GST-M1 is transcribed moreso than AKR7A2 in AFB1-exposed human monocytes and lymphocytes. (April 2015)

• Record Type: Journal Article
• Authors: Bahari, Abbas; Mehrzad, Jalil; Mahmoudi, Mahmoud; Bassami, Mohammad Reza; Dehghani, Hesam
• Is Part Of: Journal of immunotoxicology. Volume 12:Number 2(2015)
• Page Start: 194
• Page End: 198
• Publication Date: 2015-04
• Subjects: Immunotoxicology -- Periodicals; Poisons -- Immunology -- Periodicals; Environmental health -- Periodicals; 616.97
• DOI: 10.3109/1547691X.2014.925994
• Languages: English
• ISSNs: 1547-691X

Abstract

<abstract> <title>Abstract</title> <p>Glutathione-S-transferases (GST) and aldo-keto reductases (AKR) are key aflatoxin (AF)-detoxifying enzymes. In this study, the expression of <italic>GST-M1, GST-T1, AKR-7A2</italic>, and <italic>AKR-7A3</italic> genes in human monocytes and lymphocytes was analyzed after <italic>in vitro</italic> exposure to 10 or 100 ng AFB<sub>1</sub>/ml for 2 h. Unlike in pilot studies that showed that all four examined genes were present in HepG2 cells, in lymphocytes and monocytes, only <italic>GST-M1</italic> and <italic>AKR-7A2</italic> were detected. In fact, the induced expression of both <italic>GST-M1</italic> and <italic>AKR-7A2</italic> genes in human monocytes was moreso than that seen in AFB<sub>1</sub>-exposed lymphocytes. In addition, analyses of the effects of the exposures on cell cycle status were performed as, in cells lacking adequate detoxification capacities, it would be expected the cells would arrest at checkpoints in the cell cycle or progress to apoptotic/necrotic states. The results here indicated that only the high dose of AFB<sub>1</sub> led to a change in cell cycle profiles and only in the monocytes (i.e. cells in S phase were significantly reduced). In general, the results here strongly suggest that human immune cell lineages appear to be able to increase their expression of AFB<sub>1</sub>-detoxifying enzymes (albeit to differing degrees) and, as a result, are able to counter potential toxicities from AFB<sub>1</sub> and (likely) its metabolites.</p> </abstract>