Argemone Oil and Butter Yellow Induced Toxicity in Hepatic and Extra Hepatic Tissues
|Vivek Mishra1,2*, Manjari Mishra1, Bhushan P Chaudhari1, Raj Khanna2 and Mukul Das1|
|1 CSIR- Indian Institute of Toxicology Research, Council of Scientific and Industrial Research, Lucknow, India|
|2 Department of Biochemistry, University of Lucknow, Lucknow, India|
|Corresponding Author :||Vivek Mishra
CSIR- Indian Institute of Toxicology Research
Council of Scientific and Industrial Research
Post Box#80, Lucknow-226 001, India
E-mail: [email protected]
|Received December 06, 2013; Accepted January 01, 2014; Published February 10, 2014|
|Citation: Mishra V, Mishra M, Chaudhari BP, Khanna R, Das M (2014) Argemone Oil and Butter Yellow Induced Toxicity in Hepatic and Extra Hepatic Tissues. Bioenergetics 3:111. doi:10.4172/2167-7662.1000111|
|Copyright: © 2014 Mishra V, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.|
Objective: The present study was designed to evaluate the toxicological potential of argemone oil (AO) and butter yellow (BY).
Methods: Short term treatment through intraperitoneal administration in hepatic tissue and long term treatment through diet in hepatic and extra hepatic tissues was performed in mice.
Results: Short term study showed that female mice were more prone towards risk associated with liver damage than the males. Further investigations in female mice given AO (1%) and BY (0.06%) through diet for 180 days, showed significant weight loss and increase in liver weight. Phase I and Phase II enzymes, antioxidant enzymes and glutathione content were significantly decreased with concomitant increase in lipid peroxidation (LPO) in AO and BY treated mice. Animal fed with AO and BY showed profuse hyperplasia along with fluid filled spaces and patches of hemorrhage in hepatic tissue. AO treated animals showed tumorigenic growth, while BY treatment caused multiple nodule formation in hepatic tissue. Other organs like heart, lungs, kidney and spleen also showed substantial histopathological changes.
Conclusion: The results suggest that AO and BY treatment may cause oxidative stress and inhibited phase I and II enzymes leading to accumulation of parent compound(s) or their metabolites, which may result in the tumorigenic/toxic responses in hepatic and extra hepatic tissues.