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Accumulation Patterns of Sub-chronic Aluminum Toxicity Model After Gastrointestinal Administration in Rats. / Drobyshev, Evgenii J.; Solovyev, Nikolay D.; Gorokhovskiy, Boris M.; Kashuro, Vadim A.

In: Biological Trace Element Research, Vol. 185, No. 2, 10.2018, p. 384-394.

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Drobyshev, Evgenii J. ; Solovyev, Nikolay D. ; Gorokhovskiy, Boris M. ; Kashuro, Vadim A. / Accumulation Patterns of Sub-chronic Aluminum Toxicity Model After Gastrointestinal Administration in Rats. In: Biological Trace Element Research. 2018 ; Vol. 185, No. 2. pp. 384-394.

BibTeX

@article{478887cc809d43b4b4e34709a5ed6126,
title = "Accumulation Patterns of Sub-chronic Aluminum Toxicity Model After Gastrointestinal Administration in Rats",
abstract = "Although aluminum chronic neurotoxicity is well documented, there are no well-established experimental protocols of Al exposure. In the current study, toxic effects of sub-chronic Al exposure have been evaluated in outbreed male rats (gastrointestinal administration). Forty animals were used: 10 were administered with AlCl3 water solution (2 mg/kg Al per day) for 1 month, 10 received the same concentration of AlCl3 for 3 month, and 20 (10 per observation period) saline as control. After 30 and 90 days, the animals underwent behavioral tests: open field, passive avoidance, extrapolation escape task, and grip strength. At the end of the study, the blood, liver, kidney, and brain were excised for analytical and morphological studies. The Al content was measured by inductively coupled plasma mass-spectrometry. Essential trace elements—Co, Cr, Cu, Fe, Mg, Mn, Mo, Se, and Zn—were measured in whole blood samples. Although no morphological changes were observed in the brain, liver, or kidney for both exposure terms, dose-dependent Al accumulation and behavioral differences (increased locomotor activity after 30 days) between treatment and control groups were indicated. Moreover, for 30 days exposure, strong positive correlation between Al content in the brain and blood for individual animals was established, which surprisingly disappeared by the third month. This may indicate neural barrier adaptation to the Al exposure or the saturation of Al transport into the brain. Notably, we could not see a clear neurodegeneration process after rather prolonged sub-chronic Al exposure, so probably longer exposure periods are required.",
keywords = "Aluminum, Neurotoxicity, Per oral administration, Rats, Sub-chronic exposure, Trace elements, INDUCED ALZHEIMERS-DISEASE, FREQUENCY MODULATION POLARIZATION, OXIDATIVE STRESS, TRACE-ELEMENTS, PLASMA-MASS SPECTROMETRY, IN-VIVO, RENAL-FAILURE, DIALYSIS ENCEPHALOPATHY, INDUCED NEUROTOXICITY, BLOOD",
author = "Drobyshev, {Evgenii J.} and Solovyev, {Nikolay D.} and Gorokhovskiy, {Boris M.} and Kashuro, {Vadim A.}",
year = "2018",
month = oct,
doi = "10.1007/s12011-018-1247-8",
language = "English",
volume = "185",
pages = "384--394",
journal = "Biological Trace Element Research",
issn = "0163-4984",
publisher = "Humana Press",
number = "2",

}

RIS

TY - JOUR

T1 - Accumulation Patterns of Sub-chronic Aluminum Toxicity Model After Gastrointestinal Administration in Rats

AU - Drobyshev, Evgenii J.

AU - Solovyev, Nikolay D.

AU - Gorokhovskiy, Boris M.

AU - Kashuro, Vadim A.

PY - 2018/10

Y1 - 2018/10

N2 - Although aluminum chronic neurotoxicity is well documented, there are no well-established experimental protocols of Al exposure. In the current study, toxic effects of sub-chronic Al exposure have been evaluated in outbreed male rats (gastrointestinal administration). Forty animals were used: 10 were administered with AlCl3 water solution (2 mg/kg Al per day) for 1 month, 10 received the same concentration of AlCl3 for 3 month, and 20 (10 per observation period) saline as control. After 30 and 90 days, the animals underwent behavioral tests: open field, passive avoidance, extrapolation escape task, and grip strength. At the end of the study, the blood, liver, kidney, and brain were excised for analytical and morphological studies. The Al content was measured by inductively coupled plasma mass-spectrometry. Essential trace elements—Co, Cr, Cu, Fe, Mg, Mn, Mo, Se, and Zn—were measured in whole blood samples. Although no morphological changes were observed in the brain, liver, or kidney for both exposure terms, dose-dependent Al accumulation and behavioral differences (increased locomotor activity after 30 days) between treatment and control groups were indicated. Moreover, for 30 days exposure, strong positive correlation between Al content in the brain and blood for individual animals was established, which surprisingly disappeared by the third month. This may indicate neural barrier adaptation to the Al exposure or the saturation of Al transport into the brain. Notably, we could not see a clear neurodegeneration process after rather prolonged sub-chronic Al exposure, so probably longer exposure periods are required.

AB - Although aluminum chronic neurotoxicity is well documented, there are no well-established experimental protocols of Al exposure. In the current study, toxic effects of sub-chronic Al exposure have been evaluated in outbreed male rats (gastrointestinal administration). Forty animals were used: 10 were administered with AlCl3 water solution (2 mg/kg Al per day) for 1 month, 10 received the same concentration of AlCl3 for 3 month, and 20 (10 per observation period) saline as control. After 30 and 90 days, the animals underwent behavioral tests: open field, passive avoidance, extrapolation escape task, and grip strength. At the end of the study, the blood, liver, kidney, and brain were excised for analytical and morphological studies. The Al content was measured by inductively coupled plasma mass-spectrometry. Essential trace elements—Co, Cr, Cu, Fe, Mg, Mn, Mo, Se, and Zn—were measured in whole blood samples. Although no morphological changes were observed in the brain, liver, or kidney for both exposure terms, dose-dependent Al accumulation and behavioral differences (increased locomotor activity after 30 days) between treatment and control groups were indicated. Moreover, for 30 days exposure, strong positive correlation between Al content in the brain and blood for individual animals was established, which surprisingly disappeared by the third month. This may indicate neural barrier adaptation to the Al exposure or the saturation of Al transport into the brain. Notably, we could not see a clear neurodegeneration process after rather prolonged sub-chronic Al exposure, so probably longer exposure periods are required.

KW - Aluminum

KW - Neurotoxicity

KW - Per oral administration

KW - Rats

KW - Sub-chronic exposure

KW - Trace elements

KW - INDUCED ALZHEIMERS-DISEASE

KW - FREQUENCY MODULATION POLARIZATION

KW - OXIDATIVE STRESS

KW - TRACE-ELEMENTS

KW - PLASMA-MASS SPECTROMETRY

KW - IN-VIVO

KW - RENAL-FAILURE

KW - DIALYSIS ENCEPHALOPATHY

KW - INDUCED NEUROTOXICITY

KW - BLOOD

UR - http://www.scopus.com/inward/record.url?scp=85041895555&partnerID=8YFLogxK

UR - http://www.mendeley.com/research/accumulation-patterns-subchronic-aluminum-toxicity-model-after-gastrointestinal-administration-rats

U2 - 10.1007/s12011-018-1247-8

DO - 10.1007/s12011-018-1247-8

M3 - Article

AN - SCOPUS:85041895555

VL - 185

SP - 384

EP - 394

JO - Biological Trace Element Research

JF - Biological Trace Element Research

SN - 0163-4984

IS - 2

ER -

ID: 23856040