Bilirubin: An Endogenous Inducer of Nrf2 Pathway and Its Possible Application in Therapy- Juniper Publishers


JUNIPER PUBLISHERS-OPEN ACCESS JOURNAL OF TOXICOLOGY

Bilirubin: An Endogenous Inducer of Nrf2 Pathway and Its Possible Application in Therapy


Authored by Mohammed Qaisiya

Abstract

It has been asked, why convert-in a step that consumes energy-biliverdin a non-toxic easily excretable waste product, into bilirubin, that is excretable, neurotoxic, and must be further metabolized for dispose? This two page opinion focus on the possible effects of bilirubin on an important cyto-protective pathway named Nrf2 antioxidant signaling. In animals, the product of oxidative degradation of heme results in a yellow pigment named un-conjugated bilirubin [UCB] that has a significant importance role during physiological and pathological conditions. UCB once produced is transferred into liver and then conjugated with glucuronic acid by the enzyme UGT1A1. UCB is responsible for neonatal jaundice that occurs in most newborn during the first week of life. However, UCB is a potential neurotoxic and in very few cases, such as Crigler Najjar syndrome type I in which the activity of UGT1A1 is completely absent; UCB leads to neurotoxicity or kernicterus. UCB plays a major role as a significant antioxidant at physiological levels, although we are still far from a complete understanding of this phenomenon. The antioxidant ability of UCB arises from a popular explanation of redox consuming cycling mechanism that act between the conversions of UCB in biliverdin. Several in vitro studies support the "direct" antioxidant properties of UCB.

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