Muscarinic M1, M3, Nicotinic,GABAA and GABAB Receptor ...

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Discussion
Haces et al., 2010). Furthermore, increased lipoperoxidation has been observed in
the hippocampus, cerebral cortex and the striatum of hypoglycemic animals not
subjected to a coma period (Patockova et al., 2003). These observations together
with the present results support the hypothesis that the hypoglycemic condition is
sufficient to stimulate RS production.
Pancreas
SOD is implicated in the pathophysiology of various disease states
including diabetes mellitus. Oxygen free radicals exert their cytotoxic effect by
peroxidation of membrane phospholipids leading to change in permeability and
loss of membrane integrity (Meerson et al., 1982). Pancreatic β-cell death
underlies the pathogenesis of Type I (insulin-dependent) diabetes mellitus and
liver is an important organ which offers an adequate site for various metabolic
functions. Oxygen free radicals have been implicated in β cell destruction as well
as in liver injury (Roza et al., 1995; Poli et al., 1989; Paty et al., 1990). Our results
showed a decreased expression of SOD in the pancreas of hypoglycemic and
diabetic rats when compared to control which suggest the oxidative stress in
pancreas during hypoglycemia and hyperglycemia. Increases in oxidative stress
following hyper/hypoglycemia results from modulation of anti-oxidant pathways.
BAX PROTEIN IN BRAIN AND PANCREAS
Bax, a member of the Bcl-2 family proteins, are distinct regulators of
early stages of the apoptotic process by forming oligomers onto the mitochondrial
outer membrane and creating a channel for the release of cytochrome C and other
apoptotic substances (Eskes et al., 2000; Antonsson et al., 2001). Study also
suggested that Bax can bind to the voltage-dependent anion channel (VDAC) and
promote the release of cytochrome C from VDAC, despite the fact the opening
and closing of VDAC is Bax independent (Vander Heiden et al., 1997). Bax