Silicon Reverses Lipid Peroxidation but not Acetylcholinesterase Activity Induced by Long-Term Exposure to Low Aluminum Levels in Rat Brain Regions

Abstract

Aluminum (Al) is the most widely distributed metal in the environment and is extensively used in daily life leading to easy exposure to human beings. Besides not having a recognized physiological role, Al may produce adverse effects through the interaction with the cholinergic system contributing to oxidative stress. The present study evaluated, in similar conditions of parenteral nutrition, whether the reaction of silicon (SiO2) with Al(3+) to form hydroxyaluminosilicates (HAS) reduces its bioavailability and toxicity through intraperitoneal administrations of 0.5 mg Al/kg/day and/or 2 mg Si/kg/day in Wistar rats. Al and Si concentrations were determined in rat brain tissue and serum. Acetylcholinesterase (AChE) activity and lipid peroxidation (LPO) were analyzed in the cerebellum, cortex, hippocampus, striatum, hypothalamus, and blood. An increase in the Al concentration was verified in the Al + Si group in the brain. All the groups demonstrated enhanced Si compared to the control animals. Al(3+) increased LPO measured by thiobarbituric acid reactive substances (TBARS) in cerebellum and hippocampus, whereas SiO2 reduced it when compared with the control group. An increase of AChE activity was observed in the Al-treated group in the cerebellum whereas a decrease of this enzyme activity was observed in the cortex and hippocampus in the Al and Al + Si groups. Al and Si concentrations increased in rat serum; however, no effect was observed in blood TBARS levels and AChE activity. SiO2 showed a protective effect in the hippocampus and cerebellum against cellular damage caused by Al(3+)-induced lipid peroxidation. Thus, SiO2 may be considered an important protector in LPO induced by Al(3+).

The Nutritional Components of Beer and Its Relationship with Neurodegeneration and Alzheimer’s Disease

“…However, AChE activity is increased within and around the Aβ plaques. Noremberg et al [18] showed the contrary, that is, a decrease of the AChE activity in the presence of aluminum in the hippocampus and cortex, which would be a precursor of Alzheimer’s disease. It is important to emphasize that since cerebral AChE is an important regulator of behavioral process, the decreased AChE activity found in the cortex and hippocampus may be an indicator of aluminum-induced damage in the brain.…”

“…In line with the González-Muñoz et al [43] study, aluminum nitrate intoxication impairs the brain antioxidant status. Noremberg et al [18], based on many investigations, suggested that the brain may be particularly vulnerable to oxidative damage due the relationship between aluminum accumulation and oxidative damage in the brain [171]. As previously commented on, although aluminum is not a transition metal and therefore cannot initiate peroxidation, aluminum induces alteration in brain metal homeostasis [17], mainly affecting minerals with antioxidant properties [40].…”

“…It has been reported that amyloid beta peptide (Aβ) acts as an antimicrobial; thus, its accumulation would amplify the immune-response and the subsequent brain inflammation [15]. In addition, epigenetic factors, such as the exposition to some toxics, like lead and aluminum [16,17,18], have been proposed as a risk factor of dementia. It is well known that lead is a neuronal enhancer of oxidative stress, as it induces free radical accumulation and is able to modify the cellular patron of genome methylation [16].…”

Understanding Aspects of Aluminum Exposure in Alzheimer's Disease Development

“…Al causes changes in acetylcholinesterase activity from acute and subacute exposure as well as significant deterioration in cognitive functions in rats (21,66,78,108,166). Observation of the central cholinergic system after Al exposure, of 10 mg/kg of body weight/ day for 4 weeks, revealed a deleterious effect on the activities of biosynthetic (choline acetyltransferase) and hydrolytic (acetylcholinesterase) enzymes of the neurotransmitter acetylcholine.…”

Impact of aluminium toxicity on vital human sperm parameters—Protective effects of silymarin

“…Aluminium exerts its adverse effects in different organs, including the nervous (Bondy, 2016;Noremberg et al, 2015), skeletal muscle (Aghilinejad, Mousavi, Nouri, & Ahmadi, 2012), respiratory (Shaaban, Zayet, Aboufaddan, & Elghazally, 2016), cardiovascular (Schmidt et al, 2016) and urogenital system (Berihu, 2015;Farajbakhsh, Amjadi, Manzoori, Ardalan, & Jouyban, 2016;Sombra et al, 2003).…”