Kade I J, Nogueira C W, Rocha J B T
Postgraduate Programme in Biochemical Toxicology, Centre for Natural and Exact Sciences, Federal University of Santa Maria, CEP 97105-900, Camobi, Santa Maria, RS, Brazil.
Brain Res. 2009 Aug 11;1284:202-11. doi: 10.1016/j.brainres.2009.04.003. Epub 2009 Apr 9.
Neuronal malfunction is a characteristic feature of diabetic mellitus. Hence, the present study therefore sought to evaluate the effect of diphenyl diselenide (DPDS) on the antioxidant status, sodium pump, cholinergic and glutamatergic system in the rat brain of streptozotocin (STZ) induced diabetes. The results show that although STZ evoke a significant diminution on the antioxidant status and activity of Na(+)/K(+)-ATPase, the activity of acetylcholinesterase and glutamate uptake and release was not altered. However, DPDS was able to markedly restore the observed imbalance in cerebral antioxidant status and also relieve the inhibition of Na(+)/K(+)-ATPase caused by streptozotocin. Hence, we conclude that DPDS is a potential candidate in the management of neuronal dysfunction that often accompanied complications associated with diabetic hyperglycemia.
神经元功能障碍是糖尿病的一个特征性表现。因此，本研究旨在评估二苯基二硒醚（DPDS）对链脲佐菌素（STZ）诱导的糖尿病大鼠脑内抗氧化状态、钠泵、胆碱能和谷氨酸能系统的影响。结果表明，尽管STZ显著降低了抗氧化状态和Na(+)/K(+)-ATP酶的活性，但乙酰胆碱酯酶的活性以及谷氨酸的摄取和释放并未改变。然而，DPDS能够显著恢复所观察到的脑内抗氧化状态失衡，并且还能缓解链脲佐菌素对Na(+)/K(+)-ATP酶的抑制作用。因此，我们得出结论，DPDS是治疗常伴随糖尿病高血糖并发症的神经元功能障碍的潜在候选药物。
