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Long-term oral administration of melatonin does not improve beta-amyloid deposition, caspase 3, and SOD2 levels in 3 aluminum-treated Tg2576 mice 

Celeste Di Paolo, Jordi Blanco, Maria Cabré, Tania García, Mercedes Gómez, and Jose L. Domingo

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Volume 35 (2018) p. 20 - 31

Abstract

Trace Elements and Electrolytes, Vol. 35 – No. 1/2018 (20-31)

Long-term oral administration of melatonin does not improve beta-amyloid deposition, caspase 3, and SOD2 levels in 3 aluminum-treated Tg2576 mice 

Celeste Di Paolo¹, Jordi Blanco², Maria Cabré³, Tania García¹#³, Mercedes Gómez¹#³, and Jose L. Domingo¹

¹Laboratory of Toxicology and Environmental Health, ²Physiology Unit, and ³Biochemistry Unit, School of Medicine, IISPV, Universitat Rovira i Virgili, Reus, Catalonia, Spain
Objective: Alzheimer’s disease (AD) is characterized by the production and deposition of amyloid-β peptide (Aβ) and neurofibrillary degeneration. It has been demonstrated that aluminum (Al) may be considered as a risk factor for developing the disease, while it is well established that Aβ induces oxidative stress, neurotoxicity and apoptosis. On the other hand, melatonin is a potent antioxidant whose levels are reduced in patients of AD in relation with the progression of the disease. Therefore, restoring the suitable melatonin levels could be considered a good strategy against AD. Materials and methods: The quantity of soluble and insoluble Aβ (Aβ1-40 and Aβ1-42, respectively), the main pro-apoptotic caspase (caspase-3), and the anti-apoptotic SOD2 protein levels in cortex and hippocampus of Tg2576 mice were evaluated. Animals were chronically exposed to Al and melatonin from diet and drinking water, respectively. Results: The quantity of Aβ40 was higher than the quantity of Aβ42 in brain tissues. However, no significant differences between groups were found. Regarding Casp-3 and SOD2, an interaction “genotype × treatment” was found in both tissues tested, but no significant differences between groups of treatment were noted. Conclusion: The results of the present study did not corroborate the anti-amyloidogenic and anti-apoptotic properties of melatonin. Further studies are required to confirm the tendencies here observed. Correspondence to:
Professor Jose L. Domingo
 Laboratory of Toxicology and Environmental Health
School of Medicine, IISPV, Universitat Rovira i Virgili
Reus, Catalonia, Spain 
Email: [email protected]

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