Metal detection in hair as biomarker to monitor the health status in rats

Objectives. Epidemiological indications suggest that the exposure to neurotoxin agents (i.e. pesticide, Cu, Fe, Mn, etc) during pregnancy and early childhood is involved in the neurodevelopmental disorders and subclinical brain dysfunction (1). During early age, when the neurodevelopmental process is the most rapid/intense, individuals may be more susceptible to pollutants, leading to potential effects on the brain even at very low doses. Our previous studies indicated that pup rats treated with the pyrethroid insecticide permethrin, during brain development (from 6th to 21th day of life) develop long term effects leading to a Parkinson-like disease (PD) (2). Methods. Permethrin was administered orally to Wistar rats for 15 days, from PND6 to PND21 and their hair were processed in adult age (150 days). Hair from neck of treated and control groups were analyzed with two different techniques: 1) ICP-MS instrumentation treating samples with closed vessel mineralization in acidic conditions and 2) polarized light microscopy combined with remote sensing and digital camera at high resolution. Results Data on hair of PD animal model show a significant decrease of Se, Hg and Sn, while Cu resulted increased with ICP-MS analysis, while only Hg resulted significantly reduced with the other method. However the polarized light microscopy shows a great potentiality because it permits to screen also aminoacids, vitamins and hormone (i.e. noradrenaline, dopamine and progesterone). Conclusions Considering that Se protects cells from oxidative damage, and the PD animal model presents high level of oxidative stress, the decrease of Se in hair of PD rats can be considered as an useful biomarker indicative for neurodegeneration process. Similarly, Cu results indicative of the disease, because high Cu level is associated with the oligomerization of alpha-synuclein and the copper-alpha-synuclein complex induces changes in copper’s redox properties, since it promotes H2O2 production, which leads to dopamine and GSH oxidation (3). Acknowledgements We thank the “Cassa di Risparmio di Fabriano and Cupramontana Foundation” for grant support. References: 1) Grandjean, P; Landrigan, PJ. Lancet. 2006, 368(9553),2167-2178. 2) Carloni et al., Brain Res. 2013, 7;1515:19-28. 3) Montes S. et al., Oxidative Medicine and Cellular Longevity 2014, ID 147251, 15.