Abstract
Hepatic fibrosis occurs after many years of iron overload in liver. An effective iron deposition model induced by ferric nitrilotriacetate (FeNTA) in cultured rat hepatocytes was assumed. It has been shown that treatment of rat hepatocytes with FeNTA lead to oxidative stress and hepatocyte apoptosis. Hepatocyte apoptosis can promote liver fibrosis. The mechanisms of hepatocyte apoptosis induced by FeNTA have not yet been fully elucidated. The present study demonstrated that FeNTA-induced hepatocyte apoptosis was related to Bax translocation, cytochrome c release, and caspase-3 activation.
Publication types
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Comparative Study
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Apoptosis / drug effects*
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Blotting, Western
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Caspase 3
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Caspases / metabolism
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Colorimetry
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Cytochromes c / metabolism
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Enzyme Activation / drug effects
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Ferric Compounds / toxicity*
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Fluoresceins
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Hepatocytes / drug effects
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Hepatocytes / metabolism*
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Indoles
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Male
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Models, Biological
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Nitrilotriacetic Acid / analogs & derivatives*
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Nitrilotriacetic Acid / toxicity*
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Protein Transport / drug effects
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Proto-Oncogene Proteins c-bcl-2 / metabolism*
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Rats
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Rats, Wistar
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Reactive Oxygen Species / metabolism
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bcl-2-Associated X Protein
Substances
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Bax protein, rat
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Ferric Compounds
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Fluoresceins
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Indoles
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Proto-Oncogene Proteins c-bcl-2
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Reactive Oxygen Species
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bcl-2-Associated X Protein
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diacetyldichlorofluorescein
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DAPI
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Cytochromes c
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Casp3 protein, rat
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Caspase 3
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Caspases
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Nitrilotriacetic Acid
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ferric nitrilotriacetate