Abstract
Oxidative stress has been involved in neurodegenerative diseases. The growth hormone (GH) counteracts the levels of reactive oxygen species. Previously, we showed that the prolonged exposure to ozone causes oxidative stress in the hippocampus and memory deficits. In this work, we analyzed the effects of the growth hormone on the memory deficit generated by ozone exposure, growth hormone effects on the Insulin-like growth factor I (IGF-I), and the serinethreonine protein kinase (Akt) activation in the dentate gyrus. Our results show that GH prevents memory deficits in early stages of the neurodegenerative process.
Highlights
Oxidative stress in cells is generated because of an imbalance between the reactive oxygen species (ROS) and antioxidants
In this work we evaluated the effects of the growthhormone treatment on the memory deficit generated by the oxidative stress, produced by low doses of ozone, in the water maze and passive-avoidance tasks and on the Insulin-like growth factor I (IGF-I)-Akt signaling in the dentate gyrus
For the acquisition of spatial memory, the repeatedmeasures ANOVA indicated no significant differences between the groups in the latency to reach the hidden platform during the training block for 3 days (Figure 1(a))
Summary
Oxidative stress in cells is generated because of an imbalance between the reactive oxygen species (ROS) and antioxidants. It has been demonstrated that ozone inhalation generates oxidative damage through the formation of the ROS [1,2]. Oxidative stress produced by ozone inhalation causes damage in the central nervous system [3,4,5], increases lipid peroxidation (LPO) levels in brain structures [5,6], and causes memory deficits [5,6,7]. It has been reported that the GH-IGF-I axis is involved in cognitive functions [12,14,15]. In previous studies we demonstrated that oxidative stress generated by exposure to ozone causes memory deficit [5], and neurogenesis alterations in rats [6]
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