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.

*Original abstract online at https://pubmed.ncbi.nlm.nih.gov/25577494/

• Related Studies :

  • Effects of chronic fluorosis on the brain.

    Highlights Reviewing the mechanism of brain injury caused by chronic fluorosis is of great significance for protecting residents in fluorosis endemic areas. Abstract This article reviews the effects of chronic fluorosis on the brain and possible mechanisms. We used PubMed, Medline and Cochraine databases to collect data on fluorosis, brain injury,

  • Black berry juice attenuates neurological disorders and oxidative stress associated with concurrent exposure of aluminum and fluoride in male rats

    The objective of this study was to assess the protective effect of black berry juice (BBJ) on the neurological disorders and oxidative stress induced by co-exposure to ALCL3 and NaF in male albino rats. Administration of either AlCl3 (200?mg/kg bw) or NaF (10?mg/kg bw) or both of them caused a

  • Protective effect of resveratrol against neuronal damage through oxidative stress in cerebral hemisphere of aluminum and fluoride treated rats.

    Aluminum has no defined biological function and it is potentially involved in the pathogenesis of neurodegenerative disorders. Furthermore, the presence of fluoride causes more aluminum to accumulate in the brain, resulting in increased neuronal damage. In recent years, resveratrol through its ameliorative effects was found to be a neuroprotectant. This

  • Co-exposure to arsenic and fluoride on oxidative stress, glutathione linked enzymes, biogenic amines and DNA damage in mouse brain.

    We studied the effects of combined exposure to arsenic and fluoride on (i) brain biogenic amines, oxidative stress and its correlation with glutathione and linked enzymes; (ii) alterations in the structural integrity of DNA; and (iii) brain and blood arsenic and fluoride levels. Efficacy of alpha-tocopherol in reducing these changes

  • [Influence of free radical inducer on the level of oxidative stress in brain of rats with fluorosis].

    OBJECTIVE:  To study changes in content of lipid peroxide and composition of fatty acids in the brain of rats affiliated with chronic fluorosis after treatment with free radical inducer (ferric ion). METHODS:  Thirty-six Wistar rats were divided into three groups, fed with similar fodder and varied concentrations of fluoride in drinking

• Related FAN Content :

  • Fluoride & IQ: 76 Studies

    Note: See the Updated list of fluoride IQ studies at https://fluoridealert.org/researchers/fluoride-iq-studies/the-fluoride-iq-studies/ • As of July 18, 2022, a total of 85 human studies have investigated the relationship between fluoride and human intelligence. • Of these investigations, 76 studies have reported that elevated fluoride exposure is associated with reduced IQ in humans. • The studies

  • Fluoride content in tea and its relationship with tea quality.

    J Agric Food Chem. 2004 Jul 14;52(14):4472-6. Fluoride content in tea and its relationship with tea quality. Lu Y, Guo WF, Yang XQ. Department of Tea Science, Zhejiang University, 268 Kaixuan Road, Hangzhou 310027, People's Republic of China. Abstract: The tea plant is known as a fluorine accumulator. Fluoride (F) content in fresh leaves collected

  • NRC (2006): Fluoride's Neurotoxicity and Neurobehavioral Effects

    The NRC's analysis on fluoride and the brain.

  • Fluoride's Direct Effects on Brain: Animal Studies

    The possibility that fluoride ingestion may impair intelligence and other indices of neurological function is supported by a vast body of animal research, including over 40 studies that have investigated fluoride's effects on brain quality in animals. As discussed by the National Research Council, the studies have consistently demonstrated that fluoride, at widely varying concentrations, is toxic to the brain.

  • Fluoride & Oxidative Stress

    A vast body of research demonstrates that fluoride exposure increases oxidative stress. Based on this research, it is believed that fluoride-induced oxidative stress is a key mechanism underlying the various toxic effects associated with fluoride exposure. It is also well established that fluoride's toxic effects can be ameliorated by exposure