Iron Overload-Induced Hepatotoxicity: An Overview

Document Type : Original Article

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Abstract

Iron is an important vital micronutrient; nevertheless, iron excess may induce cellular
toxicity via mediating reactive oxygen species generation, ensuing in oxidative stress and
harm to various organs, including the liver, kidney, heart, and others. Iron overload, also
called hemochromatosis, is the most severe manifestation of excessive iron accumulation
that can occur despite the body's regulatory processes and results in a systemic buildup of
iron in the body leading to many adverse effects. Several factors can contribute in including
consuming significant amounts of additional iron, iron loading anaemias, frequent blood
transfusions, and some genetic mutations. Liver is particularly at risk of the damaging
consequences of iron overload due to the fact it's the primary site for storing iron. However,
when the liver's iron storage and anti-oxidant capacity is surpassed, iron overload can
result in oxidant-mediated hepatotoxicity. Iron is 'kept safe' in health by a regular balance
of iron absorption, transport, storage, and use. Further, efficient regulation of systemic iron
homeostasis, along with the effective antioxidant systems, is essential to prevent the
harmful effects of excessive ROS generation and oxidative damage. Consequently, a
thorough understanding of iron metabolism, mechanisms of iron overload-induced toxicity
concomitantly with characterization the optimal methods of assessment and monitoring its
adverse effects is crucial for preventing iron-related disorders and for employing successful
treatment and control. 

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