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
Recommended Citation
Agas, Agnieszka; Ravula, Arun Reddy; Ma, Xiaotang; Cheng, Yiming; Belfield, Kevin D.; and Haorah, James, "Hemolytic iron regulation in traumatic brain injury and alcohol use" (2023). Faculty Publications. 1675.
https://digitalcommons.njit.edu/fac_pubs/1675