The mechanism of microbial inactivation by aqueous ClO2 has been explored, but it is not fully understood. ClO2 has been shown to react readily with amino acids (cysteine, tryptophan, and tyrosine), but not with viral ribonucleic acid (RNA) [44,45]. Bernarde et al.  suggested that the primary inactivation mechanism was the disruption of protein synthesis. However, Roller et al.  indicated that the inhibition of protein might not be the primary inactivation mechanism. The increase of the permeability of the outer membrane was considered as another mechanism due to reactions of the outer membrane protein and lipids with ClO2 [13,45,47]. Berg et al.  reported that gross cellular damage involving significant leakage of intracellular macromolecules did not occur for ClO2-treated E. coli, but the cells lost control of potassium efflux, which may be the primary lethal physiological event. Because ClO2 gas is highly water soluble, it may inactivate microorganisms in a similar way as the aqueous form of ClO2. However, ClO2 gas and/or its radicals may directly diffuse or penetrate into microbial cells to cause damage. Therefore, to understand completely the inactivation mechanism of aqueous and/or gaseous ClO2, extensive research is needed.
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