Biochemical alterations in rat brain following aluminum exposure: Protection with centrophenoxine

Abstract

Aluminum (Al) is a neurotoxicant potentially affecting ionic, cholinergic, and dopaminergic neurotransmission in the central nervous system. These alterations are known to be associated with learning ability, adaptive responses, and other aspects of behavior. The present experiment was designed to study the neurotoxic consequences of Al exposure on neurotransmitters like dopamine (DA), serotonin (5-HT), norepinephrine (NE) along with the activity of acetylcholinesterase (AChE). Furthermore, Centrophenoxine (CpH) was administered as a post treatment to evaluate its potential in Al-induced neurotoxicity. The cognitive functions and memory loss were also studied after both Al and CpH administration. Al was administered orally at a dose of 40 mg kg À1 day À1 for a period of 8 weeks, whereas CpH was administered intraperitoneally at a dose of 100 À1 mg kg À1 day À1 for a period of 6 weeks. The study was carried out in four regions of the brain, namely cerebrum, cerebellum, medulla oblongata, and hypothalamus. A significant reduction in AChE activity and different neurotransmitters was observed after Al exposure in the regions. CpH as a post treatment proved beneficial in restoring these alterations. Al exposure also affected the cognitive functions and short-term memory, which were significantly improved following CpH post treatment.

Inhibitory potentials of Cymbopogon citratus oil against aluminium-induced behavioral deficits and neuropathology in rats

“…This study showed the possible neuroprotective/neuromodulatory potentials of ESO before and after AlCl 3 exposure on rat's cerebellar morphology and functions through behavioral, biochemical, and histoarchitectural evaluations. The use of neurobehavioral studies in risk assessment is premised on the fact that behavior/emotions can be regarded as the net output of memory, motor, locomotor and cognitive functions occurring in the nervous system and can serve as potentially sensitive endpoints of chemically induced-neurotoxicity [22]. AlCl 3 is a neurotoxicant that permeates and functionally alters the blood-brain barrier and potentially produces changes in the ionic, cholinergic, dopaminergic, and noradrenergic neurotransmission in the central nervous system.…”