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PubMed2003

Computer-aided modeling of pentachlorophenol 4-monooxygenase and site-directed mutagenesis of its active site.

Homology modeling was used to construct a model of the three-dimensional structure of pentachlorophenol 4-monooxygenase (PcpB). A PSI-BLAST homology search was initially performed to identify the 3D structure of proteins homologous with PcpB. The feasibility of modeled structures of PcpB was evaluated by Verify3D, which calculated structural compatibility scores based on 3D-1D profiles. The predicted structure of PcpB had an acceptable 3D-1D self-compatibility score, beyond the incorrect fold score threshold. A PcpB-pentachlorophenol (PCP) complex was then constructed utilizing the modeled PcpB structure. After energy minimization of the complex, and successive minimizations of the system that consisted of the complex and the water layer surrounding the complex, the molecular dynamics of the system were simulated. The active-site residues of PcpB were identified on the basis of the modeled structure, and PcpB mutants were then designed to change the active site residues, expressed, and purified by affinity chromatography. The mutant activity was compared with that of the wild-type to investigate the validity of the modeled structure. The experimental results suggested that Phe85, Tyr216, and Arg235 were relevant to enzyme activity, and that Tyr397 and Phe87 were important for stabilization of the structure of PcpB.

Binding Sites↗
PubMed1996

Mortality in a cohort of pentachlorophenol manufacturing workers, 1940-1989.

Mortality in a cohort of 770 workers with potential pentachlorophenol (PCP) exposure was evaluated from 1940 through 1989. The study cohort is a subset of a larger cohort of workers with potential exposure to higher chlorinated dioxins. Total mortality and cancer mortality in the PCP cohort were slightly lower than expected in comparison to the U.S. white male population. There were 229 total deaths with 242.5 expected (SMR = 94, 95% confidence interval 83-108), and 50 cancer deaths with 52.6 expected (SMR = 95, 95% confidence interval 71-125). In comparison with unexposed employees, the risk ratio for total mortality was 1.03 (95% confidence interval 0.90-1.17), and the risk ratio for all cancer mortality was 0.95 (95% confidence interval 0.71-1.26). In most cause of death categories of a priori interest no deaths were observed in the cohort. A small excess of other and unspecified lymphopoietic cancer deaths was observed but did not appear to be related to exposure. Excesses of deaths due to cancer of the kidney, gastric and duodenal ulcer, cirrhosis of the liver, and all accidents were observed in comparison with the U.S. white male population and with unexposed employees. These were associated with increasing estimated cumulative PCP exposure after lagging exposures by 5 and 15 years. Despite the limited size and the generally favorable total mortality experience of the cohort, it was concluded that cohort members may have incurred increased risk of death due to some specific causes. The risks could not, however, be attributed conclusively to PCP exposure and may have been associated with other occupational and nonoccupational factors. Additional mortality surveillance of this cohort will be performed.

Accidents↗
PubMed1999

Long-term exposure to wood-preserving chemicals containing pentachlorophenol and lindane is related to neurobehavioral performance in women.

BACKGROUND: The adverse neurobehavioral effects of long-term low exposure to wood-preserving chemicals (WPC) containing solvents, pentachlorophenol (PCP) and gamma-hexachlorocyclohexane (gamma-HCH; lindane), and other neurotoxicants were investigated in a neuropsychological group study. METHODS: Out of a population of 2,000 women visiting the outpatient practice of a gynecological department, a sample of 15 women aged 31-56 (mean 43) with long-term exposure to WPC verified by self-report, biological monitoring, and environmental samples was investigated. Fifteen controls aged 42 (31-56) years were drawn from the same population and pair-wise matched with respect to sex, age, education, and estimated intelligence. RESULTS: For the exposed group, mean PCP serum level was 43.6 micrograms/l and mean gamma-HCH blood level was 0.085 microgram/l. Mean duration of exposure was 10 (5-17) years. Intellectual functioning, attention, memory, and visuo-motor performance were examined, suggesting significant group differences in visual short-term memory (Benton Test; d = 1.5, P = .005), verbal memory (paired associate learning and Peterson paradigm; d = 4.3 and 1.6, P < .001), and an incidental learning task (d = 2.3; P = .001). Frequent subjective complaints as assessed by questionnaire were attenuated motivation (d = 1.7; P = .001), increased fatigue (d = 1.6; P = .001), distractibility (d = 1.0; P = .003), and depressed mood (d = 1.9; P = .004). PCP blood level was significantly associated with paired-associate learning, Benton Test, and reading/naming speed. CONCLUSIONS: Long-term low-dose exposure to WPC in the domestic environment could be related to subjective complaints (attention, mood, and motivation) and to subtle alterations of neurobehavioral performance (e.g., working memory) in women.

Adult↗
PubMed1999

Adsorption capacity as a key parameter for enzyme induction and pentachlorophenol degradation in Mycobacterium chlorophenolicum PCP-1.

Adsorption of pentachlorophenol (PCP) on induced cells of Mycobacterium chlorophenolicum PCP-1 and its influence on enzyme induction and PCP degradation of this strain were studied. Compared to non-induced cells, induced degrading cells had a lower adsorption capacity (q(ads)), particularly at prolonged induction and low PCP concentration. Unlike the effects of pH and biomass concentration previously reported for non-induced cells, the variation of q(ads) of induced cells was associated with changes of both the capacity and intensity constants of the Freundlich equation which was used to describe PCP adsorption on M. chlorophenolicum PCP-1. This indicated changes of cell surface properties during enzyme induction and PCP degradation. The latter was shown in turn to be affected by several parameters such as PCP concentration, pH value and induction time. Interestingly, irrespective of the pH and PCP concentration, the specific PCP degradation rate (q(t)(PCP)) at a given induction time was found to be solely a function of q(ads), revealing that adsorption capacity is an inherent key parameter for enzyme induction and PCP degradation. Based on this knowledge, a kinetic model was developed for q(t)(PCP) which used only q(ads) and induction time as variables. The model considered inhibition of PCP on both enzyme induction and enzyme activity and described the experimental data at different PCP concentrations and pH values well. q(ads) also turned out to be a useful criterion for choosing optimum induction concentration of PCP. Irrespective of pH and biomass concentration, an initial adsorption capacity of 2-3 micromol PCP/g cells was found to be optimum for enzyme induction in M. chlorophenolicum PCP-1.

Adsorption↗
PubMed1993

A health survey of workers in the pentachlorophenol section of a chemical manufacturing plant.

During 1968 to 1985, 109 workers who had been engaged in the production of pentachlorophenol, using non-gamma isomers of hexachloroclohexane (BHC) as the raw material, were surveyed. Endemic chloracne among them had been noted since 1974. The prevalence of chloracne was 73.4% (80/109) in total and 95.2% (20/21) in a trichlorobenzene (TCB) tank area where dioxin and dibenzofurans levels were thousands of ppm. To our knowledge, PCDDs and PCDFs have not previously been reported from thermal decomposition of BHC. Urinary porphyrins were significantly higher among exposed workers than among the controls but there was no significant difference between the workers with chloracne and those without. The conduction velocities of the median motor nerves were much slower among the workers in the TCB tank area where the highest PCDDs contamination appeared. The mortality study cohort was relatively young. Based on the three deaths observed during the follow-up, no association could be drawn.

Acne Vulgaris↗
PubMed2002

A kinetic model for surfactant inhibition of pentachlorophenol biodegradation.

A kinetic model is used to describe the effect of the nonionic surfactant Tergitol NP-10 (TNP10) on pentachlorophenol (PCP) biodegradation by Sphingomonas chlorophenolica sp. strain RA2. Different initial biomass to initial substrate ratios ranging from 13 to 418 were tested with 23 TNP10 concentrations ranging from 0 to 1500 mg/L. Tests were also conducted at 10 degrees C and 20 degrees C. No PCP biodegradation inhibition was observed at concentrations below the critical micelle concentration (CMC) of 50 mg/L. TNP10 concentrations above 100 to 200 mg/L were increasingly inhibitory to PCP biodegradation rates. This inhibition was best described by the Monod kinetic equation wherein the effect of TNP10 inhibition is reflected in the half-saturation constant (Ks). The value of the Ks increased from between 1.5 and 13.5 mg/L with no surfactant present to 44 to 131 mg/L at 1000 mg/L TNP10. Using a standard competitive inhibition approach, the inhibition constant for TNP10 was approximately 100 mg/L at both 10 degrees C and 20 degrees C.

Biodegradation, Environmental↗
PubMed2003

Flocculation behavior of Sphingobium chlorophenolicum in degrading pentachlorophenol at different life stages.

The cell flocculation behavior of degrading pentachlorophenol (PCP) by using Sphingobium chlorophenolicum (Flavobacterium sp., ATCC 39723) is investigated in the present paper. It is found that these Sphingobium cells can efficiently degrade PCP when the concentration of this toxic compound is below 150 ppm. These degradation rates of PCP can be facilitated with the additions of three supplementary carbons: glutamate (4.0 g/L), glucose (3.2 g/L), and cellobiose (3.05 g/L), among which the highest specific growth rate of cells is obtained when glucose is added. More importantly, in these biodegradation experiments described herein, in order to investigate the cell flocculation behavior, the temporal variations of cell size, zeta potential, and stability ratio of the cell suspension are also measured. It is found that, no matter what kind of supplementary carbon source is added, the highest stability ratio of the cell suspension can be always obtained at the end of the exponential growth phase, which can be well explained by using the results of cell size and zeta potential measurements according to the DLVO theory.

Alphaproteobacteria↗
PubMed2001

Enhanced selection of an anaerobic pentachlorophenol-degrading consortium.

A rapid enrichment approach based on a pentachlorophenol (PCP) feeding strategy which linked the PCP loading rate to methane production was applied to an upflow anaerobic sludge bed reactor inoculated with anaerobic sludge. Due to this strategy, over a 140-day experimental period the PCP volumetric load increased from 2 to 65 mg L(R)(-1) day(-1) with a near zero effluent concentration of PCP. Dechlorination dynamics featured sequential appearance of 3,4,5-chlorophenol, 3,5-chloro- phenol, and 3-chlorophenol in the reactor effluent. Profiling of the reactor population by denaturing gradient gel electrophoresis (DGGE) revealed a correlation between the appearance of dechlorination intermediates and bands on the DGGE profile. Nucleotide sequencing of newly detected 16S rDNA fragments suggested the proliferation of Clostridium and Syntrophobacter/Syntrophomonas spp. in the reactor during PCP degradation. Published by John Wiley & Sons, Inc.

Anaerobiosis↗
PubMed2005

Dual substrate biodegradation of a nonionic surfactant and pentachlorophenol by Sphingomonas chlorophenolica RA2.

The simultaneous biodegradation of the nonionic surfactant Tween 20 (Tw20) and pentachlorophenol (PCP) by Sphingomonas chlorophenolica sp. Strain RA2 (RA2) was measured. As a sole substrate, Tw20 biodegradation was best described by the Contois kinetic model. During concurrent biodegradation of Tw20 and PCP, the biodegradation rates of Tw20 were not significantly affected by 50 or 100 mg/L PCP, but were significantly inhibited by 500 mg/L PCP. Decreases in cell yield in the presence of PCP suggest that PCP was acting as an uncoupler. Cultures were pre-grown on PCP or Tw20 before degradation of PCP to evaluate enzyme induction effects, and long lags before PCP biodegradation after growth on Tw20 occurred. Although biokinetic models could accurately describe some of the data sets of RA2 growth and Tw20 and PCP degradation, finding a single set of kinetic parameters that predicted all dual substrate tests was not achieved. The complicating factors to modeling PCP and Tw20 interactions are described and may be more widely applicable to the biodegradation of toxic organic compounds in the presence of a biodegradable surfactant.

Biodegradation, Environmental↗
PubMed2001

Pentachlorophenol potentiates benzo[a]pyrene DNA adduct formation in adult but not infant B6C3F1 male mice.

The objective of this study is to determine whether pentachlorophenol (PCP) alters benzo[a]pyrene (B[a]P)-induced DNA adduct formation in infant and adult B6C3F1 male mice. Mice were exposed intraperitoneally to 55 microg B[a]P/g body weight (BW) alone and in combination with several doses of PCP in DMSO. The 32P-postlabeling assay was used to analyze for (+/-) anti-7,8-diol-9,10-epoxide-B[a]P-N(2)deoxyguanosine (BPDE-N(2)G) adducts formed in liver and lung DNA. Hepatic DNA also was analyzed for 8-hydroxy-2'-deoxyguanosine (8-OHdG) base damage in mice exposed to PCP. 8-OHdG was not detected at any dose of PCP in infant or adult mice. PCP exhibited an antagonistic effect on BPDE-N(2)G accumulation in infant mice exposed to B[a]P in combination with 50 microg PCP/g BW at both 12 and 24 hr. Comparatively, BPDE-N(2)G adducts were increased in adult mice exposed to binary mixtures at 24 hr in both hepatic and lung DNA (P < 0.05). Multiple comparison analysis between infant and adult mice revealed that adduct levels in infants exposed to B[a]P alone or in combination with PCP were not different from those observed in adult mice exposed to B[a]P. However, a significant increase in adducts was observed in adult mice exposed to a combination of B[a]P and PCP compared to that in all other treatment groups (P < 0.05). These results suggest that PCP alters the metabolism of B[a]P in both infant and adult mice through different mechanisms, and that infants are not susceptible to the potentiating effects of PCP observed in adult mice.

Age Factors↗
PubMed1991

Effect of pentachlorophenol on the activation of 2,6-dinitrotoluene to genotoxic urinary metabolites in CD-1 mice: a comparison of GI enzyme activities and urine mutagenicity.

2,6-Dinitrotoluene (2,6-DNT) and pentachlorophenol (PCP) are used for industrial purposes and are found in the environment as hazardous contaminants. Because concurrent exposure to both compounds can occur, it is of interest to determine if organochlorine compounds potentiate the effect of nitroaromatic chemicals. CD-1 mice were treated with PCP (42.8 mg/kg) for 4 weeks. On weeks 1, 2, and 4 after the initial PCP dose, mice were treated p.o. with 2,6-DNT (75 mg/kg) and 24 hr urines were collected. After concentration, the urines were tested for their mutagenic activity in Salmonella typhimurium strain TA98 without metabolic activation in a microsuspension bioassay. A significant increase (P less than .05) in mutagenicity was observed in urines from mice treated with 2,6-DNT alone and in combination with PCP. By week 4, mice that received both 2,6-DNT and PCP excreted urine that was more mutagenic than that from animals which received only 2,6-DNT. At weeks 2 and 4, mice were sacrificed and intestinal enzyme activities (nitroreductase, azo reductase, beta-glucuronidase, dechlorinase, and dehydrochlorinase) were quantitated. The enhanced genotoxicity observed in urines from 2,6-DNT/PCP-treated mice coincided with a decrease in nitroreductase and an increase in beta-glucuronidase activities in the small intestine.

Animals↗
PubMed1991

Sublethal effects of pentachlorophenol in the abalone (Haliotis rufescens) as measured by in vivo 31P NMR spectroscopy.

The sublethal biochemical effects of pentachlorophenol (PCP) were investigated in live, intact red abalones (Haliotis rufescens), using a flow-through exposure system, by in vivo 31P NMR spectroscopy. Based on rangefinding tests (6-hr LC50 = 1.6 mg/L; 6-hr no-observable-effect-level (NOEL) = 0.8 mg/L), three abalones were separately exposed to a sublethal concentration (1.2 mg/L) for 5 hr, followed by a 13 hr recovery period. Effects in foot muscle included both a decrease in phosphoarginine and an increase in inorganic monophosphate concentrations ([PA] and [Pi], respectively); both foot muscle concentrations of adenosine triphosphate [ATP] and intracellular pH (pHi) also declined. Parallel in vitro experiments revealed that concentrations of glycerol 3-phosphate, lactate, citrate, succinate, malate, and alanine (Ala) all increased, while those of glyceraldehyde 3-phosphate and glutamine (Gln) remained stable. Also, these effects were not evident until 2 hr into exposure, possibly the time required for PCP to attain an effective concentration in foot muscle. During recovery, while Pi declined to pre-exposure levels, [PA] completely recovered in only one individual. Also, realkalinization of pHi was similar to recovery of [Pi], and ATP returned to near-initial levels, as did glycerol 3-phosphate, lactate, succinate, malate, and Ala; glyceraldehyde 3-phosphate, citrate, and Gln levels declined. Recovery responses corresponded to the time for PCP clearance from foot muscle. The effects of PCP were similar to those of hypoxia, fatigue, hypersalinity, and arginine kinase inhibitors, and so sublethal PCP concentrations may also inhibit electron transport and arginine kinase as well as uncouple mitochondrial oxidative phosphorylation in intact molluscs. Thus, the effects of pollutants on key biochemical processes may now be measured in intact aquatic organisms as they occur, improving our ability to accurately assess the environmental effects of pollutants in the laboratory.

Animals↗
PubMed1993

Toxicokinetics and biotransformation of pentachlorophenol in the topsmelt (Atherinops affinis).

The toxicokinetics and biotransformation of pentachlorophenol (PCP) were determined in the topsmelt (Atherinops affinis). In a static system, topsmelt (n = 9) were exposed to 50 micrograms/L of [U-14C]PCP for 24 hours to determine the absorption rate constant (Ka), the whole-body bioconcentration (at steady-state conditions), the elimination rate constant (Ke), and the elimination half-life (t1/2). Kinetics were determined by direct quantitation of radioactivity in the exposure water. Following exposure, fish were placed in a flow-through metabolism chamber for 24 hours to allow depuration of retained residues, which were collected on XAD-4 resin. Excreted residues were identified and quantified by high-pressure liquid co-chromatography, fraction collection, and liquid scintillation counting. The Ka and Ke, calculated using a simplified model, were 0.012 +/- 0.005/h and 0.014 +/- 0.003/h, respectively, while the 24 hour total concentration factor was 278.0 +/- 182.0 and the t1/2 was 52.7 +/- 11.2. During 24 hours of exposure to clean seawater, topsmelt depurated 32.9% of retained residues, and while PCP was primarily excreted unchanged (64.9%), significant amounts of both pentachlorophenylsulfate (18.9%) and pentachloro-beta-D-glucuronide (16.2%) were also formed.

Absorption↗
PubMed1992

Pharmacokinetic concepts in assessing intake of pentachlorophenol by rats after exposure through drinking water.

The objective of this study was to predict concentrations of a toxicant in plasma after exposure to the toxicant through drinking water using basic pharmacokinetic principles. As an example, we studied pentachlorophenol (PCP), a widely used wood preservative of public health concern as an environmental pollutant. We added PCP to the drinking water (30 micrograms/mL) of five rats for 3 days. Blood was sampled, and water consumption was monitored every 12 h on the days 1 and 2 and every 3 h on day 3. After a 4-day washout, a PCP dose of 2.5 mg/kg was given intravenously, and blood was withdrawn at selected times for 2 days. PCP concentrations in plasma were measured by capillary gas chromatography. A one-compartment model with zero-order input and kinetic parameters (clearance, volume of distribution, and bioavailability) estimated after intravenous administration adequately predicted PCP concentrations in plasma during exposure to PCP. The average steady-state concentration (Css), which reflects the overall exposure, was predicted using the clearance (CL) concept [i.e., Css = (bioavailability.rate of intake)/CL] and compared with the observed value. The data for PCP demonstrate the potential utility of CL and other kinetic concepts in assessing exposure to a toxicant in drinking water, food, or air.

Administration, Oral↗
PubMed2003

Skin tumor-promoting potential and systemic effects of pentachlorophenol and its major metabolite tetrachlorohydroquinone in CD-1 Mice.

The mouse skin carcinogenesis model provides a conceptual framework to study the carcinogenesis process. It has been used extensively to assess whether a chemical or physical agent carries a carcinogenic hazard to humans and to define the mechanism involved with the carcinogenic effects. We conducted a study to evaluate whether the tumor-promoting activity of pentachlorophenol (PCP) is mainly from its major metabolite tetrachlorohydroquinone (TCHQ). We applied the mouse skin model to CD-1 mice and the results showed that PCP and TCHQ are much weaker promoters than 12-O-tetradecanoylphorbol-13-acetate (TPA) in mouse skin during a 25-wk experiment. Both PCP and TCHQ could induce mice skin epidermal hyperplasia and proliferating cell nuclear antigen (PCNA) labeling index in the epidermis. However, TCHQ caused a more significant induction of epidermal hyperplasia and PCNA positive cells than PCP. Topical application of PCP, but not TCHQ, induced significant organ enlargement and lymphoma in mice, whereas short-term treatment of TCHQ increased tumor necrosis factor-alpha (TNF-alpha) gene expression in mouse skin. We did not observe a significant association between the carcinogenic process and serum TNF-alpha or interleukin-1 beta (IL-1 beta) levels in mice.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed2005

Persistent inhibition of human natural killer cell function by ziram and pentachlorophenol.

Ziram is a currently used agricultural fungicide. It is also used as an additive in the production of latex gloves. Because of these uses, there is a potential for human exposure to this compound. Pentachlorophenol (PCP) has been used as an insecticide, fungicide, disinfectant, and ingredient in antifouling paints. Currently, it is used as a wood preservative for power-line poles and fence posts. Measurable levels of PCP have been detected in human blood and urine. In previous studies we demonstrated that both these compounds could cause very significant inhibition of the tumor-killing function of human natural killer (NK) cells. NK lymphocytes play a central role in immune defense against viral infection and the formation of primary tumors. So interference with their function could increase the risk of tumor development. In the present study we examined the effects of exposure to ziram or PCP of brief duration (1 h) on the ability of NK cells to destroy tumor cells. NK cells were exposed to either ziram (5-0.5 microM) or PCP (10-5 microM) for 1 h followed by 0 h, 24 h, 48 h, or 6 days in compound-free media and then were tested for the ability to lyse as well as to bind tumor cells. A 1-h exposure to as little as 2.5 microM ziram decreased the ability of NK cells to lyse target tumor cells, which persisted up to 6 days following exposure. The loss of lytic function for from 24 h to 6 days following exposure was accompanied by a comparable loss of NK capacity to bind tumor cells. Exposure to 10 microM PCP for 1 h caused a progressive loss (greater than 80%) of lytic function within 6 days of exposure. In contrast to ziram, PCP exposure caused no accompanying loss of binding function.

Cells, Cultured↗
PubMed1995

Veratryl alcohol-mediated indirect oxidation of pentachlorophenol by lignin peroxidase.

The oxidation of pentachlorophenol (PCP) by lignin peroxidase (LiP) is characterized by a rapid loss of activity during which time the enzyme is quickly converted to compound III, an inactive form of the enzyme. We investigated the indirect oxidation of PCP by LiP using veratryl alcohol (VA) as a mediator. The oxidation of VA to veratryl aldehyde by LiP was inhibited by PCP. Inhibition was characterized by lag period followed by the same rate of VA oxidation. The lag period before VA oxidation was increased by increasing concentrations of PCP. During the lag period, PCP was oxidized and the extent of PCP oxidation increased with increasing concentrations of VA. The enzyme stayed as compound II during PCP oxidation in the presence of VA, suggesting that VA has a protective role in the LiP catalysis. The kinetics of PCP oxidation in the presence of VA were similar to those of VA oxidation. All these results suggest that PCP is oxidized indirectly via the veratryl alcohol cation radical. 2,3,5,6-Tetrachloro-p-benzoquinone was a stoichiometric product during PCP oxidation in both the presence and the absence of VA. An equivalent amount of inorganic chloride was formed by oxidative 4-dechlorination during PCP oxidation in the presence of VA. The increase in the rate and extent of PCP oxidation by VA results from mediation of PCP oxidation and reversion of inactive compound III to native enzyme, both by the veratryl alcohol cation radical.

Basidiomycota↗
PubMed2000

Evidence for production of hydroxyl radicals by pentachlorophenol metabolites and hydrogen peroxide: A metal-independent organic Fenton reaction.

The production of hydroxyl radicals by tetrachlorohydroquinone (TCHQ, a major metabolite of the widely used biocide pentachlorophenol) in the presence of H(2)O(2) was studied by salicylate hydroxylation method. HPLC with electrochemical detection was used to measure the levels of 2,3- and 2,5-dihydroxybenzoic acid (DHBA) formed when the hydroxyl radicals react with salicylate. We found that TCHQ and H(2)O(2) could produce both 2,3- and 2,5-DHBA when incubated with salicylate. Their production was markedly inhibited by hydroxyl radical scavenging agents dimethyl sulfoxide and ethanol, as well as by tetrachlorosemiquinone radical scavengers desferrioxamine and other hydroxamic acids. In contrast, their production was not affected by the nonhydroxamate iron chelators diethylenetriaminepentaacetic acid (DTPA), bathophenanthroline disulfonic acid, and phytic acid, as well as the copper-specific chelator bathocuprione disulfonic acid. A comparison of product formation and distribution from the reaction of ferrous iron with hydrogen peroxide (the classic Fenton system) strongly suggests that the same hydroxyl radical adducts are formed as in the TCHQ/H(2)O(2) experiments. Taken together, we propose that hydroxyl radicals were produced by TCHQ in the presence of H(2)O(2), probably through a metal-independent organic Fenton reaction.

Chelating Agents↗