Direct Emission of I_2 Molecule and IO Radical from the Heterogeneous Reactions of Gaseous Ozone with Aqueous Potassium Iodide Solution

Recent studies indicated that gaseous halogens mediate key tropospheric chemical processes. The inclusion of halogen-ozone chemistry in atmospheric box models actually closes the ~50% gap between estimated and measured ozone losses in the marine boundary layer. The additional source of gaseous halogens is deemed to involve previously unaccounted for reactions of O_3(g) with sea surface water and marine aerosols. Here, we report that molecular iodine, I_2(g), and iodine monoxide radical, IO(g), are released ([I_2(g)] > 100[IO(g)]) during the heterogeneous reaction of gaseous ozone, O_3(g), with aqueous potassium iodide, KI(aq). It was found that (1) the amounts of I_2(g) and IO(g) produced are directly proportional to [KI(aq)] up to 5 mM and (2) IO(g) yields are independent of bulk pH between 2 and 11, whereas I_2(g) production is markedly enhanced at pH < 4. We propose that O_3(g) reacts with I− at the air/water interface to produce I_2(g) and IO(g) via HOI and IOOO− intermediates, respectively

Weak Acids Enhance Halogen Activation on Atmospheric Water’s Surfaces

We report that rates of I_2(g) emissions, measured via cavity ring-down spectroscopy, during the heterogeneous ozonation of interfacial iodide: I^–(surface, s) + O_3(g) + H+(s) →→ I_2(g), are enhanced several-fold, whereas those of IO·(g) are unaffected, by the presence of undissociated alkanoic acids on water. The amphiphilic weak carboxylic acids appear to promote I_2(g) emissions by supplying the requisite interfacial protons H^+(s) more efficiently than water itself, at pH values representative of submicrometer marine aerosol particles. We infer that the organic acids coating aerosol particles ejected from ocean’s topmost films should enhance I_2(g) production in marine boundary layers

Heterogeneous Reaction of Gaseous Ozone with Aqueous Iodide in the Presence of Aqueous Organic Species

The fast reaction of gaseous ozone, O_3(g), with aqueous iodide, I−(aq), was found to be affected by environmentally relevant cosolutes in experiments using cavity ring-down spectroscopy (CRDS) and electrospray ionization mass spectrometry (ESIMS) for the detection of gaseous and interfacial products, respectively. Iodine, I_2(g), and iodine monoxide radical, IO(g), product yields were suppressed in the presence of a few millimolar phenol (pK_a = 10.0), p-methoxyphenol (10.2), or p-cresol (10.3) at pH ≥ 3 but unaffected by salicylic acid (pK_(a2) = 13.6), tert-butanol, n-butanol, or malonic acid. We infer that reactive anionic phenolates inhibit I_2(g) and IO(g) emissions by competing with I−(aq) for O_3(g) at the air/water interface. ESIMS product analysis supports this mechanism. Atmospheric implications are discusse

Conversion of gaseous nitrogen dioxide to nitrate and nitrite on aqueous surfactants

The hydrolytic disproportionation of gaseous NO2 on water's surface (2 NO_2 + H_2O → HONO + NO_3- + H+) (R1) has long been deemed to play a key, albeit unquantifiable role in tropospheric chemistry. We recently found that (R1) is dramatically accelerated by anions in experiments performed on aqueous microjets monitored by online electrospray mass spectrometry. This finding let us rationalize unresolved discrepancies among previous laboratory results and suggested that under realistic environmental conditions (R1) should be affected by everpresent surfactants. Herein, we report that NO_2(g) uptake is significantly enhanced by cationic surfactants, weakly inhibited by fulvic acid (FA, a natural polycarboxylic acid) and anionic surfactants, and unaffected by 1-octanol. Surfactants appear to modulate interfacial anion coverage via electrostatic interactions with charged headgroups. We show that (R1) should be the dominant mechanism for the heterogeneous conversion of NO_2(g) to HONO under typical atmospheric conditions throughout the day. The photoinduced reduction of NO_2 into HONO on airborne soot might play a limited role during daytime

Surgical Treatment for Biliary Carcinoma Arising After Pancreatoduodenectomy

The clinicopathological features and surgical treatment of biliary carcinoma around the major hepatic duct confluence arising after pancreatoduodenectomy (PD) due to initial bile duct carcinoma are described in three patients. Occurrence of biliary carcinoma more than 12 years after initial surgery and a histological finding of cholangiocellular carcinoma mixed with hepatocellular carcinoma suggested metachronous incidence of biliary carcinoma after PD. Extended right hemihepatectomy with complete removal of the residual extrahepatic bile duct and segmental, resection of the jejunal loop were carried out safely without operative death or severe postoperative complications. Two patients died of tumor recurrence 6 months after surgery, and the remaining patient is currently living a normal life without evidence of recurrence 17 months after surgery. These surgical procedures are a therapeutic option in patients with biliary carcinoma around the major hepatic duct confluence arising after PD

Stable and functional expression of the CIC-3 chloride channel in somatic cell lines

AbstractThe CIC family is the superfamily of voltage-gated Cl− channels. Although the CIC channels expressed in Xenopus oocytes have been characterized, their channel properties are still poorly understood. We recently cloned a unique member of the CIC family, CIC-3, that is expressed abundantly in neurons. Its channel activity was regulated by phorbol esters. Now, we have established a stably transfected somatic cell line expressing functional CIC-3 channels and examined the CIC-3 single-channel current by patch-clamp techniques. In inside-out patches from the stably transfected cells, a rise of bath Ca2+ concentration in the physiological range of intracellular Ca2+ concentrations inhibited the CIC-3 single-channel currents. This inhibition by Ca2+ was independent of phosphorylation and ATP. Thus, the CIC-3 channel is a Ca2+-sensitive CI− channel localized in neuronal cells, and its Ca2+ sensitivity implies a physiological role in neuronal functions