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Acetaminophen Induced Liver Injury

Reply from: ironjustice
Date: 03 May 2008, 06:18
Acetaminophen Induced Liver Injury

Is propolis an iron chelator like deferoxamine ?
Deferoxamine has been known to blind.
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Propolis reverses acetaminophen induced acute hepatorenal alterations:
A biochemical and histopathological approach.
Nirala SK, Bhadauria M
Arch Pharm Res 2008 Apr; 31(4):451-61.

The present study has been conducted to evaluate the curative effect
of propolis extract, a honey bee-hive product, against acetaminophen
(APAP) induced oxidative stress and dysfunction in liver and kidney.
Animals were challenged with APAP (2 g/kg, p.o.) followed by treatment
of propolis extract (100 and 200 mg/kg, p.o.) once only after 24 h.
Release of transaminases, alkaline phosphatase, lactate dehydrogenase,
and serum bilirubin were increased, whereas hemoglobin and blood sugar
were decreased after APAP administration. Antioxidant status in both
the liver and kidney tissues were estimated by determining the
glutathione, malondialdehyde content and activities of the CYP
enzymes, which showed significant alterations after APAP intoxication.
In addition, activities of adenosine triphosphatase, acid phosphatase,
alkaline phosphatase, and major cell contents (total protein, glycogen
and cholesterol) were also altered due to APAP poisoning. Propolis
extract successfully reversed the alterations of these biochemical
variables at higher dose. Improvements in hepatorenal
histoarchitecture were also consistent with biochemical observations.
The results indicated that ethanolic extract of propolis has ability
to reverse APAP-induced hepatorenal biochemical and histopathological
alterations probably by increasing the antioxidative defense
activities due to various phenolic compounds present in it.
Archives of pharmacal research [Arch Pharm Res]
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Protection against acetaminophen-induced liver injury in vivo by and
iron chelator, deferoxamine
Auteur(s) / Author(s)
SAKAIDA I. ; KAYANO K. ; WASAKI S. ; NAGATOMI A. ; MATSUMURA Y. ;
OKITA K. ;
Affiliation(s) du ou des auteurs / Author(s) Affiliation(s)
Yamaguchi univ., school medicine, first dep. internal medicine, Ube,
Yamaguchi Prefecture 755, JAPON

Abstract
Background:
Recent data indicate that iron play a major role in lipid
peroxidation, a hepatotoxic effect of acetaminorphen (APAP). Methods:
We investigated whether an iron chelator, deferoxamine (DFO), can
protect against APAP-induced liver injury in vivo in rats.
Results:
DFO diminished the increase in serum alanine aminotransferase (ALAT)
in a dose-dependent manner after APAP administration and also reduced
mortality. Administration of 750 mg/kg APAP resulted in an increased
ALAT (11,666±4633) after 8 h, and the mortality at 24 h was 88%
Revue / Journal Title
Scandinavian journal of gastroenterology ISSN 0036-5521 CODEN
SJGRA4
Source / Source
1995, vol. 30, no1, pp. 61-67 (23 ref.)
Scandinavian University Press, Oslo, NORVEGE (1966) (Revue)

INIST-CNRS, Cote INIST : 12513, 35400005811428.0100
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"Irreversible ocular toxicity"

Desferrioxamine related maculopathy: a case report.
Arora A, Wren S, Gregory Evans K
Am J Hematol 2004 Aug; 76(4):386-8.

Desferrioxamine is used for the treatment of chronic iron overload,
acute iron poisoning, and certain anaemias. Ocular toxicity secondary
to prolonged treatment with desferrioxamine may result in night
blindness, visual field constriction, cataract, pigmentary retinopathy
and optic neuropathy. To avoid such complications an ophthalmic
screening has been suggested for patients taking desferrioxamine. We
report an 81-year-old patient who developed irreversible ocular
toxicity despite undergoing ophthalmic screening.
American journal of hematology. [Am J Hematol]
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