Iron Overload-Induced Hepatotoxicity: An Overview

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.