First report on the electrooxidation of vinpocetine using a modification free sensing platform: application to pharmaceutical formulations.

This study presents the first insights into vinpocetine (VIN) behavior, a nootropic compound, on a glassy carbon electrode (GCE). Cyclic voltammetry (CV) revealed an irreversible oxidation peak at +1.0 V (vs. Ag/AgCl), with pH dependency indicating proton involvement in the electrochemical reaction. Density functional theory (DFT) optimized VIN's molecular geometry, while Fukui functions and dual descriptors elucidated its reactivity for a more straightforward exploration of the complete electrooxidation mechanism. Differential pulse voltammetry (DPV) demonstrated VIN sensing capabilities within a concentration range of 0.20 to 12.8 mg L-1, with a theoretical limit of detection (LOD) at 0.07 mg L-1, using optimized conditions of supporting electrolyte. The method showed selectivity in the presence of excipients and interfering species commonly found in pharmaceutical formulations. Recovery tests yielded 95.5% (n = 3), and quantification in pharmaceutical formulations showed no significant differences compared to the reference method based on HPLC DAD. This novel electroanalytical method holds promise for VIN nootropic sensing and routine pharmaceutical analysis.

Selenofuranoside improves long-term memory deficits in rats after exposure to monosodium glutamate: Involvement of Na+, K+-ATPase activity.

Monosodium glutamate (MSG) is the most widely used additive in the food industry; however, some adverse effects of this additive, including functional, learning, and behavioral alterations, have been observed in experimental animals and humans. Studies have shown learning and memory impairment in adult animals exposed to MSG. However, studies relating exposure to MSG to acetylcholinesterase (AChE) and Na+, K+-ATPase activities and memory damage are still scarce in the literature. The aim of the present study was to assess the possible protective effects of selenofuranoside, an organoselenium compound, against the impairment of long-term memory, Na+, K+-ATPase and AChE activities, and oxidative stress after MSG exposure in rats. MSG (2g/kg) and/or selenofuranoside (5mg/kg) were administered orally to 5-week-old male Wistar rats for 10days. On the 10th day, after the administration of last dose of the drug(s), the rats were subjected to behavioral tests: the open-field test and step-down passive avoidance task (SDPA). The blood, liver, kidney, cortex, and hippocampus were removed to determine the oxidative stress parameters, such as the levels of reactive species, lipid peroxidation, antioxidant enzyme activities, and endogenous nonenzymatic antioxidant content. Furthermore, the cortex and hippocampus were used to determine the Na+, K+-ATPase and AChE activities. The results demonstrate that the administration of MSG led to long-term memory impairment, as shown in the SDPA task, and also hippocampal and cortical Na+, K+-ATPase inhibition. There were no alterations in the AChE activity and oxidative stress parameters. Treatment with selenofuranoside attenuated memory impairment associated with MSG exposure by improving the hippocampal Na+, K+-ATPase activity.