Effect of Nanosilver Particles on Procaspase-3 Expression in Newborn Rat Brain


Mostafa Ganjuri, M.Sc, 1Jamal Moshtaghian, Ph.D, 1,*Kamran Ghaedi, Ph.D, 1,2,*
Department of Biology, School of Sciences, University of Isfahan, Isfahan, Iran
Department of Cellular Biotechnology, Cell Science Research Center, Royan Institute for Biotechnology, ACECR, Isfahan, Iran
Department of Biology, School of Sciences, University of Isfahan, Isfahan, Iran
Department of Cellular Biotechnology, Cell Science Research Center, Royan Institute for Biotechnology, ACECR, Isfahan, Iran
*Corresponding Address: P.O.Box: 81746-73441 Department of Biology School of Sciences University of Isfahan Hezarjarib Avenue Isfahan Iran Emails:jmoshtaghian@sci.ui.ac.ir,kamranghaedi@sci.ui.ac.ir
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Abstract

Objective

Nanotechnology focuses on materials having at least one dimension of less than 100 nanometers. Nanomaterials such as Nanosilver (NS) have unique physical and chemical properties such as size, shape, surface charge. NS particles are thought to in- duce neuronal degeneration and necrosis in the brain. It has been reported that NS parti- cles generate free radicals and oxidative stress which alters gene expression and induces apoptosis. This study was designed to evaluate whether the detrimental effect of NS parti- cles is through the activation of Procaspase-3 during fetal neural development.

Materials and Methods

In this experimental study, thirty Wistar female rats at day one of pregnancy were semi-randomly distributed into three groups of ten. Group 1, the control group, had no treatment. From day 1 to the end of pregnancy, groups 2 and 3 received 1 and 10 ppm NS respectively via drinking water. Newborn rats were sacrificed immediately after birth and their brains were dissected and kept frozen. Total RNA, extracted from brain homogenates, was reverse transcribed to cDNA. Quantitative real-time polymerase chain reaction (PCR) analysis was undertaken to estimate the expression level of Procaspase-3.

Results

Developmental exposure to NS induced neurotoxicity and apoptosis. This corre- lated with a significant increase in Procaspase-3 expression level especially at 10 ppm NS.

Conclusion

The pro-apoptotic activity of NS in cells is likely to due to the dysregula- tion of Procaspase-3.