Hepatic transcriptional analysis in rats treated with Cassia occidentalis seed: Involvement of oxidative stress and impairment in xenobiotic metabolism as a putative mechanism of toxicity

author Gati Krushna Panigrahi, Ashish Yadav, Anuradha Yadav, Kausar M. Ansari, Rajnish K. Chaturvedi, Vipin M. Vashistha, S. Raisuddin, Mukul Das
his workplace 1Food, Drug and Chemical Toxicology Division, Council of Scientific and Industrial Research-Indian Institute of Toxicology Research (CSIR-IITR), Lucknow,Uttar Pradesh, India2Developmental Toxicology Division, CSIR-IITR, Lucknow, Uttar Pradesh, India3Mangla Hospital and Research Centre, Bijnor, Uttar Pradesh, India4Department of Medical Elementology and Toxicology, Jamia Hamdard, New Delhi, India
periodicalToxicology Letters, 2014, Vol.229 (1), pp.273-283
sourceElsevier Journal
key word Cassia occidentalis seed; Children; Oxidative stress; Xenobiotic metabolism; Microarray;
Original abstractAbstract(#br)The present study was undertaken to investigate the effect of Cassia occidentalis (CO) seeds on the transcriptional expression patterns of mRNAs in rat liver by microarray analysis. The results indicated that exposure of CO (0.5%) seeds in diet to rats differentially regulated 60 transcripts belonging to various metabolic pathways including, oxidative stress, xenobiotic metabolism, carbohydrate metabolism, cell cycle, apoptosis etc. The expression of AKT1, CAT, SOD1, CYP1A1, CYP2B1, TGF-β, BAX, CREB1, JNK1 and IL-6 were validated by the qRT-PCR. In addition, involvement of oxidative stress was observed due to marked depletion of glutathione, increase in lipid peroxidation and modulation of antioxidant enzymes in hepatic tissue of rats treated with 0.5–2.0% CO in diet. Furthermore, significant decrease in the levels of Phase 1 (EROD, MROD and PROD) and Phase 2 (QR and GST) enzymes following 0.5–2.0% CO exposure indicates the impairment of xenobiotic metabolism and possible accumulation of toxic ingredients of the seeds in liver. Overall, the study predicts the involvement of multiple pathways and related biomolecules in CO induced hepatotoxicity and the data may be useful in formulating strategies for therapeutic interventions of suspected CO poisoning study cases.
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