Dietary Iron Overload and Hfe-/- Related Hemochromatosis Alter Hepatic Mitochondrial Function.

ABSTRACT: Iron is an essential co-factor for many cellular metabolic processes, and mitochondria are main sites of utilization. Iron accumulation promotes production of reactive oxygen species (ROS) via the catalytic activity of iron species. Herein, we investigated the consequences of dietary and genetic iron overload on mitochondrial function. C57BL/6N wildtype and Hfe-/- mice, the latter a genetic hemochromatosis model, received either normal diet (ND) or high iron diet (HI) for two weeks. Liver mitochondrial respiration was measured using high-resolution respirometry along with analysis of expression of specific proteins and ROS production. HI promoted tissue iron accumulation and slightly affected mitochondrial function in wildtype mice. Hepatic mitochondrial function was impaired in Hfe-/- mic

SUBMITTER: Fischer C 

PROVIDER: S-EPMC8615072 | biostudies-literature | 2021 Nov

REPOSITORIES: biostudies-literature