Bacterial Toxicity of Potassium Tellurite: Unveiling an Ancient Enigma

Abstract

Biochemical, genetic, enzymatic and molecular approaches were used to demonstrate, for the first time, that tellurite (TeO3 2−) toxicity in E. coli involves superoxide formation. This radical is derived, at least in part, from enzymatic TeO3 2− reduction. This conclusion is supported by the following observations made in K2TeO3-treated E. coli BW25113: i) induction of the ibpA gene encoding for the small heat shock protein IbpA, which has been associated with resistance to superoxide, ii) increase of cytoplasmic reactive oxygen species (ROS) as determined with ROS-specific probe 2′7′-dichlorodihydrofluorescein diacetate (H2DCFDA), iii) increase of carbonyl content in cellular proteins, iv) increase in the generation of thiobarbituric acid-reactive substances (TBARs), v) inactivation of oxidative stress-sensitive [Fe-S] enzymes such as aconitase, vi) increase of superoxide dismutase (SOD) activity, vii) increase of sodA, sodB and soxS mRNA transcription, and viii) generation of superoxide radical during in vitro enzymatic reduction of potassium tellurite.

Escherichia coli YqhD Exhibits Aldehyde Reductase Activity and Protects from the Harmful Effect of Lipid Peroxidation-derived Aldehydes

“…We found that YqhD was highly induced when cells were grown in the presence of K 2 TeO 3 . This result and the fact that an important pathway of tellurite toxicity involves superoxide generation (4,27) prompted us to evaluate the role that YqhD could have in E. coli resistance to tellurite and other oxidative stress elicitors.…”

“…Although cells overexpressing yqhD showed increased tolerance to compounds whose toxicity involves superoxide generation like paraquat and potassium tellurite (4,27), the hydroxyl radical-generating chromate anion (5), and hydrogen peroxide, E. coli ⌬yqhD showed increased sensitivity to all these compounds (Table 2). To assess whether YqhD-mediated resistance phenotype was also related to cytoplasm thiol depletion (especially GSH), the effect of YqhD on E. coli resistance to oxidant compounds that involve thiol oxidation like diamide and cadmium chloride (28) was determined.…”

“…4 Hydrogen peroxide (H 2 O 2 ), superoxide (O 2 . ), and hydroxyl radical (OH ⅐ ) are typical side products of the aerobic metabolism.…”

“…), and hydroxyl radical (OH ⅐ ) are typical side products of the aerobic metabolism. ROS compounds are also formed during cell exposure to redox-cycling chemicals like paraquat or metals and metalloids like chromate and potassium tellurite (K 2 TeO 3 ) (3)(4)(5). To alleviate ROS-generated oxidative damage, Escherichia coli cells induce the synthesis of a variety of antioxidant enzymes including catalases and superoxide dismutases (3,6).…”

Site-Directed Mutagenesis as a Tool for Unveiling Mechanisms of Bacterial Tellurite Resistance

“…It has been argued that tellurite toxicity results from the ability of tellurite to act as a strong oxidizing agent that damages a number of cell components (Taylor, 1999;Pérez et al, 2007). In the last years, however, available evidence shows that tellurite toxicity results from the generation of reactive oxygen species (ROS) (Borsetti et al, 2005;Calderón et al, 2006;Tremaroli et al, 2007;Pérez et al, 2007). ROS, such as hydrogen peroxide (H 2 O 2 ), superoxide anion (O 2 -) and hydroxyl radical (OH˙), are typical byproducts of aerobic metabolism.…”