"Hemolytic iron regulation in traumatic brain injury and alcohol use" by Agnieszka Agas, Arun Reddy Ravula et al.
 

Hemolytic iron regulation in traumatic brain injury and alcohol use

Document Type

Article

Publication Date

6-1-2023

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.

Identifier

85150051929 (Scopus)

Publication Title

Alcohol

External Full Text Location

https://doi.org/10.1016/j.alcohol.2023.01.001

e-ISSN

18736823

ISSN

07418329

PubMed ID

36690222

First Page

1

Last Page

12

Volume

109

Grant

5R21AA028340-02

Fund Ref

National Institutes of Health

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