• Miroslav Pohanka, Martina Hrabinova, Filip Zemek, Lucie Drtinova, Hana Bandouchova, and Jiri Pikula.
• Faculty of Military Health Sciences, University of Defence, Hradec Kralove, Czech Republic. miroslav.pohanka@gmail.com
• Neuroendocrinol Lett. 2011 Jan 1; 32 Suppl 1: 95-100.

ObjectivesAlzheimer's disease (AD) is a neurodegenerative disorder. Symptomatic treatment is available by inhibitors of acetylcholinesterase (AChE) such as rivastigmine, galantamine and donepezil. As huperzine is a promising compound for AD treatment, our study was aimed at evaluating its pertinent implications in oxidative stress.MethodsLaboratory guinea pigs were exposed to huperzine A at doses of 0, 5, 25, 125 and 625 µg/kg. The animals were observed for cognitive disorders and sacrificed one hour after exposure. Tonic-clonic seizures were noticed, but only in highly dosed animals. Ferric reducing antioxidant power (FRAP), thiobarbituric acid reactive substances (TBARS), glutathione reductase and glutathione S-transferase were assessed in frontal, temporal and parietal lobes, the cerebellum, liver, spleen and kidney.ResultsOnly minimal changes in enzymatic markers were recognized. Huperzine was not implicated in oxidative stress enhancement as the TBARS values remained quite stable. Surprisingly, antioxidants accumulated in the examined brain compartments as the FRAP value was significantly elevated following all doses of huperzine.ConclusionsWe discuss the potency of huperzine in enhancing the antioxidant capacity of the central nervous system. Huperzine is probably implicated in more processes than cholinesterase inhibition only.

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