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Melatonin, a pineal secretory product, and its precursors, tryptophan and serotonin, were examined for their metal binding affinities for both essential and toxic metals: aluminium, cadmium, copper, iron, lead, and zinc. An electrochemical technique, adsorptive stripping voltammetry, showed the varying abilities of melatonin and its precursors to bind the metals in situ. The results show that the following metal complexes were formed: aluminium with melatonin, tryptophan, and serotonin; cadmium with melatonin and tryptophan; copper with melatonin and serotonin; iron(III) with melatonin and serotonin; lead with melatonin, tryptophan, and serotonin; and zinc with melatonin and tryptophan. Iron(II) showed the formation of an in situ complex with tryptophan only. These studies suggest a further role for melatonin in the reduction of free radical generation and metal detoxification, and they may explain the accumulation of aluminium in Alzheimer's disease.

Research demonstrates that antioxidants and metal chelators may be of beneficial use in the treatment of neurodegenerative diseases, such as Alzheimer's disease (AD). This study investigated the antioxidant and metal-binding properties of curcumin, capsaicin, and S-allylcysteine, which are major components found in commonly used dietary spice ingredients turmeric, chilli, and garlic, respectively. The DPPH assay demonstrates that these compounds readily scavenge free radicals. These compounds significantly curtail iron- (Fe2+) and quinolinic acid (QA)-induced lipid peroxidation and potently scavenge the superoxide anion generated by 1 mM cyanide in rat brain homogenate. The ferrozine assay was used to measure the extent of Fe2+ chelation, and electrochemistry was employed to measure the Fe3+ binding activity of curcumin, capsaicin, and S-allylcysteine. Both assays demonstrate that these compounds bind Fe2+ and Fe3+ and prevent the redox cycling of iron, suggesting that this may be an additional method through which these agents reduce Fe2+-induced lipid peroxidation. This study demonstrates the antioxidant and metal-binding properties of these spice ingredients, and it is hereby postulate that these compounds have important implications in the prevention or treatment of neurodegenerative diseases such as AD.

This study investigated the neuroprotective effects of the curcuminoids against lead-induced neurotoxicity. The results show that lead significantly increases lipid peroxidation and reduces the viability of primary hippocampal neurons in culture. This lead-induced toxicity was significantly curtailed by the co-incubation of the neurons with the curcuminoids. In a whole animal experiment, rats were trained in a water maze and thereafter dosed with lead and/or curcumin (CURC), demethoxycurcumin (DMC), or bisdemethoxycurcumin (BDMC) for 5 days. Animals treated with curcumin and demethoxycurcumin but not bisdemethoxycurcumin had more glutathione and less oxidized proteins in the hippocampus than those treated with lead alone. These animals also had faster escape latencies when compared to the Pb-treated animals indicating that CURC- and DMC-treated animals retain the spatial reference memory. The findings of this study indicate that curcumin, a well-established dietary antioxidant, is capable of playing a major role against heavy metal-induced neurotoxicity and has neuroprotective properties.