Significance The Fenton reaction, Fe 2+ + H 2 O 2 , plays fundamental roles in vivo and in advanced oxidation processes. Its mechanism and the identity of the intermediates involved, however, remain controversial. Here we present direct, mass-specific evidence of the prompt formation of mono- and poly-iron Fe IV =O (ferryl) species on the surface of aqueous FeCl 2 microjets exposed to gaseous H 2 O 2 or O 3 beams. Remarkably, Fe 2+ ions at the aqueous surface react with H 2 O 2 and O 3 >10 3 times faster than Fe(H 2 O) 6 2+ in bulk water. Our results suggest that interfacial Fenton and Fenton-like chemistries could play a more significant role than hitherto envisioned.

SI text Experimental detailsThe cavity ring-down mirrors (Research Electro-Optics, 7.8 mm dia. and 1 m curvature) had a specified maximum reflectivity of 0.9994 and were mounted 1.04 m apart. Light leaking from the end mirror was detected by a photomultiplier tube (Hamamatsu Photonics, R212UH) through a band pass filter. The ring-down signal of the light intensity was recorded in a personal computer. The decay of the light intensity is represented by equation (I) 1 ;where I 0 and I(t) are the light intensities at time 0 and t, respectively. τ 0 is the cavity ring-down time without any absorbed species (about 20 µs at 435 nm), τ the measured cavity ring-down time with absorbed species, c the velocity of light, l and L are the length of the reaction surface where absorbers are considered to be present (l = 70 + 10 cm) and the length between mirrors (L = 104 cm), N and σ are the concentration and absorption cross section of the species of interest, respectively. Each ring-down trace was digitized with a time resolution of 100 MHz. The digitized traces were transferred to a personal computer and averaged over 16 runs to calculate the ring-down rate, τ −1 .

Ethylene ozonolysis was investigated in laboratory experiments using a Teflon bag reactor. A negative ion chemical ionization mass spectrometer (NI-CIMS) using SO2Cl(-) and Cl(-) as reagent ions was used for product analysis. In addition to the expected gas-phase products, such as formic acid and hydroperoxymethyl formate, oligomeric hydroperoxides composed of the Criegee intermediate (CH2OO) as a chain unit were observed. Furthermore, we observed secondary organic aerosol (SOA) formation from the ethylene ozonolysis, and the particle-phase products were also analyzed by NI-CIMS. The CH2OO oligomers were also observed as particle-phase components, suggesting that the oligomeric hydroperoxides formed in the gas phase partition into the particle phase. By adding methanol as a stabilized Criegee intermediate scavenger, both the gas-phase oligomer formation and SOA formation were strongly suppressed. This indicates that CH2OO plays a critical role in the formation of oligomeric hydroperoxides followed by SOA formation in ethylene ozonolysis. A new formation mechanism for the oligomeric hydroperoxides, which includes sequential addition of CH2OO to hydroperoxides, is proposed.

Fifty-seven years after NO(x) (NO + NO(2)) were identified as essential components of photochemical smog, atmospheric chemical models fail to correctly predict *OH/HO(2)* concentrations under NO(x)-rich conditions. This deficiency is due, in part, to the uncertain rates and mechanism for the reactive dissolution of NO(2)(g) (2NO(2) + H(2)O = NO(3)(-) + H(+) + HONO) in fog and aerosol droplets. Thus, state-of-the-art models parametrize the uptake of NO(2) by atmospheric aerosol from data obtained on "deactivated tunnel wall residue". Here, we report experiments in which NO(3)(-) production on the surface of microdroplets exposed to NO(2)(g) for approximately 1 ms is monitored by online thermospray mass spectrometry. NO(2) does not dissolve in deionized water (NO(3)(-) signals below the detection limit) but readily produces NO(3)(-) on aqueous NaX (X = Cl, Br, I) microdroplets with NO(2) uptake coefficients gamma that vary nonmonotonically with electrolyte concentration and peak at gamma(max) approximately 10(-4) for [NaX] approximately 1 mM, which is >10(3) larger than that in neat water. Since I(-) is partially oxidized to I(2)(*-) in this process, anions seem to capture NO(2)(g) into X-NO(2)(*-) radical anions for further reaction at the air/water interface. By showing that gamma is strongly enhanced by electrolytes, these results resolve outstanding discrepancies between previous measurements in neat water versus NaCl-seeded clouds. They also provide a general mechanism for the heterogeneous conversion of NO(2)(g) to (NO(3)(-) + HONO) on the surface of aqueous media.

Gaseous biogenic volatile organic compounds (BVOCs) are immediately oxidized by gaseous oxidants to form BVOC-acids that rapidly condense onto aqueous aerosol phase and thus contribute to the growth of atmospheric particles. Because BVOC-acids are highly hydrophobic and hence surface-active in nature, it seems critical to study the oxidation by gaseous hydroxyl radical (·OH(g)) at the air-water interface. Here we report on the fast (≤10 μs) oxidation of aqueous cis-pinonic acid (C10H16O3, CPA, cis-pinonate anion's m/z = 183), a representative BVOC-acid, by ·OH(g) at the air-water interface for the first time. We find that cis-pinonate anion is more enriched at the air-water interface by ∼4 and ∼14 times than n-octanoate anion at 10 and 100 μM, respectively, as revealed by an interface-specific mass spectrometry of the equimolar mixture of microjets. Exposure of aqueous CPA microjets to ·OH(g) pulses from the 266 nm laser photolysis of O3(g)/O2(g)/H2O(g)/N2(g) mixtures yields pinonic peroxyl radicals (m/z = 214) that lead to the functionalization products carbonyls (m/z = 197), alcohols (m/z = 199), and pinonic hydroperoxides (m/z = 215) in addition to smaller-mass products including carbonyls (m/z = 155 and 157). We confirmed the formation of the corresponding alcohols, aldehydes, and hydroperoxides in experiments performed in D2O solvent. The analysis of total mass balance implies a significant amount (>70%) of products would be emitted into the gas-phase during the heterogeneous ·OH-oxidations. Our results suggest ·OH-oxidations of amphiphilic BVOC-acids at the air-water interface may play a far more significant role in photochemical aging process of aqueous aerosols than previously assumed.

BackgroundKinesin family member 4A (KIF4A), a microtubule-based motor protein, was implicated in regulation of chromosomal structure and kinetochore microtubule dynamics. Considering the functions of KIF4A, we assumed that KIF4A is involved in progression of oral squamous cell carcinomas (OSCCs) via activation of the spindle assembly checkpoint (SAC). However, little is known about the relevance of KIF4A in the behavior of OSCC. We investigated the KIF4A expression status and its functional mechanisms in OSCC.MethodsThe KIF4A expression levels in seven OSCC-derived cells were analyzed by quantitative reverse transcriptase-polymerase chain reaction and immunoblotting analyses. Using a KIF4A knockdown model, we assessed the expression of (SAC)-related molecules (BUB1, MAD2, CDC20, and cyclin B1), cell-cycle, and cellular proliferation. In addition to in vitro data, the clinical correlation between the KIF4A expression levels in primary OSCCs (n = 106 patients) and the clinicopathologic status by immunohistochemistry (IHC) also were evaluated. ResultsKIF4A mRNA and protein were up-regulated significantly (P < 0.05) in seven OSCC-derived cells compared with human normal oral keratinocytes. In the KIF4A knockdown cells, SAC activation was observed via increased BUB1 expression on the kinetochores, appropriate kinetochore localization of MAD2, down-regulation of CDC20, up-regulation of cyclin B1, and cell-cycle arrested at G2/M phase. The results showed that cellular proliferation of KIF4A knockdown cells decreased significantly (P < 0.05) compared with control cells. IHC showed that KIF4A expression in primary OSCCs was significantly (P < 0.05) greater than in the normal oral counterparts and that KIF4A-positive OSCCs were correlated closely (P < 0.05) with tumoral size. ConclusionsOur results proposed for the first time that KIF4A controls cellular proliferation via SAC activation. Therefore, KIF4A might be a key regulator for tumoral progression in OSCCs.

BackgroundAdenosine A2b receptor (ADORA2B) encodes an adenosine receptor that is a member of the G protein-coupled receptor superfamily. This integral membrane protein stimulates adenylate cyclase activity in the presence of adenosine. Little is known about the relevance of ADORA2B to human malignancy including oral squamous cell carcinoma (OSCC). We aimed to characterize the expression state and function of ADORA2B in OSCC.MethodsThe ADORA2B expression levels in nine OSCC-derived cells were analyzed by quantitative reverse transcriptase-polymerase chain reaction and immunoblotting analyses. Using an ADORA2B knockdown model, we assessed cellular proliferation and expression of hypoxia-inducible factor1α (HIF-1α). We examined the adenosine receptor expression profile under both normoxic and hypoxic conditions in the OSCC-derived cells. In addition to in vitro data, the clinical correlation between the ADORA2B expression levels in primary OSCCs (n = 100 patients) and the clinicopathological status by immunohistochemistry (IHC) also was evaluated.ResultsADORA2B mRNA and protein were up-regulated significantly (p < 0.05) in seven OSCC-derived cells compared with human normal oral keratinocytes. Suppression of ADORA2B expression with shRNA significantly (p < 0.05) inhibited cellular proliferation compared with the control cells. HIF-1α also was down-regulated in ADORA2B knockdown OSCC cells. During hypoxia, ADORA2B expression was induced significantly (p < 0.05) in the mRNA and protein after 24 hours of incubation in OSCC-derived cells. IHC showed that ADORA2B expression in primary OSCCs was significantly (p < 0.05) greater than in the normal oral counterparts and that ADORA2B-positive OSCCs were correlated closely (p < 0.05) with tumoral size.ConclusionOur results suggested that ADORA2B controls cellular proliferation via HIF-1α activation, indicating that ADORA2B may be a key regulator of tumoral progression in OSCCs.Electronic supplementary materialThe online version of this article (doi:10.1186/s12885-015-1577-2) contains supplementary material, which is available to authorized users.

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