Gene Expression and Activity of Some Antioxidant Enzyme in Oxidative Stress Induced by Long-Term Iron Overload in Rat Liver and Kidney.

International Congress of the Molecular Biology Association, İzmir, Türkiye, 10 - 12 Ekim 2014, ss.1, (Özet Bildiri)

Although the trace elements such as iron are vital for various cellular events, excessive intake of iron

causes the production of reactive oxygen species (ROS) [1, 2] that induces hepatoxicity [3] and

nephrotoxicity [4] in living organisms. Since ROS are highly reactive and oxygen-containing

molecules, it has to be neutralized by antioxidant defense system to protect cells against its damage [5,

6, 7]. The present study was designed to examine the effect of long-term iron overload on renal and

hepatic antioxidant system at the enzymatic and molecular level. A reduced glutathione (GSH) level,

which is a marker for oxidative stress, markedly decreased with a long-term iron overload in rat kidney

and liver. While the content of iron in the blood and kidney was not affected, hepatic iron content was

increased by iron toxicity. The gene expression of antioxidant related enzymes was affected by iron

overload. However, the actual effect of long-term iron overload on renal and hepatic antioxidant

system is observed at protein level. The gene expression of antioxidant related enzymes did not

correlate to enzyme activity. Furthermore, the impact of iron on the renal antioxidant system is

different from its effect on the hepatic antioxidant system [8, 9, 10].

Keywords: iron, toxicity, antioxidant enzymes, mRNA expression, enzyme activity.