Analysis of Density Changes of Selected Brain Receptors After a 14-Day Supply of Chromium(III) and Evaluation of Chromium(III) Affinity to Selected Receptors and Transporters

Abstract

Chromium(III) is one of the most controversial biometals. Although, it is no longer on the list of minerals necessary for the proper functioning of the human body, and its pharmacological effect is still under discussion. One of the purposes of Cr(III) administration is to use it in patients with mood disorders and it is strictly related to its pharmacological, not dietary effect. This is because its high doses are necessary to obtain the results and additionally, no deficiencies in human population have been noted. In this study, the affinity of chromium(III) to selected receptors and transporters in the rat brain was evaluated, and the effect of the 14-day administration of this metal was assessed on the density of selected receptors. All analyses were performed in vitro using radioligand binding assays, and the results indicated lack of affinity to β 1 and α 1 receptors and serotonin transporter (SERT), furthermore very weak affinity to the 5-HT 1A receptor (30% inhibition at 10 −4 and 10 −5 M). Analysis of the α 1 and β 1 adrenergic receptor density indicated lack of any adaptive effects after 14 days of Cr(III) administration through intraperitoneal injections (doses 6 and 12 mg/kg). The antidepressant activity of chromium(III) indicated in clinical trials concerned patients with atypical, seasonal, or dystonic symptoms. This effect, as it seems based on the presented results, does not depend on direct affinity to serotonin receptors and transporter nor is the result of adaptive changes in the adrenoreceptor system.

Neuroprotective effect of sodium alginate against chromium-induced brain damage in rats

“…Hence, disturbance in 5-HT levels is responsible for many neurological diseases and neuropsychiatric disorders, so it was selected in the current study as a potent neurobiochemical marker. Previous studies proved the high affinity of Cr to bind to the 5-HT 1A receptors, which regulates 5-HT release in neurons via the negative feedback mechanism, affecting postsynaptic events and 5-HT release [ 46 ]. These results are in agreement with our findings and demonstrate that Cr(VI) can be considered as a serotoninergic neurotoxin, as indicated by the significant decrease in the 5-HT levels detected in the Cr-intoxicated group compared to the standard control group.…”