Chlorpyrifos-induced parkinsonian model in mice: Behavior, histopathology and biochemistry.
Pestic Biochem Physiol. 2018 Jan ;144:36-41. Epub 2017 Nov 10. PMID: 29463406
Haci Ahmet Deveci
INTRODUCTION: The aim of this study was to investigate the protective effect of caffeic acid phenethyl ester (CAPE) on Paraoxonase (PON1) activity, and levels of lipid profile, total sialic acid (TSA), total antioxidant capacity (TAC) and total oxidant capacity (TOC) in the plasma and brain tissue of mice with chlorpyrifos-ethyl (CPF)-induced Parkinson.
MATERIAL AND METHOD: In the study, 35 male Swiss albino mice were divided into 5 groups including equal number of mice as follows; intraperitoneal injection of saline for mice in control (C) group, subcutaneous injection of 80mg/kg CPF for CPF group, intraperitoneal injection of 10μmol/kg CAPE for CAPE group, subcutaneous injection of 80mg/kg CPF and intraperitoneal injection of 10μmol/kg CAPE for CPF+CAPE group and intraperitoneal injection of 10% ethanol diluted in physiological saline solution for 21days for ethanol (E) group. All the mice were fed with normal feed and tap water ad libitum. At the end of the study, PON1 activity, lipid profile (except for brain), and TSA, TAC and TOC levels in the plasma and brain tissue were analyzed. Tissue samples of brain substantia nigra were evaluated histopathologically.
RESULTS: Levels of plasma TAC, high density lipoprotein (HDL) and PON1 activity were statistically lower in CPF group than the other groups (P<0.001). Also, levels of plasma TOC, TSA, total cholesterol, triglycerides, low density lipoprotein (LDL) and very low density lipoprotein (VLDL) were statistically higher in CPF group than the other groups(P<0.001). PON1 activity and level of TAC were significantly lower in brain tissue of CPF groups (P<0.001). In addition, TOC and TSA levels were significantly higher in brain tissue in CPF group (P<0.001).
CONCLUSION: In conclusion, CAPE showed a protective effect on PON1 activity and levels of lipid profile, TSA, TAC and TOC in plasma and brain tissue and prevented the neurodegenerations in brain tissue in CPF-induced Parkinson's disease.