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Pathophysiology. 2015 Mar;22(1):39-48. doi: 10.1016/j.pathophys.2014.12.001. Epub 2014 Dec 13.

Interplay of glia activation and oxidative stress formation in fluoride and aluminium exposure.

Author information

1
Department of Anatomy, College of Health Sciences, Bingham University, P.M.B. 005, New Karu 961106, Nasarawa State, Nigeria; Department of Anatomy, College of Health Sciences, Olabisi Onabanjo University, Olabisi Onabanjo University, P.M.B. 1515, Remo Campus, Ikenne, Ogun State, Nigeria. Electronic address: bisibk@gmail.com.
2
Department of Anatomy, College of Health Sciences, Bingham University, P.M.B. 005, New Karu 961106, Nasarawa State, Nigeria. Electronic address: jokememudu@gmail.com.
3
Neural Systems Lab, Department of Comparative Biomedical Sciences, Louisiana State University, Baten Rouge 70802, LA, USA. Electronic address: ogundele@lsu.edu.
4
Department of Histopathology, University of Jos Teaching Hospital, Jos, Nigeria. Electronic address: lanreajetunmobi@yahoo.com.

Abstract

BACKGROUND:

Oxidative stress formation is pivotal in the action of environmental agents which trigger the activation of glial cells and neuroinflammation to stimulate compensatory mechanisms aimed at restoring homeostasis.

AIM:

This study sets to demonstrate the interplay of fluoride (F) and aluminium (Al) in brain metabolism. Specifically, it reveals how oxidative stress impacts the activation of astrocytes (GFAP), mediates proinflammatory responses (microglia and B-cells: CD68 and CD 20 respectively) and shows the pattern of lipid peroxidation in the brain following fluoride and (or) aluminium treatment in vivo.

METHOD:

Male adult Wistar rats were treated with low and high doses of fluoride, aluminium or combination of fluoride-aluminium for 30 days. The control group received distilled water for the duration of the treatment. Blood and brain tissue homogenates were prepared for colorimetric assay of stress biomarkers [malonialdehyde (MDA) and superoxide dismutase (SOD)]. Subsequent analysis involved immunodetection of astrocytes (anti-GFAP), microglial (anti-CD68) and B-cells (anti-CD20) in coronal sections of the prefrontal cortex using antigen retrieval immunohistochemistry.

RESULT AND CONCLUSION:

Aluminium, fluoride and a combination of aluminium-fluoride treatments caused an increase in brain lipid peroxidation products and reactive oxygen species (ROS) formation. Similarly, an increase in glial activation and inflammatory response were seen in these groups versus the control. Oxidative stress induced glial activation (GFAP) and increased the expression of B cells (CD20). This also corresponded to the extent of tissue damage and lipid peroxidation observed. Taken together, the results suggest a close link between oxidative stress neuroinflamation and degeneration in aluminium-fluoride toxicity.

KEYWORDS:

Astrocytes; B cells; Microglia; Oxidative stress; Prefrontal cortex

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