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It of inflammatory bowel disease (MacDonald et

It has been reported that cytokines play an integral role in the
pathogenesis of inflammatory bowel disease (MacDonald et al. 2000).
It was increased following acetic acid instillation
in our experiment. Sod sel treatment inhibits TNF and IL1? production which may
be due to inhibition of their synthesis or release.

Previous studies have linked selenium with decreasing inflammation,
Gazdik  et al. (Gazdik et al. 2002) reported significantly decreased
consumption of corticosteroids after Se supplementation with 200??g/day for 96
weeks in corticoid-dependent asthmatics. There have been some data
demonstrated  that there was an
improvement in lung function in patients with Cystic Fibrosis
with selenium supplementation (Wood et al. 2003). In
a small study involving 46 patients with rheumatoid arthritis and 48
age-matched controls, serum se levels were significantly reduced (Pemberton et al. 2009). 

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Sodium
Selenite was further shown to inhibit the levels of other inflammatory
mediators in colon tissue, such as the intercellular adhesion molecule, ICAM-1,
which helps in the recruitment of leukocytes as well as the initiation and
perpetuation of intestinal inflammation in IBD (Li et al. 2005; Sun et al. 2001; Woywodt
et al. 1999). Inhibition of ICAM-1 by sod sel was
previously shown by Zhang et al. (Zhang et al. 2002). However, sod sel was found to
preserve the levels of another adhesion molecule, named junctional adhesion
molecule (JAM-a) which belongs to an immunoglobulin super family found in tight junctions of epithelial cells (Ebnet et al. 2003) and primarily involved in interactions
with ?2 integrins during inflammatory responses, and it inhibits the synthesis
of eicosanoids and oxidative DNA injury (Osakabe et al. 2004). This shows that the drug, by increasing
JAM-A, might reduce impairment of the epithelial barrier function and the
consequent intestinal inflammation.

In the current
study, oxidative stress was evaluated in the erythrocytes. Erythrocytes (RBCs)
are more exposed to oxidative stress than other cells owing to plenty of heme
iron and oxygen, which can generate superoxides, H2O2 and
lipid peroxides. The hydroperoxides themselves are not very reactive but are
readily transformed to hydroxyl and alkoxyl radicals in the existence of free
iron and electron donor molecules, which indiscriminately inflict damage on
biomolecules. Therefore, RBCs are believed to have a very effective defense
mechanism against peroxides (Giulivi and Davies 1990) that may explain depletion in RBCS
and hemoglobin in the present study which were restored in treated groups due
to antioxidant effect of sod sel.

The generation of free radicals is considered to
be the primary cause of the hepatic and renal damages. These free radicals
combined with the cellular lipid and proteins which in turn, initiate lipid
peroxidation process and protein carbonylation, resulting in structural changes
in bio-membranes, loss of integrity, and damage of cellular membranes.
Accordingly, serum transaminases activities as well as urea and creatinine
levels were increased in acetic acid control rats. Treatment with sod sel was
able to restore normal level of the liver enzymes, urea and creatinine,
probably due to its antioxidant properties

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