Metal Utilization and Oxidative Stress
Frank Gherardini, Julie Boylan and Paul Brett
from: Pathogenic Treponema: Molecular and Cellular Biology (Edited by: Justin D. Radolf and Sheila A. Lukehart). Caister Academic Press, U.K. (2006)
Abstract
Spirochetes living in oxygen-rich environments or when challenged by host immune cells are exposed to reactive oxygen (ROS) and reactive nitrogen (RNS) species. These can harm polyunsaturated lipids, cysteinyl residues, iron-sulfur clusters and DNA (Fenton Reaction) leading to inhibition of growth and, if the damage is too extensive, cell death. As is the case with other bacteria, spirochetes harbor genes encoding proteins such as superoxide dismutases (SOD), superoxide reductase (SOR), alkylhydroperoxide reductases (AhpR), peroxidases and small molecular weight thiols (i.e., thioredoxin, glutathione, CoA) to protect cellular components and maintain intracellular oxidation/reduction potential (redox). While defending against an oxidative challenge, cells must also maintain sufficient, biochemically relevant intercellular concentrations of the metals which constitute a major ROS/RNS target. To maintain this balance, bacterial cells coordinately regulate metal transport and defense enzymes using oxidative stress response regulators and metal-dependent repressors. Within the Spirochetales, different systems have evolved to deal with the interplay between the requirements for metals and oxidative challenge. In this chapter, we compare the more "conventional" mechanisms seen in Treponema denticola and Leptospira interrogans with the more limited systems seen in Treponema pallidum and Borrelia burgdorferi read more ...
