Molecular mechanisms of aluminium ions neurotoxicity in brain cells of fish from various pelagic areas
Date
2017Author
Sukharenko, E. V. and Samoylova, I. V. and Nedzvetsky, V. S.
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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 S100 beta 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 S100 beta (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 S100
beta 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 S100 beta. 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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