Biofabricated zinc oxide nanoparticles impair cognitive function via modulating oxidative stress and acetylcholinesterase level in mice

Abstract

Current work was designed to explore the effect of ZnO nanoparticles (ZnONP) biofabricated by using Trianthema portulacastrum (TP) leaves extract on mice brain hippocampus. ZnO nanoparticles of TP leaves (ZnOTP) were synthesized by co‐precipitation method and further characterized by using various techniques such as UV‐Vis spectrophotometer, Field Emission Scanning Electron Microscopy (FESEM), Fourier Transform Infrared (FTIR), and Energy Dispersive X‐ray (EDX). ZnOTP were evaluated for in vitro antioxidant activity, in vivo behavior models (for assessment of cognitive ability), acetylcholinesterase (AChE) activity along with other neurotransmitters content determination, estimation of various oxidative stress parameters and analysis of zinc content in the brain as well as plasma. Histopathological evaluation of the brain hippocampus of each group was performed to corroborate the statistical results. Spherical ZnOTP of 10 to 20 nm size embedded with different phytoconstituents of TP was confirmed. Results of our study revealed a significant memory deficit in mice treated with ZnOTP. Neuronal degeneration was also observed via a significant increase in AChE activity and oxidative stress levels in the brain of mice administered with ZnOTP. Exposure of ZnOTP was also found responsible for modulation of neurotransmission in hippocampus area. Further, ZnOTP disturbed the zinc homeostasis in hippocampus via elevation of zinc content in brain as well as plasma. Histopathology of hippocampus supported the damaging impact of ZnOTP by an increase in vacuolated cytoplasm and focal gliosis in groups treated with ZnOTP. Results demonstrated the neurotoxic effect of ZnOTP on brain hippocampus via cognitive impairment by alteration of neurotransmitter level, zinc content and oxidative stress.

Environmental Nanoparticles Reach Human Fetal Brains

“…There is a deep concern regarding uterine environmental exposures, the developmental origins of disease, and the fetal programming model predicting lifelong consequences from early intrauterine and/or postnatal exposures to insults significant in length, cumulative doses, and properties favoring specific cell damage [ 19 , 20 , 21 , 22 , 23 , 24 , 25 , 26 , 27 ]. Experimentally, NPs cause fetal developmental toxicity, and the early stages of brain organogenesis are highly vulnerable to reactive oxygen species (ROS); ultrastructural alterations in mitochondria, endoplasmic reticulum (ER), and Golgi complexes; downregulation of neuronal glutamate transporters; and, ultimately, the impairment of cognition and alterations in animal behavior [ 23 , 24 , 25 , 26 , 27 , 28 , 29 , 30 ]. The early development of the radial microvasculature in the telencephalon cortical plate (CP) and the correct micro vessel formation are the basis for the later perivascular glia coverage formation and endothelial barrier maturation critical for setting up the brain–blood barrier (BBB) [ 31 , 32 , 33 , 34 ].…”