Novel neuroprotective and hepatoprotective effects of citric acid in acute malathion intoxication
10.1016/j.apjtm.2016.11.005
- Author:
Omar M.E. ABDEL-SALAM
1
;
Eman R. YOUNESS
2
;
Nadia A. MOHAMMED
2
;
Safinaz Ebrahim EL-TOUKHY
2
;
Noha N. YASSEN
3
;
Yasser A. KHADRAWY
4
;
Amany A. SLEEM
5
Author Information
1. Department of Toxicology and Narcotics, National Research Centre
2. Department of Medical Biochemistry, National Research Centre
3. Department of Pathology, National Research Centre
4. Department of Physiology, National Research Centre
5. Department of Pharmacology, National Research Centre
- Publication Type:Journal Article
- Keywords:
Cholinesterase;
Citric acid;
Comet assay;
Malathion;
Oxidative stress;
Paraoxonase 1
- From:
Asian Pacific Journal of Tropical Medicine
2016;9(12):1181-1194
- CountryChina
- Language:Chinese
-
Abstract:
Objective To study the effect of citric acid given alone or combined with atropine on brain oxidative stress, neuronal injury, liver damage, and DNA damage of peripheral blood lymphocytes induced in the rat by acute malathion exposure. Methods Rats were received intraperitoneal (i.p.) injection of malathion 150 mg/kg along with citric acid (200 or 400 mg/kg, orally), atropine (1 mg/kg, i.p.) or citric acid 200 mg/kg + atropine 1 mg/kg and euthanized 4 h later. Results Malathion resulted in increased lipid peroxidation (malondialdehyde) and nitric oxide concentrations accompanied with a decrease in brain reduced glutathione, glutathione peroxidase (GPx) activity, total antioxidant capacity (TAC) and glucose concentrations. Paraoxonase-1, acetylcholinesterase (AChE) and butyrylcholinesterase activities decreased in brain as well. Liver aspartate aminotransferase and alanine aminotransferase activities were raised. The comet assay showed increased DNA damage of peripheral blood lymphocytes. Histological damage and increased expression of inducible nitric oxide synthase (iNOS) were observed in brain and liver. Citric acid resulted in decreased brain lipid peroxidation and nitric oxide. Meanwhile, glutathione, GPx activity, TAC capacity and brain glucose level increased. Brain AChE increased but PON1 and butyrylcholinesterase activities decreased by citric acid. Liver enzymes, the percentage of damaged blood lymphocytes, histopathological alterations and iNOS expression in brain and liver was decreased by citric acid. Meanwhile, rats treated with atropine showed decreased brain MDA, nitrite but increased GPx activity, TAC, AChE and glucose. The drug also decreased DNA damage of peripheral blood lymphocytes, histopathological alterations and iNOS expression in brain and liver. Conclusions The study demonstrates a beneficial effect for citric acid upon brain oxidative stress, neuronal injury, liver and DNA damage due to acute malathion exposure.
