<p>This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</p> <p>Oxidative damage has been suggested to be a contributing
factor in the development to diabetic nephropathy
(DN). Recently, there has been evidence that pentoxifylline
(PTX) has free radical-scavenging properties; thus, its antiinflammatory
and renoprotective effects may be related to a
reduction in reactive oxygen species production. It is likely
that the pharmacological effects of PTX include an antioxidant
mechanism as shown in in vitro assays. The aim of
this study was to evaluate whether the reported renoprotective
effects of PTX could be the result of its antioxidant
actions in streptozotocin (STZ)-induced DN in rats. The administration
of PTX over a period of 8 weeks, in addition
to displaying renoprotective effects, caused a significant reduction
in lipoperoxide levels (LPOS) in the diabetic kidney
(<italic>P</italic> &lt; 0.05), compared to untreated rats. These levels were
comparable to those in the healthy kidney of experimental
animals (<italic>P</italic> &gt; 0.05). All untreated STZ rats exhibited
an increase in LPOS as opposed to healthy controls (H)
(<italic>P</italic> &lt; 0.001). The total antioxidant activity (TAA) in plasma
was increased significantly already after 2 days of STZ
(<italic>P</italic> &lt; 0.05). When we examined the progression of TAA in
STZ rats, there was a significant decrease over 8 weeks
(<italic>P</italic> &lt; 0.05). PTX treatment caused an increase in TAA
when compared to untreated STZ rats (<italic>P</italic> &lt; 0.05).
Renal hypertrophy was less evident in PTX-treated
STZ than in untreated STZ rats, evaluated by kidney
weight/body weight ratio. These results indicate
that PTX decreases the oxidative damage induced by these experimental procedures and may increase antioxidant
defense mechanisms in STZ-induced diabetes in rats.</p>
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Exp Diabesity Res. 2004; 5(4):245-251