Induction of oxidative stress by non-lethal dose of
mercury in rat liver:
Possible relationships between
apoptosis and necrosis
Bharat
Bhusan Patnaik*1,
Atish Roy2, Soumik
Agarwal2 and Shelley
Bhattacharya2
1Department of
Biotechnology, Iase
University (Off Campus Centre), Mancheswar Industrial Estate, Bhubaneswar - 751010, India
2Environmental
Toxicology Laboratory, Department of Zoology, Visva-Bharathi University,
Santiniketan - 731235, India
(Received: November 19, 2008; Revised
received: July
20, 2009; Accepted: August 07, 2009)
Abstract: Sprague Dawley
strain of male rats weighing 200 ? 10.0 g, were exposed intramuscularly to
non-lethal dose of mercury for short acute duration of 24 and 48 hr. Mercury
treatment increased thio-barbituric acid reactive
substance (TBARS) and conjugated diene (CD) content
with increase in duration when compared with control. This reflects possible
increase in lipid peroxidation, revealing that
sufficient intoxication was generated by non-lethal dose of mercury. Furthermore,
mercury treatment decreased tissue glutathione (GSH) content to 2.07 and 1.49 ?g GSH mg protein-1 with concomitant decrease in glutathione-S-transferase (GST) activity by 26.06 and 36.40% after 24 and
48hr of exposure respectively. The elevations of aspartate
transaminase (AST) and alanine
transaminase (ALT) levels measured exhibited increase
of 287.5 and 214.5% after 48 hr of exposure respectively which were found to be
highly significant compared with control. Western blot analysis indicated upregulation of caspase-9 and upsurge in effector caspase-3 activity leading to apoptosis. The
concluded findings of the present investigation suggests? possible role of early mercury exposure in
inducing oxidative stress mediated apoptosis in mammalian model systems as an
indicator component of environmental toxicology.
Keywords: Mercury, Oxidative stress, Lipid peroxidation, Glutathione, Apoptosis
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