Hypochlorous acid is purported to be an reliable bleaching agent when provided through a proprietary additive (sassist to be a C-2 monoalkyl amine) that protects cellulose from acid hydrolysis.

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From: Biermann's Handbook of Pulp and Paper (Third Edition), 2018

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Hae-Jo Kim, in Comprehensive Supramolecular Chemistry II, 2017

8.06.3.3.2 Hypochlorous acid (HOCl)

Hypochlorous acid (HOCl) is developed largely in leukocytes, consisting of neutrophils, macrophperiods, and monocytes, by myeloperoxidase (MPO)-catalyzed peroxidation of chloride ions. It plays an essential role in killing a vast variety of pathogens and also affords an inherent organize defense. On the other hand, oxidative tension because of extreme generation of ROS is implicated in many kind of human illness, and also it is assumed that neutrophil-acquired HOCl contributes to inflammation-associated tissue injury, such as hepatic ischemia-reperfusion injury, atherosclerosis, lung injury, and rheumatoid arthritis.

Approximately half of the HOCl (pKa = 7.463) dissociates to the hypochlorite anion (OCl−), among the many effective natural oxidants under physiological conditions. Thus, hypochlorite is likely to injure microorganisms oxidatively in living units.


Nagano et al.56 brought out pioneering research on NIR fluorescent probes for HClO through rhodamine analogs (Fig. 21). Although the spirothioether probe was nonfluorescent initially, a large and prompt rise of fluorescence intensity was oboffered upon addition of HOCl owing to the development of highly fluorescent rhodamine derivative (Amax/Fmax = 652/670 nm, Φ = 0.31 in PBS). In contrast, various other ROS such as hydroxy radical and also H2O2 did not elicit any fluorescence. In addition, they examined the fluorescence response in the presence of an HOCl-generating enzymatic system, MPO. The fluorescence boost was suppressed by an MPO inhibitor. In addition, they assessed the capacity of the probe to visualize HOCl in a mouse peritonitis design with a much more hydrophilic derivative (R = CON(CH2CO2−)2). After mice were given an i.p. injection of zymosan to induce neutrophils to attack the peritoneal cavity and then injected i.p. through the hydrophilic probe and PMA, fluorescence dimensions confirmed a far-ranging rise in the PMA-treated region of the mice. In contrast, uncreated mice that were i.p. injected through the probe followed by saline just (no zymosan or PMA) confirmed no substantial fluorescence improvement.



Yoon et al.57–59 reported another rhodamine-based NIR probe for hypochlorite. Upon treatment via HClO, both the boronate and thioester teams were oxidized to afford fluorescein or rhodamine moieties, which shown strong fluorescence in living cells. They successfully applied the probes to imaging bacteria-induced HOCl manufacturing in the mucosa of live animals.

Two photon absorption fluorescent probes for HOCl were also occurred by Chang et al.60 A thioketal was transdeveloped right into a keto team in the presence of HOCl, which produced two photon active acedan derivatives, targeting lysosomes or mitochondria of live cells. They properly applied the probe to an inflammation design of mice.

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A myeloperoxidase (MPO)-linked hypochlorous acid probe (SNAPF) was additionally occurred by Libby et al.61 (Fig. 22). A protected ether team was easily removed by reaction with hypochlorite, which developed a strongly fluorescent naphthoquinone (Amax at 614 nm and Fmax at 676 nm). They gave direct evidence of the visibility of HOCl within huguy atherosclerotic plaques. The outcomes indicated that SNAPF could administer an useful tool to selectively monitor the influence of HOCl on the atherogenic procedure, in vivo.