Aluminum‐induced pro‐oxidant effects in rats: protective role of exogenous melatonin

Abstract

In recent years, it has been suggested that oxidative stress is a feature of Alzheimer's disease in which aluminum (Al) could exacerbate oxidative events. The goal of the present study was to assess in rats the pro-oxidant effects induced by Al exposure, as well as the protective role of exogenous melatonin. Two groups of male rats were intraperitoneally injected with Al only or melatonin only, at doses of 5 and 10 mg/kg/day, respectively for 8 wk. During this period, a third group of animals received Al (5 mg/kg/day) and melatonin (10 mg/kg/day). At the end of the treatment period, rats were anesthesized and arterial blood was obtained. Thereafter, animals were killed and liver and brain (cortex, hippocampus and cerebellum) were removed. These tissues were processed to examine oxidative stress markers: glutathione transferase (GST), reduced glutathione (GSH), oxidized glutathione (GSSG), superoxide dismutase (SOD), glutathione reductase (GR), glutathione peroxidase (GPx), catalase (CAT), thiobarbituric acid reactive substances (TBARS), as well as protein content. Samples of these tissues were also used to determine Al, Fe, Mn, Cu and Zn concentrations. The results show that Al exposure promotes oxidative stress in different neural areas, including those in which Al concentrations were not significantly increased. The biochemical changes observed in neural tissues show that Al acts as pro-oxidant, while melatonin exerts an antioxidant action in Al-treated animals. The protective effects of melatonin against cellular damage caused by Al-induced oxidative stress, together with its low toxicity, make melatonin worthy of investigation as a potential supplement to be included in the treatment of neurological disorders in which the oxidative effects must be minimized.

Melatonin is a potent modulator of antioxidative defense and cellular proliferation against aluminum toxicity in rats

“…This decrease in GSH levels could be due to the exhaustion of GSH reserves and the increase in oxidative stress. Esparza et al (2003) suggested increased generation of free radicals and oxidative stress in the toxic mechanism of Al. Here, GSH levels were depleted, indicating that Al-induced histoid damage was associated with oxidative stress.…”

“…All rats were clinically healthy. The animals were randomly divided into five groups (n = 8 per group): Group I: control animals injected intraperitoneally with physiological saline; group II: Mel control animals injected subcutaneously with physiological saline containing 2% ethanol (Mel dissolved in 2% ethanol); group III: animals injected subcutaneously with 10 mg/kg Mel; group IV: rats injected intraperitoneally with 5 mg/kg [Al 2 (SO 4 ) 3 ]; group V: animals receiving 5 mg/kg Al 2 (SO 4 ) 3 intraperitoneally and 10 mg/kg Mel subcutaneously (Esparza et al, 2003;Salido et al, 2013). All chemicals were purchased from Sigma-Aldrich (St. Louis, MO, USA).…”

Oxidative stress status and RNA expression in hippocampus of an animal model of Alzheimer's disease after chronic exposure to aluminum

“…It is well known that the central nervous system is highly vulnerable to attacks from ROS due to the brain's high oxygen consumption rate, the abundant lipid contents, as well as the relatively low levels of antioxidant enzymes in comparison with other tissues (Esparza et al, 2003Kaneko et al, 2004;Gómez et al, 2005).…”

Effects of Ellagic acid and Hesperetin on Levels of Some Elements in Livers of Aluminum-Induced Rats

“…Esparza et al demonstrated that Mn concentrations were higher in the melatonin-treated group than the one in Altreated group in liver [30]. Moreover, in this study, it has been suggested that the protective effects of melatonin against cellular damage caused by Al-induced oxidative stress, together with its low toxicity, make melatonin worthy of investigation as a potential supplement to be included in the treatment of neurological disorders in which the oxidative effects must be minimized.…”