caa a22 4500 606237054 CHVBK 20210128101251.0 cr unu---uuuuu 210128e20150301xx s 000 0 eng 10.1007/s11010-014-2306-x doi (NATIONALLICENCE)springer-10.1007/s11010-014-2306-x Activation of oxidative stress and inflammatory factors could account for histopathological progression of aflatoxin-B1 induced hepatocarcinogenesis in rat [Elektronische Daten] [Krishna Singh, Brajesh Maurya, Surendra Trigun] Aflatoxin-B1 (AFB1) intoxication is known to develop hepatocellular carcinoma (HCC). However, pathogenesis and diagnosis of AFB1-induced HCC remain undefined. This article describes histopathological progression versus kinetics of the placental glutathione S-transferase (GST-pi) expression and profiles of the antioxidant enzymes, pro-inflammatory cytokines, and proliferative cell nuclear antigen (PCNA) in the liver from the rats administered with two doses of 1mg AFB1/kg b.w. Histopathologically, hepatocytes necrosis could be observed after 4weeks of the AFB1 treatment, which subsequently developed into the well-defined foci of altered hepatocytes (FAH) at 10weeks post-treatment stage. This was consistent with an increasing trend of GST-pi immunostaining especially in the liver foci as a function of FAH progression and thus, suggesting that GST-pi over expression may serve as a marker for AFB1-induced hepatocarcinogenesis. The liver from AFB1-treated rats showed significantly enhanced level of reactive oxygen species coinciding with the declined immunostaining for superoxide dismutase-1, a committed enzyme of the antioxidant pathway, in the FAH regions and also with declined activity of the other antioxidant enzymes. Concordantly, the liver from the AFB1-treated rats showed over expression of pro-inflammatory cytokines; TNF-α & IL-1α and a cell proliferative marker PCNA. These findings present histological characterization of AFB1-induced HCC development and provide evidence for activation of oxidative stress-pro-inflammatory pathway during hepatocarcinogenesis induced by AFB1 toxicity. Springer Science+Business Media New York, 2014 Hepatocarcinogenesis nationallicence Aflatoxin-B1 nationallicence Antioxidant enzymes nationallicence SOD1 nationallicence TNF-α nationallicence PCNA nationallicence Singh Krishna Biochemistry Section, Centre of Advanced Study in Zoology, Banaras Hindu University, 221005, Varanasi, India aut Maurya Brajesh Biochemistry Section, Centre of Advanced Study in Zoology, Banaras Hindu University, 221005, Varanasi, India aut Trigun Surendra Biochemistry Section, Centre of Advanced Study in Zoology, Banaras Hindu University, 221005, Varanasi, India aut Molecular and Cellular Biochemistry Springer US; http://www.springer-ny.com 401/1-2(2015-03-01), 185-196 0300-8177 401:1-2<185 2015 401 11010 https://doi.org/10.1007/s11010-014-2306-x text/html Onlinezugriff via DOI BK010053 XK010053 XK010000 Metadata rights reserved Springer special CC-BY-NC licence nationallicence 1 research-article jats NATIONALLICENCE NATIONALLICENCE NL-springer NATIONALLICENCE 856 40 https://doi.org/10.1007/s11010-014-2306-x text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Singh Krishna Biochemistry Section, Centre of Advanced Study in Zoology, Banaras Hindu University, 221005, Varanasi, India aut NATIONALLICENCE 700 1- Maurya Brajesh Biochemistry Section, Centre of Advanced Study in Zoology, Banaras Hindu University, 221005, Varanasi, India aut NATIONALLICENCE 700 1- Trigun Surendra Biochemistry Section, Centre of Advanced Study in Zoology, Banaras Hindu University, 221005, Varanasi, India aut NATIONALLICENCE 773 0- Molecular and Cellular Biochemistry Springer US; http://www.springer-ny.com 401/1-2(2015-03-01), 185-196 0300-8177 401:1-2<185 2015 401 11010