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Nicotinamide: A
cytoprotectant against streptozotocin-induced diabetic
damage in Wister rat brains
Safinaz S.
Ibrahim1* and Sherine M. Rizk2
Biochemistry Department, Faculty of Pharmacy, Cairo
University, Cairo, Egypt.
*Corresponding author: E-mail:
safinazsibrahim@cu.edu.eg. Mobile: 002 010 1595025. Fax:
002-02-23628426
Accepted
25 June 2008 |
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Nicotinamide is being used in experimental and clinical
trials examining the prevention of type-1 diabetes mellitus.
However,
the precise
mechanisms underlying the antidiabetic and neuroprotective
effects of nicotinamide require further analysis.
Our goals are to evaluate the protective effect and the
cellular and molecular mechanisms of nicotinamide against
brain damage induced by type-1 diabetes in rats. Type-1
diabetes was induced by i.p injection of streptozotocin (50
mg/kg). Ten days after the induction of diabetes, rats were
divided into two groups, control diabetic group and
nicotinamide-treated group. Nicotinamide was i.p administered
at daily dose of 100 mg/kg for a period of 4 weeks. Another
group of normal animals was
served as
normal control group.
The
diabetic group showed a significant (p < 0.05) decrease in
the content of brain DNA, RNA and glutathione, whereas, the
contents of lipid peroxide, as malondialdehyde, and nitric
oxide were significantly increased. The activities of aldose
reductase, sorbitol dehydrogenase and cytochrome oxidase
were significantly increased, whereas, the activities of
glutathione reductase, glutathione peroxidase,
glutathione-S-transferase and superoxide dismutase were
significantly decreased.
Nicotinamide administration produced
restoration of brain malondialdehyde, nitric oxide,
glutathione, RNA, DNA levels and the activities of the most
measured enzymes.
In conclusion,
nicotinamide could ameliorate brain damage induced by type-1
diabetes in Wistar rats. The present data provide new
approaches for the precise cellular and molecular mechanisms
of the neuroprotective effect of nicotinamide.
Key
words:
Nicotinamide, STZ-diabetes, rat brain, polyol pathway,
oxidative status, antioxidant systems, DNA and RNA levels. |
