Rate Of Oxidant Production Research Articles

Local and Regional Contributions to Tropospheric Ozone Concentrations

The Wasatch Front in Utah, USA is currently a non-attainment area for ozone according to the Environmental Protection Agency’s (EPA) National Ambient Air Quality Standards (NAAQS). Nitrogen oxides (NOx = NO2 + NO) and volatile organic compounds (VOCs) in the presence of sunlight lead to ozone formation in the troposphere. When the rate of oxidant production, defined as the sum of O3 and NO2, is faster than the rate of NOx production, a region is said to be NOx-limited and ozone formation will be limited by the concentration of NOx species in the region. The inverse of this situation makes the region VOC-limited. Knowing if a region is NOx-limited or VOC-limited can aid in generating effective mitigation strategies. Understanding the background or regional contributions to ozone in a region, whether it be from the transport of precursors or of ozone, provides information about the lower limit for ozone concentrations that a region can obtain with regulation of local precursors. In this paper, measured oxidant and NOx concentrations are analyzed from 14 counties in the state of Utah to calculate the regional and local contributions to ozone for each region. This analysis is used to determine the nature of the atmosphere in each county by determining if the region is VOC- or NOx-limited. Furthermore, this analysis is performed for each county for the years 2012 and 2022 to determine if there has been a change in the oxidative nature and quantify the regional and local contributions to ozone over a 10-year period. All studied counties—except for Washington County—in Utah were found to be VOC-limited in 2012. This shifted in 2022 to most counties being either in a transitional state or being NOx-limited. Local contributions to ozone increased in two major counties, Cache and Salt Lake Counties, but decreased in Carbon, Davis, Duchesne, Uinta, Utah, Washington, and Weber Counties. Generally, the regional contributions to oxidant concentrations decreased across the state. A summertime spike in both regional and local contributions to oxidants was seen. Smoke from wildfires was seen to increase the regional contributions to oxidants and shift the local regime to be more NOx-limited.

PH Dependence of Hydroxyl Radical, Ferryl, and/or Ferric Peroxo Species Generation in the Heterogeneous Fenton Process.

The heterogeneous Fenton process in the presence of Fe-containing minerals is ubiquitous in nature and widely deployed in wastewater treatment. While there have been extensive relevant studies, the dependence on pH of the nature and extent of oxidant generation and key reaction pathways remain unclear. Herein, the adsorption and decomposition of formate and H2O2 were quantified in the presence of ferrihydrite within the pH range of 3.0-6.0, and experiments with methyl phenyl sulfoxide were conducted to distinguish between HO• and weaker oxidant(s) which react via oxygen atom transfer including ferryl ion ([FeIVO]2+) and/or ferric hydroperoxo intermediates (≡FeIII(O2H)). Both HO• and [FeIVO]2+/≡FeIII(O2H) are concurrently produced on the surface over the acidic to near-neutral pH range. Despite the simultaneous formation of both oxidants, HO• is the major oxidant responsible for substrate oxidation in the interfacial boundary layer with [FeIVO]2+/≡FeIII(O2H) exhibiting limited exposure to substrates. With an increase of pH, the yield of both oxidants is inhibited by the decreasing availability of surface sites due to ferrihydrite particle aggregation. Increasing pH also favors the nonradical decay of H2O2 as evident from the consistent oxidant production rate relative to the surface area (SSA) despite an accelerated H2O2 decay rate relative to SSA with pH increase.

Impact of COVID-19 lockdown on ambient levels and sources of volatile organic compounds (VOCs) in Nanjing, China

A lot of restrictive measures were implemented in China during January–February 2020 to control rapid spread of COVID-19. Many studies reported impact of COVID-19 lockdown on air quality, but little research focused on ambient volatile organic compounds (VOCs) till now, which play important roles in production of ozone and secondary organic aerosol. In this study, impact of COVID-19 lockdown on VOCs mixing ratios and sources were assessed based on online measurements of VOCs in Nanjing during December 20, 2019-Feburary 15, 2020 (P1-P2) and April 15–May 13, 2020 (P3). Average VOCs levels during COVID-19 lockdown period (P2) was 26.9 ppb, about half of value for pre-lockdown period (P1). Chemical composition of VOCs also showed significant changes. Aromatics contribution during decreased from 13% during P1 to 9% during P2, whereas alkanes contribution increased from 64% to 68%. Positive matrix factorization (PMF) was then applied for non-methane hydrocarbons (NMHCs) sources apportionment. Five sources were identified, including a source related to transport and background air masses, three sources related to petrochemical industry or chemical industry (petrochemical industry#1-propene/ethene, petrochemical industry#2-C7-C9 aromatics, and chemical industry-benzene), and a source attributed to gasoline evaporation and vehicular emission. During P2, NMHCs levels from petrochemical industry#2-C7-C9 aromatics showed the largest relative decline of 94%, followed by petrochemical industry#1-propene/ethene (67%), and gasoline evaporation and vehicular emission (67%). Furthermore, ratios of OH reactivity of NMHCs versus NO2 level (ROH,NMHCs/NO2) and total oxidant production rate (P (OX)) were calculated to assess potential influences of COVID-19 lockdown on O3 formation.

Formation of S-(carboxymethyl)-cysteine in rat liver mitochondrial proteins: effects of caloric and methionine restriction

Maillard reaction contributes to the chemical modification and cross-linking of proteins. This process plays a significant role in the aging process and determination of animal longevity. Oxidative conditions promote the Maillard reaction. Mitochondria are the primary site of oxidants due to the reactive molecular species production. Mitochondrial proteome cysteine residues are targets of oxidative attack due to their specific chemistry and localization. Their chemical, non-enzymatic modification leads to dysfunctional proteins, which entail cellular senescence and organismal aging. Previous studies have consistently shown that caloric and methionine restrictions, nutritional interventions that increase longevity, decrease the rate of mitochondrial oxidant production and the physiological steady-state levels of markers of oxidative damage to macromolecules. In this scenario, we have detected S-(carboxymethyl)-cysteine (CMC) as a new irreversible chemical modification in mitochondrial proteins. CMC content in mitochondrial proteins significantly correlated with that of the lysine-derived analog N (ε)-(carboxymethyl)-lysine. The concentration of CMC is, however, one order of magnitude lower compared with CML likely due in part to the lower content of cysteine with respect to lysine of the mitochondrial proteome. CMC concentrations decreases in liver mitochondrial proteins of rats subjected to 8.5 and 25 % caloric restriction, as well as in 40 and 80 % methionine restriction. This is associated with a concomitant and significant increase in the protein content of sulfhydryl groups. Data presented here evidence that CMC, a marker of Cys-AGE formation, could be candidate as a biomarker of mitochondrial damage during aging.

Quantification of the Oxidizing Capacity of Nanoparticulate Zero-Valent Iron

Addition of nanoparticulate zero-valent iron (nZVI) to oxygen-containing water results in oxidation of organic compounds. To assess the potential application of nZVI for oxidative transformation of organic contaminants, the conversion of benzoic acid (BA) to p-hydroxybenzoic acid (p-HBA) was used as a probe reaction. When nZVI was added to BA-containing water, an initial pulse of p-HBA was detected during the first 30 min, followed by the slow generation of additional p-HBA over periods of at least 24 h. The yield of p-HBA increased with increasing BA concentration, presumably due to the increasing 'ability of BA to compete with alternate oxidant sinks, such as ferrous iron. At pH 3, maximum yields of p-HBA during the initial phase of the reaction of up to 25% were observed. The initial rate of nZVI-mediated oxidation of BA exhibited a marked reduction at pH values above 3. Despite the decrease in oxidant production rate, p-HBA was observed during the initial reaction phase at pH values up to 8. Competition experiments with probe compounds expected to exhibit different affinities for the nZVI surface (phenol, aniline, o-hydroxybenzoic acid, and synthetic humic acids) indicated relative rates of reaction that were similar to those observed in competition experiments in which hydroxyl radicals were generated in solution. Examination of the oxidizing capacity of a range of Fe0 particles reveals a capacity in all cases to induce oxidative transformation of benzoic acid, but the high surface areas that can be achieved with nanosized particles renders such particles particularly effective oxidants.

Short-term CR decreases cardiac mitochondrial oxidant production but increases carbonyl content.

Lifelong caloric restriction (CR) reduces the rate of mitochondrial oxidant production and the accumulation of oxidized proteins and prevents some of the age-associated decline in 20S proteasome activity. However, few studies have investigated how rapidly the beneficial effects of CR take place. We investigated whether 2 mo of CR in 6-mo-old rats would be of sufficient duration to elicit these beneficial changes. Mitochondrial oxidant production was significantly diminished in the CR rats compared with the ad libitum-fed animals. Short-term CR also caused a significant decrease in mitochondrial superoxide dismutase (SOD) and glutathione peroxidase (GPX) activities, but there were no differences in cytosolic SOD and GPX activities, whereas mitochondrial and cytosolic catalase (CAT) activity was increased with CR. However, protein carbonyl content was significantly elevated in both the mitochondrial and cytosolic fractions from CR rats. Of the three major 20S proteasome activities (chymotrypsin-like, trypsin-like, and peptidylglutamyl-peptide hydrolase), the peptidylglutamyl-peptide hydrolase activity was significantly elevated in the CR animals, possibly because of the fact that there were more oxidized proteins to be degraded. Although fewer oxidants were produced in the CR animals, it is possible that the ability to scavenge oxidants was transiently suppressed because of the reduction in mitochondrial antioxidant enzyme activities, which may explain the observed increases in carbonyl content.

Two subpopulations of mitochondria in the aging rat heart display heterogenous levels of oxidative stress.

Cardiac mitochondria are composed of two distinct subpopulations: one beneath the sarcolemma (subsarcolemmal mitochondria: SSM), and another along the myofilaments (interfibrillary mitochondria: IFM). Previous studies suggest a preferential loss of IFM function with age; however, the age-related changes in oxidative stress in these mitochondrial subpopulations have not been examined. To this end, the changes in mitochondrial antioxidant capacity, oxidant output, and oxidative damage to Complex IV in IFM and SSM from young and old rats were studied. Results show no apparent differences in any parameters examined between IFM and SSM from young rats. However, relative to young, only IFM from old rats had a significantly higher rate of oxidant production and a decline in mitochondrial ascorbate levels and GSH redox status. The age-related decline in mitochondrial antioxidant capacity in IFM was accompanied by a marked loss in glutaredoxin and GSSG reductase activities, suggesting a diminished reductive capacity in IFM with age. Moreover, the loss in Complex IV activity was limited to the IFM of old rats, which was accompanied by a 4-fold increase in 4-hydroxynonenal-modified Complex IV. Thus, mitochondrial decay is not uniform and further indicates that myofibrils may be uniquely under oxidative stress in the aging heart.

Ectopic expression of catalase in Drosophila mitochondria increases stress resistance but not longevity.

The goal of this study was to test the hypothesis that the rate of mitochondrial oxidant production governs the aging process of the fruit fly, Drosophila melanogaster. Catalase, an antioxidative enzyme expressed in the cytosol and peroxisomes of Drosophila, was targetted ectopically to the mitochondrial matrix by fusion of a leader peptide derived from ornithine aminotransferase with its N-terminus. The presence of the transgene encoding this fusion protein was associated with moderate (35 +/- 13%) increases in total catalase activity in most lines, and measurable levels of catalase activity in the mitochondria (30-140 U/mg protein). There was no impact on the life span of the flies at 25 degrees C, even in an exceptional line with a 149% increase in total catalase activity, and there was a small decrease in longevity at 29 degrees C. There were no compensatory changes in the rate of metabolism or physical activity, or in the levels of other major antioxidants, suggesting that the aging process was largely unaffected. Resistance to exogenous hydrogen peroxide, paraquat, and cold stress was enhanced, but there was no appreciable effect on resistance to hyperoxia. The results demonstrate the importance of mitochondrial antioxidant levels in the resistance to oxidative stress at the organismal level, and illustrate that different effects on aging and stress resistance may ensue from a single treatment. The main inferences drawn are that: (i) levels of stress resistance may neither be a cause nor a reliable indicator of the rate of aging, and (ii) bolstering antioxidant levels in Drosophila may not delay or slow down the aging process.

Mitochondrial damage in aging and apoptosis.

Mitochondria are essential to cellular aging, and free radical production by mitochondria is increased with aging. The rate of oxidant production by mitochondria correlates inversely with maximal life span of species. In many species, females live longer than males. We report that mitochondrial oxidant production by females is significantly lower than that of males. However, mitochondria from ovariectomized females have a similar oxidant production as those of males. Thus, gender difference in life span can be explained, at least in part, by different oxidant generation by mitochondria. Administration of antioxidants, such as vitamins C and E, or a Ginkgo biloba extract, protects against age-associated oxidative damage to mitochondrial DNA, oxidation of glutathione, and other signs of oxidative damage to mitochondria.

Oxidative stress in the aging rat heart is reversed by dietary supplementation with (R)-(alpha)-lipoic acid.

Oxidative stress has been implicated as a causal factor in the aging process of the heart and other tissues. To determine the extent of age-related myocardial oxidative stress, oxidant production, antioxidant status, and oxidative DNA damage were measured in hearts of young (2 months) and old (28 months) male Fischer 344 rats. Cardiac myocytes isolated from old rats showed a nearly threefold increase in the rate of oxidant production compared to young rats, as measured by the rates of 2,7-dichlorofluorescin diacetate oxidation. Determination of myocardial antioxidant status revealed a significant twofold decline in the levels of ascorbic acid (P = 0.03), but not alpha-tocopherol. A significant age-related increase (P = 0.05) in steady-state levels of oxidative DNA damage was observed, as monitored by 8-oxo-2'-deoxyguanosine levels. To investigate whether dietary supplementation with (R)-alpha-lipoic acid (LA) was effective at reducing oxidative stress, young and old rats were fed an AIN-93M diet with or without 0.2% (w/w) LA for 2 wk before death. Cardiac myocytes from old, LA-supplemented rats exhibited a markedly lower rate of oxidant production that was no longer significantly different from that in cells from unsupplemented, young rats. Lipoic acid supplementation also restored myocardial ascorbic acid levels and reduced oxidative DNA damage. Our data indicate that the aging rat heart is under increased mitochondrial-induced oxidative stress, which is significantly attenuated by lipoic acid supplementation.

Cadmium-mediated oxidative stress in alveolar epithelial cells induces the expression of gamma-glutamylcysteine synthetase catalytic subunit and glutathione S-transferase alpha and pi isoforms: potential role of activator protein-1.

Exposure of rat alveolar epithelial cells to 10 micromol/L CdCl2 causes time-dependent increases in steady-state mRNA levels of the gamma-glutamylcysteine synthetase catalytic (heavy) subunit (gamma-GCS) and of glutathione S-transferase isoforms (GST-alpha and GST-pi). The expression of gamma-GCS was significantly increased as early as 2 h after addition of cadmium. Maximal induction of gamma-GCS mRNA (approximately 4-fold), at 8 h, was subsequently followed by increases in gamma-GCS activity/protein and glutathione (GSH) levels. Maximal elevations in GST-pi (approximately 2-fold) and GST-alpha (approximately 10-fold) transcripts, at 8 and 24 h, respectively, were also accompanied by enhanced GST activity. Cadmium-induced oxidative stress, assessed by alterations in GSH homeostasis and an accelerated rate of intracellular oxidant production, could constitute early events in the signal transduction pathway mediating these responses. The dimeric transcription factor, activator protein-1 (AP-1), may also play a regulatory role in this process. This association is suggested by transcriptional activation of the immediate-early response genes, c-fos and c-jun, within 15 min after exposure to cadmium and by the enhancement of AP-1 DNA binding activity, involving a c-Jun protein complex, which is maximally induced (approximately 4-fold) by 2 h. These molecular changes likely function together to protect alveolar epithelial cells against cadmium toxicity.

Priming of neutrophil [Ca2+]i signaling and oxidative burst by human fracture fluids.

Patients with major fracture/soft-tissue injuries are at risk for adult respiratory distress syndrome after secondary infection. Fracture fluids (FF) are rich in neutrophil (PMN) -specific chemokines such as interleukin-8. PMN respond to both interleukin-8 and bacterial stimuli with calcium ([Ca2+]i) fluxes, which can initiate respiratory burst (RB). We hypothesize that small amounts of FF entering the circulation could exaggerate PMN [Ca2+]i and RB responses, potentially increasing the risk of adult respiratory distress syndrome. FF were obtained from 10 patients at open fixation of the femur 2 to 5 days postinjury. Volunteer PMN were isolated and loaded with fura dye. PMN were preincubated either in 30% autologous plasma (AP)/70% buffer, or in 5% FF/25% AP/70% buffer. Cells were resuspended in buffer with 1,2,3-dihydrorhodamine and stimulated with low-dose n-formyl-methionyl-leucyl-phenylalanine (fMLP). [Ca2+]i was assayed by fura fluorescence at 505 nm after excitation at 340/380 nm. RB was assessed by 1,2,3-dihydrorhodamine fluorescence at 530 nm after 488 nm excitation. PMN basal [Ca2+]i was higher after FF incubation than AP incubation (94+/-12 vs. 61+/-9 nmol/L, p = 0.0002). Peak [Ca2+]i response to fMLP was 475+/-47 nmol/L after FF but only 356+/-22 nmol/L after AP (p = 0.01). Two hundred seconds after fMLP, [Ca2+]i remained higher after FF (172+/-17 vs. 145+/-9 nmol/L, p = 0.04). Basal RB was slightly higher after FF than AP (13.4+/-0.3 vs. 11.3+/-0.3 units, p = 0.051) as was the maximal rate of extracellular oxidant release (1.10+/-0.17 vs. 0.76+/-0.16 units/s, p = 0.004) and total oxidant production (42.5+/-0.8 vs. 31.7+/-0.8 units, p = 0.006). Small amounts of FF in plasma can exaggerate PMN [Ca2+]i flux and RB responses to subsequent bacterial stimuli. These findings are consistent with the hypothesis that release of FF into the circulation primes PMN and, thus, may predispose to adult respiratory distress syndrome. Such PMN priming events might have important implications for both the operative and medical management of patients with major fractures.

Mitochondrial decay in aging. Reversal through supplementation of acetyl-L-carnitine and N-tert-butyl-alpha-phenyl-nitrone.

We show that mitochondrial function in the majority of hepatocytes isolated from old rats (24 mo) is significantly impaired. Mitochondrial membrane potential, cardiolipin levels, respiratory control ratio, and overall cellular O2 consumption decline, and the level of oxidants increases. To examine whether dietary supplementation of micronutrients that may have become essential with age could reverse the decline in mitochondrial function, we supplemented the diet of old rats with 1% (w/v) acetyl-L-carnitine (ALCAR) in drinking water. ALCAR supplementation (1 month) resulted in significant increases in cellular respiration, mitochondrial membrane potential, and cardiolipin values. However, supplementation also increased the rate of oxidant production, indicating that the efficiency of mitochondrial electron transport had not improved. To counteract the potential increase in oxidative stress, animals were administered N-tert-butyl-alpha-phenyl-nitrone (30 mg/kg) (PBN) with or without ALCAR. Results showed that PBN significantly lowered oxidant production as measured by 2,7'-dichlorofluorescin diacetate (DCFH), even when ALCAR was coadministered to the animals. Thus, dietary supplementation with ALCAR, particularly in combination with PBN, improves mitochondrial function without a significant increase in oxidative stress.

A model for radiation energy deposition in natural uranium-bearing systems and its consequences to water radiolysis

Water radiolysis is of great concern in the concept of final disposal of nuclear waste in geological formations. In this paper, a model is developed for radiation energy deposition and its consequences to water radiolysis. The model concepts are based on radiation energy deposition in the porewater and other constituents of a uranium ore (the Cigar Lake uranium deposit). Radiation is randomly generated within grains of uranium minerals in the ore, by the Monte Carlo method. The radiation energy is then allowed to deposit into the various constituents of the ore. The fraction of the total radiation energy absorbed by water is obtained, and the oxidant production rate is calculated with G-values of water. When back-reactions of the oxidants and reductants projected by other researchers in similar systems are accounted for, the calculated oxidant production rate is in agreement with that predicted by mass transport models.

Determination of photochemically available iron in ambient aerosols

Experiments to determine the concentration of photochemically available Fe in ambient aerosol samples were carried out using a novel photochemical extraction procedure. Ambient aerosol samples, which were collected on Teflon filters, were suspended in an aqueous solution within a photochemical reactor and irradiated. Under these conditions, which were favorable to the photochemical weathering of aerosol particles, the relative amount of Fe(II)aq to Fetotal was shown to increase. The extent and rate of Fe(II)aq photoproduction was used to characterize the Fe in aerosol samples collected from Whiteface Mountain, New York, Pasadena, California, San Nicholas Island, California, and Yosemite National Park, California. Photochemically available Fe concentrations found ranged from <4 ng m−3 (0.07 nmole m−3) to 308 ng m−3 (5.52 nmole m−3), Fetotal concentrations ranged from 10 ng m−3 (0.18 nmole m−3) to 3400 ng m−3 (61 nmole m−3), and the percentage of photochemically available Fe to Fetotal ranged from 2.8% to 100%. Aerosol samples were also collected during biomass burning events in southern California; these samples showed insignificant changes in the photochemically available Fe (compared to nonbiomass burning samples) in conjunction with large increases of Fetotal. Calculations based on these experiments also provide further evidence that redox reactions of Fe in cloudwater could be an important in situ source of oxidants (OH, HO2/O2−). The estimated oxidant production rate in cloudwater based on these experiments is between 0 and 60 nM s−1, with an average value of 16 nM s−1. This estimated in situ oxidant production rate due to Fe chemistry is approximately equal to previous estimates of the oxidant flux to cloudwater from the gas phase.

Some Evidence of Radiolysis in a Uranium ore Body - Quantification and Interpretation

AbstractLocally oxidising conditions in the near-field of the Cigar Lake uranium deposit was observed. Ongoing processes of water radiolysis has also been predicted previously by our mass transport model. In the ore there was an enhanced concentration of helium, hydrogen and sulphate. Sulphate is the only oxidising species of substantial amount in the groundwater samples, and is possibly indirectly produced by water radiolysis and oxidation of sulphides. The ongoing oxidant production rate has been calculated by the mass transport model.In this paper, the issue of water radiolysis is addressed from a more fundamental angle of approach. The maximum oxidant production rate is calculated based on the assumptions of geometric dispersion of the ore constituents, the estimate of the total radiation energy, the fraction of energy deposited into the pore water, and the G-values of water. The results show that only a few percent of the total radiation energy is deposited into the pore water to cause water radiolysis. If the recombination factor projected by other researchers are accounted for, the oxidant production rate thus calculated agrees with the present-day ongoing oxidant production rate predicted by the mass transport model.

Oxygen-Reactive Species and Antioxidant Responses during Development: The Metabolic Paradox of Cellular Differentiation

Metabolic gradients are established during early phases of development and their existence influences subsequent developmental events. Variations in oxygen supply and oxygen metabolism associated with the gradation of metabolic rate in embryos appear to form one basis for the influence of metabolic gradients on development. The rate of oxygen metabolism affects the rate of oxidant generation by various cellular biochemical pathways. Cells contain antioxidant defenses that respond to variations in cellular oxidant production. Large changes in the activity of the antioxidant enzyme superoxide dismutase and changes in cellular redox state occur during the differentiation of many types of cells. These changes correspond to an increased rate of oxidant production; the cellular environment becomes more prooxidizing during differentiation. Evidence is presented that implicates oxidants as a factor that can stimulate alterations in gene expression. Possible mechanisms by which oxidants influence gene expression are also discussed.