ArticleMolecular and cellular biochemistry2015
Activation of oxidative stress and inflammatory factors could account for histopathological progression of aflatoxin-B1 induced hepatocarcinogenesis in rat.
Article in Molecular and cellular biochemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 64 citations in OpenAlex.
- Review
- Prenatal Aflatoxin BToxins · 2026Review
- Aflatoxin B1: Challenges and Strategies for the Intestinal Microbiota and Intestinal Health of Monogastric Animals.Toxins · 2025Review
- The Potential Influence of the Presence of Mycotoxins in Human Follicular Fluid on Reproductive Outcomes.Toxins · 2024Article
- Amplified and distinctive genotoxicity of titanium dioxide nanoparticles in transformed yeast reporters with human cytochrome P450 (CYP) genes.Journal of hazardous materials · 2024Article
- Ashwagandha Diminishes Hippocampal Apoptosis Induced by Microwave Radiation by Acetylcholinesterase Dependent Neuro-Inflammatory Pathway in Male Coturnix coturnix Japonica.Neurochemical research · 2024Article
- Novel Insights into Total Flavonoids ofAntioxidants (Basel, Switzerland) · 2022Article
- Riboflavin (Vitamin B2) Deficiency Induces Apoptosis Mediated by Endoplasmic Reticulum Stress and the CHOP Pathway in HepG2 Cells.Nutrients · 2022Article
- Review
- In Vivo and In Vitro Models of Hepatocellular Carcinoma: Current Strategies for Translational Modeling.Cancers · 2021Review
- Environmental Pollutants, Mucosal Barriers, and Pathogen Susceptibility; The Case for Aflatoxin BPathogens (Basel, Switzerland) · 2021Review
- Protective and therapeutic effects of sildenafil and tadalafil on aflatoxin B1-induced hepatocellular carcinoma.Molecular and cellular biochemistry · 2021Article
- Genome Profiling for Aflatoxin BG3 (Bethesda, Md.) · 2020Article
- Risk assessment of aflatoxins in food.EFSA journal. European Food Safety Authority · 2020Article
- Hemoadsorption Improves Survival of Rats Exposed to an Acutely Lethal Dose of Aflatoxin BScientific reports · 2020Article
- Contamination of Aflatoxins Induces Severe Hepatotoxicity Through Multiple Mechanisms.Frontiers in pharmacology · 2020Review
- The effects of astaxanthin on liver histopathology and expression of superoxide dismutase in rat aflatoxicosis.The Journal of veterinary medical science · 2019Article
- Article
- Comparison of the toxic effects of different mycotoxins on porcine and mouse oocyte meiosis.PeerJ · 2018Article
- Hepatic transcriptomic alterations for N,N-dimethyl-p-toluidine (DMPT) and p-toluidine after 5-day exposure in rats.Archives of toxicology · 2017Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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 1 mg AFB1/kg b.w. Histopathologically, hepatocytes necrosis could be observed after 4 weeks of the AFB1 treatment, which subsequently developed into the well-defined foci of altered hepatocytes (FAH) at 10 weeks 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.
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