Non-radical Species Research Articles

Estresse oxidativo: conceito, implicações e fatores modulatórios

O estresse oxidativo decorre de um desequilíbrio entre a geração de compostos oxidantes e a atuação dos sistemas de defesa antioxidante. A geração de radicais livres e/ou espécies reativas não radicais é resultante do metabolismo de oxigênio. A mitocôndria, por meio da cadeia transportadora de elétrons, é a principal fonte geradora. O sistema de defesa antioxidante tem a função de inibir e/ou reduzir os danos causados pela ação deletéria dos radicais livres e/ou espécies reativas não radicais. Esse sistema, usualmente, é dividido em enzimático (superóxido dismutase, catalase e glutationa peroxidase) e não-enzimático. No último caso, é constituído por grande variedade de substâncias antioxidantes, que podem ter origem endógena ou dietética. Objetivou-se revisar os principais mecanismos de geração de radicais livres, bem como a ação dos agentes mais relevantes do sistema de defesa antioxidante, ressaltando suas implicações sobre os marcadores do estresse oxidativo. Também serão abordados os principais fatores exógenos moduladores do estresse oxidativo.

Effect of flavonoids on 2′-deoxyguanosine and DNA oxidation caused by singlet molecular oxygen

Antioxidant potential is generally investigated by assaying the ability of a compound to protect biological systems from free radicals. However, non-radical reactive oxygen species can also be harmful. Singlet molecular oxygen ( 1 O 2 ) is generated by energy transfer to molecular oxygen. The resulting 1 O 2 is able to oxidize the nucleoside 2′-deoxyguanosine (dGuo), which leads to the formation of 8-oxo-7,8-dihydro-2′-deoxyguanosine (8-oxodGuo) and spiroiminodihydantoin 2′-deoxyribonucleoside diastereomers (dSp) in an aqueous solution. The main objective of the present study was to verify whether the presence of flavonoids (flavone, apigenin, quercetin, morin and catechin) at different concentrations could protect dGuo from 1 O 2 damage. Of the tested flavonoids, flavone possessed antioxidant activity, as determined by a decrease in the formation of both products. Apigenin, morin, quercetin and catechin all increased the formation of 8-oxodGuo at a concentration of 100 μM. The quantification of plasmid strand breaks after treatment with formamidopyrimidine–DNA glycosylase showed that flavone protected and quercetin and catechin enhanced DNA oxidation. Our results show that compounds, such as flavonoids, may affect the product distribution of 1 O 2 -mediated oxidation of dGuo, and, in particular, high concentrations of flavonoids with hydroxyl groups in their structure lead to an increase in the formation of the mutagenic lesion 8-oxodGuo.

A novel neuroprotectant PAN-811 protects neurons from oxidative stress

AbstractHydrogen peroxide (H2O2), a major non-radical reactive oxygen species (ROS) could elicit intracellular oxidative damage and/or cause extracellular free calcium influx by activating the NMDA receptor or through calcium channels. In the present study, NMDA receptor antagonist MK-801 fully blocked H2O2-induced neuronal cell death, whereas green tea (GT) extract containing-antioxidants only partially suppressed the neurotoxicity of H2O2. These suggest that majority of ROS overproduction is downstream of H2O2-induced calcium influx. A novel neuroprotectant PAN-811 was previously demonstrated to efficiently attenuate ischemic neurotoxicity. PAN-811 hereby fully blocks H2O2-elicited neuronal cell death with a more advanced neuroprotective profile than that of GT extract. PAN-811 was also shown to protect against CaCl2-elicited neurotoxicity. Efficient protection against oxidative stress-induced neurotoxicity by PAN-811 indicates its potential application in treatment of ROS-mediated neurodegenerative diseases.

CTGF and chronic kidney fibrosis

Chronic kidney fibrosis is the unifying pathological feature of diverse renal disease leading to a progressive decline in renal function and eventually end-stage kidney failure. Many growth factors are able to induce an imbalance of extracellular matrix production and degradation, leading to excessive matrix and fibrosis in both glomeruli and in the tubulointerstitium. Over the last decade the role of connective tissue growth factor (CTGF) in renal fibrosis has been intensively studied. CTGF participates in cell proliferation, migration, and differentiation and mediates profibrotic activity by acting either directly, or as a co-factor for TGF beta 1, which is well characterised as a key cytokine mediating both the induction and promotion of fibrogenesis. CTGF also has the potential to modulate factors such as VEGF and bone morphogenic proteins, which are integral to both the development and repair process inherent in renal fibrogenesis. This review focuses on the role of CTGF in renal fibrosis and specifically its role in inducing fibrosis by factors integrally involved in the development of diabetic nephropathy, namely high glucose, angiotensin II, TGF beta 1 and AGEs.

Multiplicity of DNA Single-Strand Breaks Produced in pUC18 Exposed to the Direct Effects of Ionizing Radiation

The transition of plasmid DNA from a supercoiled to an open circle conformation, as detected by gel electrophoresis, affords an extraordinarily sensitive method for detecting single-strand breaks (SSBs), one measure of deoxyribose damage. To determine the yield of SSBs, G(ssb), by this method, it is commonly assumed that Poisson statistics apply such that, on average, one SSB occurs per supercoiled plasmid lost. For the direct effect, at a large enough plasmid size, this assumption may be invalid. In this report, the assumption that one SSB occurs per pUC18 plasmid (2686 bp) is tested by measuring free base release (fbr), which is also a measure of deoxyribose damage in films prepared under controlled relative humidity so as to produce known levels of DNA hydration. The level of DNA hydration, Gamma, is expressed in mol water/mol nucleotide. The yield of free base release, G(fbr), was measured by HPLC after exposure of the films to 70 kV X rays and subsequent dissolution in water. It is well known that damage in deoxyribose leads to SSBs and free base release. Based on known mechanisms, there exists a close correspondence between free base release and SSBs, i.e., G(fbr) congruent with G(ssb). Following this assumption, the SSB multiplicity, m(ssb), was determined, where m(ssb) was defined as the mean number of SSBs per supercoiled plasmid lost. The yield of lost supercoil was determined previously (S. Purkayastha et al., J. Phys. Chem. B 110, 26286-26291, 2006). We found that m(ssb) = 1.4 +/- 0.2 at Gamma = 2.5 and m(ssb) = 2.8 +/- 0.5 to 3.1 +/- 0.5 at Gamma = 22.5, indicating that the assumption of one SSB per lost supercoil is not likely to hold for a 2686-bp plasmid exposed to the direct effect. In addition, an increase in G(fbr), upon stepping from Gamma = 2.5 to Gamma = 22.5, was paralleled by an increase in the yield of trapped deoxyribose radicals, G(dRib)(fr), also measured previously. As a consequence, the shortfall between SSBs and trapped radicals, G(diff) = G(ssb) - G(dRib)(fr), remained relatively constant at 90-110 nmol/J. The lack of change between the two extremes of hydration is in keeping with the suggestion that non-radical species, such as doubly oxidized deoxyribose, are responsible for the shortfall.

Carbon Nanotubes as Free-Radical Scavengers

Density functional theory calculations have been used to model the potential ability of single-walled carbon nanotubes (SWCNT) to act as free-radical scavengers. The reactions of a (5,5) SWCNT fragment with six different radicals have been studied, and for hydroxyl radical, which is the most reactive and dangerous from all of the studied set, up to four additions were modeled. Energetic considerations show that, once a first radical is attached to the nanotube, further additions are increasingly feasible, suggesting that SWCNTs can act as free-radical sponges. For reactions with OH radicals, subsequent additions are expected to lead to products where the OHs are distributed in groups rather than regularly spread on the nanotube. Because nanotubes with none or an even number of OH groups attached are stable (nonradical) species that can be used for other purposes, their properties were analyzed in terms of global reactivity indexes and density of states (DOS). The results from these analyses suggest that, ...

Numerical analysis of pressure dependence on carbon nanotube growth in CH 4/H 2 plasmas

The pressure dependence of a CH 4/H 2 gas mixture plasma was analyzed for carbon nanotube (CNT) growth by one-dimensional fluid modeling and compared with the experimental results obtained under the same condition as the analysis. When the gas pressure was 10 Torr, vertically aligned CNTs are grown with a high number density. As the pressure increases, densities of the non-radical neutrals, radical neutrals and ions with a lager molecular weight than CH 4 tend to increase but those of the smaller species including CH 3 and CH 2 decrease. This is explained by the hydrogen abstraction reaction of CH 4 with H atoms and the production reaction of C 2H 5 due to incorporation of CH 3 radicals. The fluxes of these carbon-bearing species onto the substrate surface were evaluated. As the gas pressure increased, the flux of positive ions decreased. Instead, the contribution of higher-order non-radical species, including C 3H 8, to CNT formation at high gas pressure is suggested.

The role of Yap1p and Skn7p‐mediated oxidative stress response in the defence of Saccharomyces cerevisiae against singlet oxygen

The production of the reactive oxygen species superoxide and hydrogen peroxide in Saccharomyces cerevisiae induces the expression of various defence genes involved in an oxidative stress response. Expression of many of these genes has been shown to be coordinated by two transcriptional regulators, Yap1p and Skn7p, either alone or in concert. Here, we investigated the role of the Yap1p and Skn7p-mediated stress response in the defence against singlet oxygen, a non-radical reactive oxygen species produced mainly by photosensitized reactions in illuminated cells. Both, a yap1 and skn7 mutant were highly sensitive to Rose Bengal, an exogenous photosensitizer producing singlet oxygen in the light. The expression of a Yap1p-dependent reporter gene was induced by increased singlet oxygen production, showing that singlet oxygen activates general oxidative stress response mechanisms required for the resistance against Rose Bengal treatment. This response was also slightly stimulated by light in the absence of the photosensitizer, possibly due to singlet oxygen production by endogenous photosensitizers. The expression pattern of four oxidative stress genes in a yap1, skn7 and wild-type strain and the sensitivity of the corresponding mutants exposed to different oxidative stress conditions proved a role of Yap1p and Skn7p in the defence against singlet oxygen. Similarities in the genetic responses against singlet oxygen and hydroperoxides suggest an overlap in the oxidative stress response against these reactive oxygen species.

Obstructive sleep apnoea: time for a radical change?

Reactive oxygen species (ROS) are highly reactive molecules that originate from both (intra- and extracellular) endogenous sources and from exogenous sources. They can be broadly divided into free radicals and nonradical reactive species; Stocker and Keaney 1 have examined this in a more extensive review. In the basal state, ROS play an essential physiological role in cellular signalling pathways and transcriptional regulation, which act to maintain cellular homeostasis 2. In contrast, oxidative stress is characterised by an excess of ROS, which can ultimately result in cellular injury via reactions with proteins, nucleic acids and lipids. As such, oxidative stress is hypothesised to play a primary role in the development of many disease processes, including atherosclerosis. The oxidative modification hypothesis of atherosclerosis centres on the well-known association between low-density lipoprotein (LDL) cholesterol and atherosclerosis and, in particular, on the uptake of oxidised LDL by macrophages within the arterial wall to form foam cells, the earliest stage in atherogenesis. In addition to inflammatory cells, there are a number of vascular cell types, including vascular smooth muscle cells, endothelial cells and adventitial fibroblasts, which all provide a source of oxidants within the vessel wall and could play a role in the conversion of LDL into its oxidised (high-uptake) form. The metabolic and enzymatic sources of ROS include (but are not limited to) nicotinamide adenine dinucleotide phosphate oxidases, xanthine oxidase, nitric oxide synthase, myeloperoxidase, lipoxygenase and mitochondrial respiration 1 …

Polyphenols Deriving from Chalcones: Investigations of Redox Activities

The redox properties of a series of hydroxychalcones (a group of polyphenols abundantly present in plants) were investigated by cyclic voltammetry. As for many polyphenols, their beneficial properties have been mainly related to their antioxidant activities, which in turn are directly associated to their redox behavior. Two types of radicals can be produced that are localized on either one of the two aromatic systems. Their thermodynamic and kinetic parameters were extracted and compared to the predictions of density functional theory calculations. When at least one OH is present on each ring, their behaviors are dominated by the conjugated system: phenolic ring A-double bond-ketone, which is the only one to be oxidized. However, the redox properties of this conjugated system are strongly influenced by the presence of ring B. When an OH is present on ring B, an important feature is the existence of strong hydrogen bonding that remains almost unmodified even when ring A is oxidized. It does not considerably change the thermodynamics of ring A but strongly increases the rigidity of the molecule that remains planar under the neutral, anionic, or radical forms. Oxidation potentials of the phenolates range between 0.1 and 0.2 V versus a saturated calomel electrode, which correspond to species that are very easy to oxidize and lead to the rapid formation of nonradical species, underlining the potential antioxidant properties of these molecules.

Sodium Nitroprusside: Mechanism of NO Release Mediated by Sulfhydryl-Containing Molecules

Sodium nitroprusside (SNP) is among the most widely studied nitric oxide donors, and its capability of producing NO seems to depend on its interaction with sulfhydryl-containing molecules present in vivo. The aim of this research has been the study of the mechanism of interaction between SNP and sulfhydryl-containing compounds, such as cysteine and glutathione, through detection by EPR, UV-vis, and IR spectroscopy of both the radical and nonradical species involved. An electron-transfer process can be invoked as the key step, which leads to the formation of the reduced SNP radical, the main detectable radical intermediate, and the corresponding S-nitrosothiol, the ending product of NO that can be considered the real storage and transporters of NO. When cysteine was used, a second radical species (A) is detectable: it can be accounted for by the interaction of a byproduct with unreacted cysteine.

Concurrent activation of cell death‐regulating signaling pathways by singlet oxygen in Arabidopsis thaliana

Upon a dark/light shift the conditional flu mutant of Arabidopsis starts to generate singlet oxygen ((1)O(2)), a non-radical reactive oxygen species that is restricted to the plastid compartment. Immediately after the shift, plants stop growing and develop necrotic lesions. We have established a protoplast system, which allows detection and characterization of the death response in flu induced by the release of (1)O(2). Vitamin B6 that quenches (1)O(2) in fungi was able to protect flu protoplasts from cell death. Blocking ethylene production was sufficient to partially inhibit the death reaction. Similarly, flu mutant seedlings expressing transgenic NahG were partially protected from the death provoked by the release of (1)O(2), indicating a requirement for salicylic acid (SA) in this process, whereas in cells depleted of both, ethylene and SA, the extent of cell death was reduced to the wild-type level. The flu mutant was also crossed with the jasmonic acid (JA)-depleted mutant opr3, and with the JA, OPDA and dinor OPDA (dnOPDA)-depleted dde2-2 mutant. Analysis of the resulting double mutants revealed that in contrast to the JA-induced suppression of H(2)O(2)/superoxide-dependent cell death reported earlier, JA promotes singlet oxygen-mediated cell death in flu, whereas other oxylipins such as OPDA and dnOPDA antagonize this death-inducing activity of JA.

Direct superoxide anion scavenging by a highly water-dispersible carotenoid phospholipid evaluated by electron paramagnetic resonance (EPR) spectroscopy

Synthetic carotenoid analogs, with increased utility for biological applications, are sparingly reported in the literature. Synthetic modification, which may increase the water solubility and/or water dispersibility of lipophilic carotenoids, allows their use in aqueous environments as potent antioxidants against potentially deleterious reactive oxygen species (ROS) that can be generated in vivo. Superoxide anion, produced by activated human neutrophils, can be a source of additional harmful ROS and nonradical species such as singlet oxygen in vivo. In the current study, direct scavenging of superoxide anion by a well-characterized C30 carotenoid phospholipid mixture was evaluated in a standard in vitro isolated human neutrophil assay by electron paramagnetic resonance (EPR) spectroscopy, employing the spin-trap DEPMPO. The carotenoid phospholipid was tested in aqueous formulation (aqueous dispersibility >60 mg/mL), in which supramolecular assembly takes place, as well as in ethanolic formulation as a monomeric solution of the carotenoid phospholipids. The carotenoid phospholipid (a highly unsaturated zwitterionic surfactant) was compared with a previously characterized rigid, long-chain, highly unsaturated dianionic bolaamphiphile, which contains an additional three conjugated double bonds in its extended conjugated system. As previously reported, direct scavenging by the carotenoid phospholipid derivatives in monomeric ethanolic formulation was superior at each tested concentration to aqueous, aggregated formulations of the compounds. Additionally, the percent inhibition of superoxide signal was related to the apparent or effective length of the conjugated chromophore, consistent with previous reports of radical inhibition and singlet oxygen quenching by polyene carotenoids of differing length.

Application of photoactivated periodate to the decolorization of reactive dye: reaction parameters and mechanism

The decolorization of the reactive dye, reactive black 5 (RB5), by the photoactivated periodate (UV/IO 4 −) was investigated under ultraviolet (UV) irradiation at 254 nm, and its possible mechanism based on periodate photochemistry was discussed, in order to elucidate the main oxidants involved in the decolorization of RB5 as the reaction parameters, such as the light intensity, periodate concentration, dissolved oxygen, and solution pH, were varied, with the intermittent employment of an OH scavenger. The decolorization rate of RB5 increased linearly with increasing light intensity. The decolorization rate was found to increase at low periodate concentrations (0–5 mM), but slightly decrease at higher concentrations (>5 mM). Dissolved oxygen did not have any measurable effect on the decolorization rate of the reactive dye. No pH dependence of the decolorization rate was observed over the pH range of 1.5–10, regardless of the periodate speciation. Based on these results, the main oxidants responsible for the RB5 decolorization with UV 254 were found to be OH and IO 3 (I VI ), after considering the six intermediate species which are reported to be produced as a result of periodate photolysis, namely the radical species ( OH, IO 3 , and IO 4 ) and the non-radical species (O 3, IO 4 −, and IO 3 −).

Synthesis, structure, and catalytic activity of mononuclear iron and (mu-Oxo)diiron complexes with the ligand 2,6-bis(N-methylbenzimidazol-2-yl)pyridine.

Iron complexes including polyimidazole and exchangeable ligands are studied with the aim of modeling the structural and functional features of the non-heme iron centers of dinuclear proteins, such as methane monooxygenase. In [Fe(2)OL(2)(MeOH)(2)(NO(3))(2)](NO(3))(2) (1) (L = 2,6-bis(N-methylbenzimidazol-2-yl)pyridine), each Fe(III) is in a distorted octahedral environment and has a donor set of N(3)O(3) which includes three N atoms from L and three O atoms from a nitrate, micro-oxo, and methanol. In complex [FeLCl(3)] (2) (L = 2,6-bis(N-methylbenzimidazol-2-yl)pyridine), Fe(III) is coordinated to three nitrogen atoms from L and three chloride ions. Complex 1 efficiently catalyzed the oxidation of cyclohexane with 51% conversion to cyclohexanol. It also catalyzed the epoxidation of styrene, cyclohexane, 2-methyl-2-butene, and cis- and trans-2-heptene with 51-84% conversions and high selectivity (71-99%) for epoxide products. Complex 2, however, has no specific reactivity toward these substrates. From the alcohol/ketone (A/K) ratio close to 1 in the oxidation of cyclohexane, the low KIE (kinetic isotope effect K(H)/K(D) ratio = 1.8) for cyclohexanol formation, and the nonstereospecificity of the oxidation of cis-dimethylcyclohexane, it can be concluded that long-lived alkyl radicals are involved in the oxidation catalyzed by complex 1. On the other hand, the stereospecific epoxidation of alkenes, the stereoselective oxidation of cumene, and the high degree of retention of configuration in the oxidation of cis- and trans-2-heptene suggest that a nonradical species, probably a metal-based intermediate, is involved in the oxidation of alkenes and cumene.

Rapid induction of distinct stress responses after the release of singlet oxygen in Arabidopsis.

The conditional fluorescent (flu) mutant of Arabidopsis accumulates the photosensitizer protochlorophyllide in the dark. After a dark-to-light shift, the generation of singlet oxygen, a nonradical reactive oxygen species, starts within the first minute of illumination and was shown to be confined to plastids. Immediately after the shift, plants stopped growing and developed necrotic lesions. These early stress responses of the flu mutant do not seem to result merely from physicochemical damage. Peroxidation of chloroplast membrane lipids in these plants started rapidly and led to the transient and selective accumulation of a stereospecific and regiospecific isomer of hydroxyoctadecatrieonic acid, free (13S)-HOTE, that could be attributed almost exclusively to the enzymatic oxidation of linolenic acid. Within the first 15 min of reillumination, distinct sets of genes were activated that were different from those induced by superoxide/hydrogen peroxide. Collectively, these results demonstrate that singlet oxygen does not act primarily as a toxin but rather as a signal that activates several stress-response pathways. Its biological activity in Arabidopsis exhibits a high degree of specificity that seems to be derived from the chemical identity of this reactive oxygen species and/or the intracellular location at which it is generated.

Do stable nitroxide radicals catalyze or inhibit the degradation of hyaluronic acid?

Reactive oxygen-derived species and particularly OH radicals can degrade hyaluronic acid (HA), resulting in a loss of viscosity and a subsequent decrease in its effectiveness as a joint-lubricating agent. The production of OH in the vicinity of HA can be catalyzed by bound redox-active metals, which participate in the Haber-Weiss reaction. Damage to HA can also occur as a result of hypochlorite formed by myeloperoxidase (MPO). The protective reagents commonly used to inhibit oxidative stress-induced degradation of HA include antioxidative enzymes, such as SOD and catalase, chelators that coordinate metal ions rendering them redox-inactive, and scavengers of radicals, such as OH, as well as nonradical reactive species. In recent years, stable cyclic nitroxides have also been widely used as effective antioxidants. In many cases, nitroxide antioxidants operate catalytically and mediate their protective effect through an exchange between their oxidized and reduced forms. It was anticipated, therefore, that nitroxides would protect HA from oxidative degradation as well. On the other hand, nitroxides serve as catalysts in many oxidation reactions of alcohols, sugars and polysaccharides, including hyalouronan. Such opposite effects of nitroxides on oxidative degradation are particularly intriguing and the aim of the present study was to examine their effect on HA when subjected to diverse forms of oxidative stress. The results indicate that nitroxides protect HA from OH radicals generated enzymatically or radiolytically. The protective effect is attributable neither to the scavenging of OH nor to the oxidation of reduced metal, but to the reaction of nitroxides with secondary carbohydrate radicals-most likely peroxyl radicals.

Radical Pairs in Solution

AbstractFor Abstract see ChemInform Abstract in Full Text.

Minimizing oxidative injury to the developing brain: the therapeutic quest continues

EDITOR-IN-CHIEF Oxidative injury to the developing central nervous system continues to be an area of concern and controversy in perinatal medicine. The clinical examples of hypoxia‐ ischemia-induced oxidative stress in the perinatal period include antepartum and intrapartum asphyxial events and neonatal respiratory distress. In the last scenario, oxidative stress may also be produced during resuscitation secondary to hyperoxygenation. The spectrum of oxidative stress-induced neurological syndromes extends from behavioral and learning disabilities to cerebral palsy. However, the causal relationship between clinically recognized episodes of hypoxia and perinatal brain lesions is often uncertain. Most cases of perinatal neurological compromise do not demonstrate any defined antecedents and most cases of perinatal asphyxia do not result in any demonstrable neurodevelopmental deficit. These controversies reflect deficiencies in our knowledge in this field. Recent investigations, however, have made significant contributions to the elucidation of this complex problem, especially in the underlying molecular mechanisms 1 . Hypoxia‐ ischemia-induced neuronal injury essentially starts with neuronal energy failure, resulting in the excessive production of both oxygen-free and other secondary radicals, and non-radical reactive species which can injure cell constituents. There is direct evidence of oxygen-free radical generation in the developing brain in response to hypoxia 2,3 . Cells generate oxygen-free radicals during normal respiratory and metabolic activities. Oxygen-free radicals are redox intermedates produced during the sequential reduction of oxygen to water, as an integral part of the energy-regenerating process of oxidative phosphorylation. Biologically significant examples of oxygen-free radicals include superoxide, hydroxyl, lipid hydroperoxide, lipid peroxyl and lipid alkoxyl radicals, and also nitric oxide. The non-radical intermediates include hydrogen peroxide and singlet oxygen. These radical and non-radical products are often collectively called reactive oxygen species. The mechanisms for the formation of these agents are complex and multiple, and include mitochondrial respiration and various metabolic pathways 4‐7 . Additional mechanisms of free radical generation in the brain include inflammatory and immunological reactions, expression of adhesion molecules, and stimulation of polymorphonuclear

Kinetic modeling of TiO2-catalyzed photodegradation of trace levels of microcystin-LR.

A kinetic model has been developed to investigate the relative importance of major pathways for the photocatalytic degradation of trace levels of the cyanobacterial toxin microcystin-LR (MLR) in solutions containing a complex suite of dissolved organic matter and to test the sensitivity of MLR degradation to rate constants of the key processes. The kinetic model incorporates adsorption of the trace contaminant, other organics and oxygen on the particle surface, surface reactions between adsorbed radical and nonradical species, desorption of surface radical species, solution phase radical reactions, and radical termination pathways. Under conditions where the contaminant adsorbs strongly to semiconductor surface sites, rapid degradation is observed, and a primary degradation step appears to involve reaction between surface-located long-lived organic radicals (formed from hydroxyl radical scavenging by the bulk organic) and adsorbed trace contaminant. MLR degradation is relatively insensitive to changes in light intensity under these strongly adsorbing conditions but highly dependent under weakly adsorbing conditions and when solution phase degradation is important. While not verified independently, desorption of surface bound superoxide appears to lead to the production of organic peroxyl radicals through reaction of superoxide with the bulk organic. These solution phase organic peroxyl radicals are highly reactive and appear to be the primary source of trace contaminant degradation under conditions where the trace contaminant shows no observable adsorption and surface degradation is negligible. Under alkaline conditions, adsorption of carbonate onto the particle surface results in scavenging of surface hydroxyl radicals to form surface carbonate radicals that rapidly quench surface bound superoxide. This prevents organic peroxyl production, the primary agent of solution-phase trace contaminant degradation.