Asha, K K; Dr. Devadasan, K(Central Institute of Fisheries Technology, 2010)
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Abstract:
Fulminant hepatic failure (FHF) is a dramatic and challenging syndrome in clinical medicine. Although an uncommon disorder, it is usually fatal and occurs in previously healthy person. While the causes of FHF remain unclear, viral hepatitis and drug-induced liver injury account for the majority of cases. Hepatitis E causes large-scale epidemics of hepatitis in the Indian subcontinent, involving hundreds of thousands of cases with high mortality. FHF is associated with several clinical features like jaundice, shrunken liver, easy bruising, low levels of serum proteins, fatigue, multi-organ failure etc and metabolic derangements like hypoglycemia, hyperlipidemia, hyponatremia, defective protein synthesis, reduced energy production, decreased rate of urea production etc. These disturbances are predominantly attributed to oxidative stress, membrane destabilization and osmolytic imbalances. The options available for these patients are quite minimal with liver transplantation being one of them. But the procedure is ridden with issues causing it to find less favor among the patients and the caregivers. Use of hepatoprotective and cytoprotective drugs, is being considered to be a more acceptable alternative as a strategy to enhance liver regeneration. In this regard use of taurine a naturally occurring amino acid that plays a crucial role in many physiological processes would prove to be effective. In the present study, hepatoprotective effect of taurine on a rat model of induced FHF was studied. Taurine supplementation has effectively counteracted the metabolic and structural aberrations in the liver caused by D-galactosamine intoxication.
Shiny, K S; Dr. Anandan, R(Cochin University of Science and Technology, February , 2007)
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Abstract:
The present study indicate that prior administration of
taurine is effective in minimizing all the deleterious effects induced by isoproterenol,
thereby justifying its use as a potent cytoprotective agent. The overall cardioprotective
effect of taurine is probably related to its antioxidant property evidenced by its ability to
reduce lipid peroxidation and to maintain the activities of free radical enzymes and nonenzymatic
antioxidants, its membrane stabilizing action and to its hypolipidemic property.
Description:
Dept.of Marine Biology,Microbiology and Biochemistry,Cochin University of Science and Technology
Sivaperumal, P; Dr.Sankar, T V(Cochin University of Science and Technology, April , 2008)
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Abstract:
Methylparathion (MP) is an organophosphorus insecticide used world wide in
agriculture due to its high activity against a broad spectrum of insect pests. The
aim of the study is to understand the effect of methylparathion on the lipid
peroxidation, detoxifying and antioxidant enzymes namely catalase (CAT),
glutathione peroxidase (GPx), superoxide dismutase (SOD), glutathione Stransferase
(GST), total reduced glutathione (GSH), lipid peroxidation (LPO),
acetylcholinesterase (AChE) and disease diagnostic marker enzymes in liver,
sarcoplasmic (SP) and myofirbirllar (MF) proteins in muscles, lipids and
histopathlogical changes in various organs of Labeo rohita of size 75 i 6g at
lethal and sublethal level of exposure. The probit analysis showed that the lethal
concentration (LC 50%) for 24, 48, 72 and 96h were 15.5mg/L, 12.3mg/L,
11.4mg/L and 10.2mg/L respectively which is much higher compared to the LC50
for juvenile fish. The LPO level and GST activity increased five folds and two
folds respectively on exposure to methylparathion at 10.2 mg/L and the level of
the enzymes increased, on sub lethal exposure beyond 0.25mg/L. AChE activity
was inhibited by 74% at a concentration of 1.8mg/L and 90% at 5.4mg/L. The
disease diagnostic marker enzymes AST, ALT, ALP and LDH increased by about
2, 3 ,3 and 2 folds respectively at pesticide concentration of 10.2mg/L when
compared to control. On sub lethal exposure, however the enzymes did not show
any significant changes up to 0.5mg/L. At a concentration of 10.2 mg/L, there
was a three fold increase in myofibrillar proteins while the increase in
sarcoplasmic protein was above 1.5 fold. On sub lethal exposure, significant alteration was noticed up to 30 days up to 1mg/L of methylparathion
concentration. Further exposure up to 45 days increased sarcoplasmic proteins
(upto 0.5mg/L). ln the case of myofibrillar proteins, noticeable changes were
observed at 1mg/L concentration right from 15th day. The cholesterol content in
brain tissues increased by about 27% at methylparathion concentration of 5.4
mglL. However at 0.25mg/L sub lethal concentration, no significant alteration was
observed in enzyme activity, muscle proteins, lipids and histopathology of the
tissues. The results suggest that methylparathion has the potential to induce
oxidative stress in fish, and that liver, muscle and brains are more sensitive
organs of Labeo rohita, with poor antioxidant potentials at higher concentrations
of the pesticide. The various parameters studied in this investigation can also be
used as biomarkers of methylparathion exposure.
Description:
Dept.of Chemical Ocenography,Cochin University of Science and Technology