Introduction/Objective. Research has demonstrated the toxicant potential of
aluminum, but no therapeutic options have been suggested. The aim of the
study was to investigate the extent of the aluminum-induced toxicity,
evaluated by hematological/biochemical disarrangements, hepcidin
concentration and tissue accumulation after chronic aluminum exposure and to
determine possible protection with Ca2+-channel blockage, verapamil.
Methods. Experimental animals (36 rats) were treated with different doses of
AlCl3 during 8 weeks and after that their blood and tissues were analyzed.
Results. The significant differences, regardless of the aluminum dose
administered, were documented in all evaluated hematological (p < 0.001) and
biochemical parameters (p < 0.001), as well as in aluminum tissue deposition
in liver, kidneys and testicles (p < 0.001), respectively. After verapamil
administration, a significant improvement in some hematological and
biochemical parameters was demonstrated, p < 0.001, as well as the
attenuation of aluminum deposits in liver and testes, p < 0.001. Evaluated
parameters of inflammation and kidney deposition did not show significant
change after verapamil application. Conclusion. The findings indicate that
chronic AlCl3 intoxication, regardless of the dose, results in the
microcytic anemia associated with high hepcidin levels, numerous biochemical
abnormalities and significant aluminum deposition in liver, kidney and
testes and that these effects may be attenuated by verapamil administration.
Overall, the results emphasize the significance of calcium homeostasis
preservation in chronic aluminum exposure and propose possible therapeutic
option.