Distribution of glial fibrillary acidic protein in different parts of the rat brain under cadmium exposure

Kovalchuk, Y. P.; Prischepa,; U, Si; Vs, Nedzvetsky; Yg, Kot; Ee, Persky; Ушакова, Г. А.

doi:10.15407/ubj87.03.116

Cited by 5 publications

(3 citation statements)

References 19 publications

(25 reference statements)

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“…This severe activation of astrocytes is associated with an ongoing neuroinflammatory response and neurodegenerative processes in the brain. This is in agreement with several other studies that observed that CdCl2 increased the expression of GFAP [52], with morphological alterations in GFAP-expressing astrocytes [53].…”

Section: Discussionsupporting

confidence: 93%

Neuroprotective Effects of Tea Against Cadmium Toxicity

Wachira

Areba

Ngure

et al. 2019

Bioactive Compounds in Health and Disease

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Background: Cadmium (Cd) is a common pollutant and potential neuro-toxicant to humans. The main treatment for heavy metal toxicity is chelation therapy which is however replete with grave side effects. This study was designed to determine the neuroprotective effects of extracts of the tea beverage on experimentally induced cadmium toxicity in the brain of rats. Cadmiumas CdCl2 was administered subcutaneously while tea was given orally.Methods: Healthy Wister rats were used to study the effects of co-administration of Cd and tea extracts on the brain. Cadmium was injected subcutaneously while tea was administered orally to the rats. Brain tissue from euthanized rats was assayed for Zinc Fingers and Homeoboxes Protein 1 (ZHX1), reduced glutathione (GSH), and lipid peroxidation markers Thiobarbituric Acid Reactive Substances (TBARS). Neurohistochemical and histopathological studies were also carried out on the brain tissues of the rats.Results: Cadmium significantly induced neuronal damage exhibited by a significant (p < 0.05) decrease in ZHX1 in the brain tissue, significant (p <0.05) increase in TBARS, as well as significant (p < 0.05) increase in GSH implying an impaired antioxidant defense system. Co-administration of Cd with black or green tea extracts resulted in a significant decrease in lipid peroxidation as well as maintenance of GSH and ZHX1. The neurohistochemical and histopathological studies in the brain of the rats indicated that the tea extracts significantly reduced CdCl2 toxicity and preserved the normal histological architecture of the brain tissues.Conclusion: This paper reports for the first time the efficacy of tea extracts in protecting rats from cadmium induced toxicity and disturbances of antioxidant defense system in the brain.Key words: Tea; flavonoids; Cadmium; neurotoxicity; Chelating agents.

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Section: Discussionsupporting

confidence: 93%

Neuroprotective Effects of Tea Against Cadmium Toxicity

Wachira

Areba

Ngure

et al. 2019

Bioactive Compounds in Health and Disease

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“… 43 observed a reduction of GFAP network after exposure to CdCl 2 in mouse stem cell/progenitors and Kovalchuk et al . 45 showed a reduction of soluble GFAP in experiments performed in rats. In this work the presence of Cd into the lizard brain parenchyma is associated to a reduction of GFAP expression, a protein that is upregulated in many cases of cerebral damage, infection and diseases.…”

Section: Discussionmentioning

confidence: 89%

Effects of cadmium on the glial architecture in lizard brain

et al. 2017

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The glial cells are positioned to be the first cells of the brain parenchyma to face molecules crossing the blood-brain barrier with a relevant neuroprotective role from cytotoxic action of heavy metals on the nervous system. Cadmium is a highly toxic metal and its levels in the environment are increasing due to industrial activities. This element can pass the blood-brain barrier and have neurotoxic activity. For this reason we have studied the effects of cadmium on the glial architecture in the lizard Podarcis siculus, a significant bioindicator of chemical exposure due to its persistence in a variety of habitats. The study was performed on two groups of lizards. The first group of P. siculus was exposed to an acute treatment by a single i.p. injection (2 mg/kg-BW) of CdCl2 and sacrificed after 2, 7 and 16 days. The second one was used as control. The histology of the brain was studied by Hematoxylin/Eosin and Cresyl/Violet stains while the glial structures were analyzed by immunodetection of the glial fibrillary acidic protein (GFAP), the most widely accepted marker for astroglial cells. Evident morphological alterations of the brain were observed at 7 and 16 days from the injection, when we revealed also a decrease of the GFAP-immunopositive structures in particular in the rhombencephalic ventricle, telencephalon and optic tectum. These results show that in the lizards an acute exposure to cadmium provokes morphological cellular alterations in the brain but also a decrement of the expression of GFAP marker with possible consequent damage of glial cells functions.

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“…It has been earlier shown that the concentration of MT is generally down-regulated [11 -13] and that of GFAP is up-regulated [2,31,32] under various harmful conditions, while under those same conditions, changes in vimentin and GFAP levels are simultaneous [2]. All of these are changes that occur under the processes of the major pathological role played by astrocytes in the brain and spinal cord [2].…”

Section: Resultsmentioning

confidence: 99%

Corvitin restores metallothionein and glial fibrillary acidic protein levels in rat brain affected by pituitrin-izadrin

Shiyntum¹,

Dovban²,

Kovalchuk³

et al. 2017

Ukr.Biochem.J.

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In this research, we investigated the effect of pituitrin-izadrin induced injury on the levels of metallothionein (MT) and soluble and filament forms of glial fibrillary acidic protein (GFAP) in the hippocampusA strocytes are amongst the earliest and prominent to express changes under attacks [1]. They are the most numerous nonneuronal cell types in the central nervous system (CNS) and make up about 50% of the volume of the human brain [1,2]. Their functions are known to be critical, such as scavenge transmitters released during synaptic activity, control ion and water homeostasis, release neurotrophic factors, shuttle metabolite, and waste products, and to participate in the formation of the blood-brain-barrier [3,4]. Failure of any of these supportive functions of astrocytes will constitute a threat to neuronal survival. Astrocytes are home to a number of essential proteins of the CNS, including metallothionein and glial fibrillary acidic protein, which presumably carry out some astrocyte functions.Metallothioneins (MTs) are cysteine-rich, low molecular weight, heat stable proteins firstly described by Margoshes [5]. They are largely synthesized in the liver and the kidney in humans but are found at a number of other sites. In the CNS, MT-I and MT-II are conspicuously absent from neuronal populations, yet abundant in fibrous and protoplasmic astrocytes. MT is detectable in the extracellular fluid of the injured brain and astrocytes are capable of secreting MT in a regulatable manner [6].MTs have been implicated as regulatory molecules in gene expression, homeostatic control of cellular metabolism of metals, and cellular adaptation to stress. Thus, they fulfill a regulatory capacity and influence transcription, replication, protein synthesis, metabolism, as well as other zinc-dependent biological processes [7]. It has been shown that the ability of animals to recover from CNS injuries or degenerative diseases depends on the deficiency or excess availability of MT-I/-II [7][8][9][10][11]. MT has equally been demonstrated to be down-regulated in cases of induced intoxication [12] and infection [13] but its correlated effect to other astrocyte proteins has yet to be tested.GFAP is expressed in mature astrocytes in the CNS [14]. It is a member of the family of cytoskeletal proteins and is the primary intermediate filament with a size of 8-9 nm, highly specific to the CNS. However, it has been found outside the CNS in relatively low amounts [15]. It has two physicochemical GFAP forms: water-soluble (sGFAP) and filament (fGFAP) [16]. The sGFAP is unevenly distributed in various brain regions, with the maximum con-

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Distribution of glial fibrillary acidic protein in different parts of the rat brain under cadmium exposure

Cited by 5 publications

References 19 publications

Neuroprotective Effects of Tea Against Cadmium Toxicity

Neuroprotective Effects of Tea Against Cadmium Toxicity

Effects of cadmium on the glial architecture in lizard brain

Corvitin restores metallothionein and glial fibrillary acidic protein levels in rat brain affected by pituitrin-izadrin

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