Iron homeostasis and management of oxidative stress response in bacteria

Abstract

Iron is both an essential nutrient for the growth of microorganisms, as well as a dangerous metal due to its capacity to generate reactive oxygen species (ROS) via the Fenton reaction. For these reasons, bacteria must tightly control the uptake and storage of iron in a manner that restricts the build-up of ROS. Therefore, it is not surprising to find that the control of iron homeostasis and responses to oxidative stress are coordinated. The mechanisms concerned with these processes, and the interactions involved, are the subject of this review.

Iron induces bimodal population development by Escherichia coli

“…However, the mechanism by which high extracellular iron would cause intracellular reactive oxygen stress is unclear. E. coli is able to maintain a steady intracellular iron pool, regardless of extracellular iron fluctuations, due to the efficacy of iron homeostasis regulators such as Fur and RyhB (6). Fur is a transcriptional regulator that binds to ferrous iron and represses expression of iron acquisition systems.…”

“…Fur is a transcriptional regulator that binds to ferrous iron and represses expression of iron acquisition systems. RyhB is a small RNA that limits production of iron-containing proteins in low-iron conditions (6,50). Therefore, high extracellular iron should not necessarily lead to cytoplasmic-free iron stress.…”

“…Iron is an essential nutrient for almost all bacterial species, but it is efficiently sequestered by the host during an infection (5) and it is largely insoluble in aerobic environments (6). Additionally, ferrous iron can react with H 2 O 2 in the Fenton reaction to form reactive hydroxyl radicals, which can damage proteins, DNA, and lipids (7,8).…”

“…Additionally, ferrous iron can react with H 2 O 2 in the Fenton reaction to form reactive hydroxyl radicals, which can damage proteins, DNA, and lipids (7,8). To counter iron scarcity and toxicity, most bacteria express efficient iron acquisition systems and tightly regulate intracellular iron homeostasis (6,8).…”

Cells Lacking Pfh1, a Fission Yeast Homolog of Mammalian Frataxin Protein, Display Constitutive Activation of the Iron Starvation Response

“…Nevertheless, this redox-active transition metal presents a dilemma to cells, because iron can also catalyze the deleterious oxidation of biomolecules via Haber-Weiss/Fenton chemistry when combined with reactive oxygen species (ROS) (12). Accordingly, the concentration of iron in cells is tightly regulated by control of its uptake and intracellular storage (13).…”