Modulation of <sup>14</sup>C‐labeled glucose metabolism by zinc during aluminium induced neurodegeneration

Singla, Neha; Dhawan, D. K.

doi:10.1002/jnr.23596

Cited by 2 publications

(1 citation statement)

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“…The reactions of the nervous system to aluminum intoxication are quite diverse. Neurotoxicity of aluminum may be accompanied by impaired glucose metabolism, cytoskeleton changes and modulation of signal transduction mechanisms (Singla et al, 2015). The studies in vivo and in vitro have shown that aluminum affects the formation of inositol phosphate.…”

Section: Introductionmentioning

confidence: 99%

Molecular mechanisms of aluminium ions neurotoxicity in brain cells of fish from various pelagic areas

Sukharenko

Samoylova

Nedzvetsky

2017

Regul. Mech. Biosyst.

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Neurotoxic effects of aluminum chloride in higher than usual environment concentration (10 mg/L) were studied in brains of fishes from various pelagic areas, especially in sunfish (Lepomis macrochirus Rafinesque, 1819), roach (Rutilus rutilus Linnaeus, 1758), crucian carp (Carasius carasius Linnaeus, 1758), goby (Neogobius fluviatilis Pallas, 1811). The intensity of oxidative stress and the content of both cytoskeleton protein GFAP and cytosol Ca-binding protein S100β were determined. The differences in oxidative stress data were observed in the liver and brain of fish during 45 days of treatment with aluminum chloride. The data indicated that in the modeling of aluminum intoxication in mature adult fishes the level of oxidative stress was noticeably higher in the brain than in the liver. This index was lower by1.5–2.0 times on average in the liver cells than in the brain. The obtained data evidently demonstrate high sensitivity to aluminum ions in neural tissue cells of fish from various pelagic areas. Chronic intoxication with aluminum ions induced intense astrogliosis in the fish brain. Astrogliosis was determined as result of overexpression of both cytoskeleton and cytosole markers of astrocytes – GFAP and protein S100β (on 75–112% and 67–105% accordingly). Moreover, it was shown that the neurotixic effect of aluminum ions is closely related to metabolism of astroglial intermediate filaments. The results of western blotting showed a considerable increase in the content of the lysis protein products of GFAP with a range of molecular weight from 40–49 kDa. A similar metabolic disturbance was determined for the upregulation protein S100β expression and particularly in the increase in the content of polypeptide fragments of this protein with molecular weight 24–37 kDa. Thus, the obtained results allow one to presume that aluminum ions activate in the fish brain intracellular proteases which have a capacity to destroy the proteins of intermediate filaments. The data presented display the pronounced neurotoxic effect of mobile forms of aluminum on both expression level and the metabolism of molecular markers of astrocytes GFAP and protein S100β. Aluminum ions induce integrated changes, the more important of which are a significant increase in final LPO products, an increase in antioxidant enzyme activity, a reactivation of glial cells in the brain. Integrated determination of the content and polypeptide fragments of specific astrocyte proteins in fishes brains coupled with oxidative stress data may be used as valid biomarkers of toxic pollutant effects in aquatic environments.

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Section: Introductionmentioning

confidence: 99%

Molecular mechanisms of aluminium ions neurotoxicity in brain cells of fish from various pelagic areas

Sukharenko

Samoylova

Nedzvetsky

2017

Regul. Mech. Biosyst.

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Evidence of Zinc in Affording Protection Against X-Ray-Induced Brain Injury in Rats

Sharma

Singla

Dhawan

2017

Biol Trace Elem Res

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In the present world, X-rays have been regarded as one of the most efficient tools in medicine, industry and research. On the contrary, extensive human exposure to these rays is responsible for causing detrimental effects on physiological system. The aim of the present study was to investigate the role of zinc (Zn), if any, in mitigating the adverse effects induced by fractionated X-irradiation on rat brain. Female Sprague-Dawley rats weighing 170-200 g were divided into four different groups viz.: (a) normal control, (b) X-irradiated (21Gy), (c) zinc treated (227 mg/L in drinking water) and (d) X-irradiated + zinc treated. The skulls of animals belonging to groups (b) and (d) were exposed to X-rays in 30 fractions. Each fraction delivered a radiation dose of 70 rads, and rats were exposed to two fractions every day for 15 days, consecutively. X-ray treatment resulted in significant alterations in the neurobehavior, neurotransmitter levels and neuro-histoarchitecture of rats, whereas zinc co-treatment with X-rays resulted in significant improvement in these parameters. X-ray exposure also caused a significant increase in the levels of lipid peroxidation as well as activities of catalase and superoxide dismutase, which however were decreased upon simultaneous Zn treatment. On the contrary, X-ray treatment down-regulated the glutathione system, which were found to be up-regulated by zinc co-treatment. Further, protein expressions of p53 and NF-ҚB were found to be significantly elevated after X-irradiation, which were reversed following Zn supplementation. Hence, Zn seems to be an effective agent in mitigating the detrimental effects caused by exposure to X-rays.

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Modulation of ¹⁴C‐labeled glucose metabolism by zinc during aluminium induced neurodegeneration

Cited by 2 publications

References 76 publications

Molecular mechanisms of aluminium ions neurotoxicity in brain cells of fish from various pelagic areas

Molecular mechanisms of aluminium ions neurotoxicity in brain cells of fish from various pelagic areas

Evidence of Zinc in Affording Protection Against X-Ray-Induced Brain Injury in Rats

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Modulation of 14C‐labeled glucose metabolism by zinc during aluminium induced neurodegeneration

Cited by 2 publications

References 76 publications

Molecular mechanisms of aluminium ions neurotoxicity in brain cells of fish from various pelagic areas

Molecular mechanisms of aluminium ions neurotoxicity in brain cells of fish from various pelagic areas

Evidence of Zinc in Affording Protection Against X-Ray-Induced Brain Injury in Rats

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Modulation of ¹⁴C‐labeled glucose metabolism by zinc during aluminium induced neurodegeneration