol after oral administration was 2.33 g/kg. In an acute hepatotoxicity study, single-oral administration of various doses of barakol (60, 100 and 200 mg/kg) were given to rats and the animals were sacrified at 24 hours after the administration. Results from a liver biopsy revealed no sign of liver damage when compared to those from a paracetamol treated positive control group. In a subacute toxicity test, barakol at doses of 60, 120 and 240 mg/kg were orally administered daily for a period of four weeks. A half of 240 mg/kg group, called a recovery group, was maintained for 2 further weeks without barakol administration. No mortality was observed in the controlled and barakol-treated animals. Body weight gain of the barakol-treated group significantly decreased (p < 0.05). From histological examination, the barakoltreated group showed only fatty changes in the liver, but hepatocellular necrosis was not identified. Barakol did not interfere with the hematological examination values. From blood chemistry determination, bilirubin was increased (p < 0.05) in a dosedependent manner and the value return to normal values within two weeks. Barakol in doses of 60-240 mg/kg also decreased triglycerides and the effect persisted for at least two weeks in the recovery group. In conclusion, barakol may disrupt liver function, especially lipid metabolism and bilirubin, in dose-dependent manner. These effects were reversible. The data indicated that barakol may be clinically used in short-term treatment. In repeated administration, serum bilirubin should be carefully monitored. © ISHS 2005.
format Book Series
author W. Pumpaisalchai
S. Kaewvichit
T. Taesothikul
K. Sanichwankul
S. Siriaunkgul
W. Niwatananun
author_facet W. Pumpaisalchai
S. Kaewvichit
T. Taesothikul
K. Sanichwankul
S. Siriaunkgul
W. Niwatananun
author_sort W. Pumpaisalchai
title Toxicity of barakol: Hepatotoxicity and subacute toxicity
title_short Toxicity of barakol: Hepatotoxicity and subacute toxicity
title_full Toxicity of barakol: Hepatotoxicity and subacute toxicity
title_fullStr Toxicity of barakol: Hepatotoxicity and subacute toxicity
title_full_unstemmed Toxicity of barakol: Hepatotoxicity and subacute toxicity
title_sort toxicity of barakol: hepatotoxicity and subacute toxicity
publishDate 2018
url https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=84879908923&origin=inward
http://cmuir.cmu.ac.th/jspui/handle/6653943832/62046
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