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INTERNATIONAL JOURNAL OF PHARMACEUTICAL RESEARCH

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IJPR included in UGC-Approved List of Journals - Ref. No. is SL. No. 4812 & J. No. 63703

Published by : Advanced Scientific Research
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0975-2366
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IJPR 9[3] July - September 2017 Special Issue

July - September 9[3] 2017

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Early Effects of Diethylnitrosamine Contributes to Hepatocarcinogenesis

Author: UPLOADED BY-ADMIN, OMAR M. M. MOHAFEZ, MEKKY M. M. ABOUZIED
Abstract: Diethylnitrosoamine (DENA) present in many products is one of the etiological factors responsible for induction of Hepatocellular carcinoma. In this study, we injected rats with a single dose of DENA at a dose of 90 mg/kg. Rats were sacrificed after 2, 4 and 6 days. RT-PCR was used to invistigate inositol requiring enzyme-1 (IRE-1), caspase-3, glutathione reductase (GR) and TNF-a mRNA expression. We found overexpression of the endoplasmic reticulum stress sensor, IRE-1, and glutathione reductase soon after the DENA injection. Conversely, there was a gradual decrease in the level of glutathione in liver homogenates of treated animals. Moreover, The prolonged activation of the unfolded protein response (UPR) led to an apoptotic cell death, that was manifested by a gradual increase in mRNA levels of the apoptotic marker, caspase-3, and the inflammatory cytokine TNF-a starting from day four of DENA administration. On the other hand, the gradually increasing levels of thiobarbituric acid reactive substance (TBARS) and alanine transamination point at prolonged activation of UPR and liver cell injury. In consistence with the biochemical parameters, the histopathological examination showed parenchymal cell damage as indicated by numerous necrotic hepatocytes with altered nuclei and eosinophilic cytoplasm. The results indicate that ER stress is the first manifestation of DENA administration followed by apoptosis and inflammation. These events can be considered as early steps responsible for initiation and promotion of hepatocarcinogenesis.
Keyword: hepatocarcinogenesis, endoplasmic reticulum, apoptosis, inflammation, TNF-a, and caspase-3
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