Coenzyme A, acyl-CoA, and the glutathione system in CNS structures exposed to homopantothenate or in aluminum neurotoxicity

Abstract

Calcium homopantothenate (CHP, pantogam, or hopantenic acid) at a dose of 100 μg/kg was injected into white female Wistar rats weighing 180–210 g for 4 weeks. Aluminum chloride (two times at a dose of 190 mg/kg) and D-pantenol (seven times at a dose of 200 mg/kg) were injected to a subgroup of rats during the last 2 weeks of the experiment. CHP did not change the level of coenzyme A (CoA) in the hippocampus, brainstem, and cerebellum, while aluminum neurotoxicity resulted in a decrease in the CoA-SH level in the hippocampus and acyl-CoA level in the cerebellum. A decrease in glutathione level, redox status, and the total amount of glutathione and glutathione peroxidase activity was observed during aluminum neurotoxicity. Both treatments activated glutathione reductase and decreased the activity of glucose-6-phosphate dehydrogenase in the brainstem. These changes were eliminated by pantenol. The latter increased the redox status of CNS proteins in the case of the combination of treatment with CHP and aluminum neurotoxicity.