Hemolytic iron regulation in traumatic brain injury and alcohol use. Academic Article uri icon

Overview

abstract

  • Hemorrhage is a major component of traumatic brain injury (TBI). Red blood cells, accumulated at the hemorrhagic site, undergo hemolysis upon energy depletion and release free iron into the central nervous system. This iron must be managed to prevent iron neurotoxicity and ferroptosis. As prior alcohol consumption is often associated with TBI, we examined iron regulation in a rat model of chronic alcohol feeding subjected to fluid percussion-induced TBI. We found that alcohol consumption prior to TBI altered the expression profiles of the lipocalin 2/heme oxygenase 1/ferritin iron management system. Notably, unlike TBI alone, TBI following chronic alcohol consumption sustained the expression of all three regulatory proteins for 1, 3, and 7 days post-injury. In addition, alcohol significantly affected TBI-induced expression of ferritin light chain at 3 days post-injury. We also found that alcohol exacerbated TBI-induced activation of microglia at 7 days post-injury. Finally, we propose that microglia may also play a role in iron management through red blood cell clearance.

publication date

  • January 21, 2023

Research

keywords

  • Brain Injuries, Traumatic
  • Iron

Identity

PubMed Central ID

  • PMC10175116

Scopus Document Identifier

  • 85150051929

Digital Object Identifier (DOI)

  • 10.1016/j.alcohol.2023.01.001

PubMed ID

  • 36690222

Additional Document Info

volume

  • 109