Research Article | Volume: 7, Issue: 9, September, 2017

Paracetamol Overdose Induces Physiological and Pathological Aberrations in Rat Brain

Amina E. Essawy Afrah F. Alkhuriji Ahmed A. Soffar   

Open Access   

Published:  Sep 30, 2017

DOI: 10.7324/JAPS.2017.70925
Abstract

Paracetamol (Acetaminophen) is one of the most popular over the counter medications that is commonly used as an anti-inflammatory and pain killer, and to relieve fever and headaches. Despite its several therapeutic benefits, it is well known that an overdose of paracetamol can lead to hepatic and renal damage. Considering that brain cells is one of the main targets for paracetamol in the body, the effect of paracetamol on the physiology and histology of the brain is been poorly investigated. Hence, the present work investigates the possible adverse effects of paracetamol on the rat brain. Our results show that an overdose treatment of paracetamol caused significant elevation in the activity of AChE and a remarkable suppression in levels of dopamine and serotonin in treated rats. Also, applying rapid Golgi-cox staining showed that paracetamol induced morphological aberrations and a dramatic reduction in the density of dendritic spines in brain cells. Histological and ultrastructure alterations were also recorded in the neurons of paracetamol-treated rats. In conclusion, we found that an overdose of paracetamol is neurotoxic. The observed alterations point to the possibilities of higher brain impairments which is of strong public health concern.


Keyword:     Paracetamol neurotoxicity neurochemicals histopathology.


Citation:

Amina E Essawy, Afrah F Alkhuriji, Ahmed A Soffar., Paracetamol Overdose Induces Physiological and Pathological Aberrations in Rat Brain. J App Pharm Sci, 2017; 7 (09): 185-190.

Copyright: © The Author(s). This is an open-access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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