Low Concentrations Of Hydrogen Peroxide Research Articles

Effects of Hydrogen Peroxide on Wound Healing in Mice in Relation to Oxidative Damage

It has been established that low concentrations of hydrogen peroxide (H2O2) are produced in wounds and is required for optimal healing. Yet at the same time, there is evidence that excessive oxidative damage is correlated with poor-healing wounds. In this paper, we seek to determine whether topical application of H2O2 can modulate wound healing and if its effects are related to oxidative damage. Using a C57BL/6 mice excision wound model, H2O2 was found to enhance angiogenesis and wound closure at 10 mM but retarded wound closure at 166 mM. The delay in closure was also associated with decreased connective tissue formation, increased MMP-8 and persistent neutrophil infiltration. Wounding was found to increase oxidative lipid damage, as measured by F2-isoprostanes, and nitrative protein damage, as measured by 3-nitrotyrosine. However H2O2 treatment did not significantly increase oxidative and nitrative damage even at concentrations that delay wound healing. Hence the detrimental effects of H2O2 may not involve oxidative damage to the target molecules studied.

A possible future fuel cell: the peroxide/peroxide fuel cell

SUMMARY Hydrogen peroxide (H2O2) and the reduction/oxidation by-products of peroxide are non-toxic to humans and the environment. Simple, low-concentration hydrogen-peroxide solutions used as fuel and direct peroxide/peroxide fuel cells (DPPFCs) face significant challenges in the development of a new class of power generators. A power density of 10 mWcm−2 at a cell potential of 0.55 V have been achieved with a DPPFC composed of carbon-paper-supported nickel as the anode catalyst and carbon-paper PbSO4 as the cathode catalyst. The catalysts have been prepared by electroless deposition. Using non-precious metals rather than platinum in our FC makes the cell cost effective comparable to that of PEMFCs. Additionally, as a low-price fuel, H2O2 reduces the cost of this FC. Copyright © 2012 John Wiley & Sons, Ltd.

Phospholipase D participates in H2O2-induced A549 alveolar epithelial cell migration

ABSTRACTTo investigate the effects of phospholipase D (PLD) on low-concentration hydrogen peroxide (H2O2)-induced growth and migration in alveolar epithelial A549 cells, the cells were exposed to H2O2 (3–100 μM) for 12–48 hours, cell proliferation was determined by MTT assay and cell migration was tested by a modified epithelial wound healing assay. We found that one bolus of H2O2 (10–100 μM) did not affect proliferation, but significantly stimulated migration (143–161% of control) after a 12-hour exposure. Pretreatment with the antioxidants catalase (1000 U/ml), N-acetyl-cysteine (2 mM), or edaravone (10 μM) abolished the migration induced by 30 μM H2O2; the PLD inhibitor 1-butanol (0.5%) also attenuated H2O2-induced migration to the control level; while exogenous phosphatidic acid (PA) (10−7–10−4 M) mimicked the effects of PLD activation and induced migration in a dose-dependent manner. We suggest that the alveolar epithelial cell migration induced by exposure to low concentrations of H2O2 benefits tissue repair during acute lung injury (ALI) and PLD is involved in the underlying mechanism.

Oxidative stress caused by a low concentration of hydrogen peroxide induces senescence-like changes in mouse gingival fibroblasts

Periodontal tissue deteriorates under persistent oxidative stress induced by inflammatory reactions in the microflora of the oral cavity. This study aimed to evaluate the cellular properties of mouse gingival fibroblasts (MGFs) in the presence of oxidative stress. MGFs from 10-, 30- and 52-week-old mice were used to evaluate the changes in the cellular properties with aging. The study investigated the effects of oxidative stress on the cellular properties of MGFs from 10-week-old mice. The expression of p53, p21 and murine double minute 2 (Mdm2) in the MGFs in response to oxidative stress was also examined. By day 8, the number of MGFs increased in culture. However, the increase was markedly lower in MGFs derived from aged mice. Oxidative stress due to hydrogen peroxide (H2O2)-induced morphological changes characterized by a round shape with enlarged nuclei and expanded cytoplasm. The cell number of MGFs was decreased subsequent to treatment with 50 μM or a higher concentration of H2O2. MGFs treated with H2O2 at 20 μM showed a similar cell growth curve as the one seen in 52-week-old mice. Phosphorylated p53 protein was increased in MGFs subsequent to treatment with 20 μM H2O2, along with an upregulated transcription of p21 and Mdm2 mRNAs. These results suggest that treatment with a lower concentration of H2O2 in MGFs induces cell cycle arrest, resulting in stress-induced premature senescence, possibly correlated with the development of periodontal diseases.

Oxidation Levels Differentially Impact Melanocytes: Low versus High Concentration of Hydrogen Peroxide Promotes Melanin Synthesis and Melanosome Transfer

Background: UVB light can generate potentially harmful hydrogen peroxide (H₂O₂) in vivo, but it can also promote the beneficial proliferation and migration of melanocytes. The successful use of UVB monotherapy for treatment of vitiligo suggests that H₂O₂ may have a biphasic effect on melanin synthesis and melanosome transfer. Objective: To study the beneficial role of H₂O₂ on melanogenesis and melanosome transport in living melanocytes and keratinocytes. Methods: A co-culture system model was constructed using the primary human melanocytes and keratinocytes. The MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay was used to determine cell proliferation, NaOH was used to determine the melanin content, and real-time PCR was used to determine tyrosinase expression. Western blot was used to determine Rab-27A and protease-activated receptor 2 (PAR-2) expression. Results: This study demonstrated that tyrosinase was activated by low concentrations of H₂O₂ (≤0.3 mM); however, this activity was downregulated by high concentrations of H₂O₂ (>0.3 mM). Activation of high levels of melanin synthesis was induced when cells were treated with low concentrations of H₂O₂ (0.3 mM). Further observation using an in vitro co-culture system of fluorescein (carboxyfluorescein diacetate succinimidyl ester, CFDA-SE)-labeled melanocytes and keratinocytes indicated that melanosome transfer occurred in normal human epidermal melanocytes. Fluorescence microscopy revealed increased melanosome transfer into keratinocytes treated with 0.3 mM H₂O₂ in the co-culture compared to the control. Examination of melanosomes in the keratinocytes by flow cytometry confirmed these results. Furthermore, treatment with H₂O₂ (0.3 mM) upregulated the expression of Rab-27A and PAR-2, significant proteins involved in melanosome transfer, according to Western blot. Conclusion: These results confirmed that low concentration levels of H₂O₂ play a major role in the regulation of human pigmentation by increasing melanin synthesis and melanosome transfer.

Differential roles of proteasome and immunoproteasome regulators Pa28αβ, Pa28γ and Pa200 in the degradation of oxidized proteins

The response and functions of proteasome regulators Pa28αβ (or 11S), Pa28γ and Pa200 in oxidative-stress adaptation (also called hormesis) was studied in murine embryonic fibroblasts (MEFs), using a well-characterized model of cellular adaptation to low concentrations (1.0–10.0μM) of hydrogen peroxide (H2O2), which alter gene expression profiles, increasing resistance to higher levels of oxidative-stress. Pa28αβ bound to 20S proteasomes immediately upon H2O2-treatment, whereas 26S proteasomes were disassembled at the same time. Over the next 24h, the levels of Pa28αβ, Pa28γ and Pa200 proteasome regulators increased during H2O2-adaptation, whereas the 19S regulator was unchanged. Purified Pa28αβ, and to a lesser extent Pa28γ, significantly increased the ability of purified 20S proteasome to selectively degrade oxidized proteins; Pa28αβ also increased the capacity of purified immunoproteasome to selectively degrade oxidized proteins but Pa28γ did not. Pa200 regulator actually decreased 20S proteasome and immunoproteasome’s ability to degrade oxidized proteins but Pa200 and poly-ADP ribose polymerase may cooperate in enabling initiation of DNA repair. Our results indicate that cytoplasmic Pa28αβ and nuclear Pa28γ may both be important regulators of proteasome’s ability to degrade oxidatively-damaged proteins, and induced-expression of both 20S proteasome and immunoproteasome, and their Pa28αβ and Pa28γ regulators are important for oxidative-stress adaptation.

Protein polymer hydrogels by in situ, rapid and reversible self-gelation

Protein-based biomaterials are an important class of materials for applications in biotechnology and medicine. The exquisite control of their composition, stereochemistry, and chain length offers unique opportunities to engineer biofunctionality, biocompatibility, and biodegradability into these materials. Here, we report the synthesis of a thermally responsive peptide polymer-based hydrogel composed of a recombinant elastin-like polypeptide (ELP) that rapidly forms a reversibly cross-linked hydrogel by the formation of intermolecular disulfide cross-links. To do so, we designed and synthesized ELPs that incorporate periodic cysteine residues (cELPs), and show that cELPs are thermally responsive protein polymers that display rapid gelation under physiologically relevant, mild oxidative conditions. Gelation of cELPs, at concentrations as low as 2.5 wt%, occurs in ∼2.5 min upon addition a low concentration of hydrogen peroxide (0.3 wt%). We show the utility of these hydrogels for the sustained release of a model protein in vitro, and demonstrate the ability of this injectable biomaterial to pervade tumors to maximize tumor coverage and retention time upon intratumoral injection. cELPs represent a new class of injectable reversibly cross-linked hydrogels with properties intermediate between ELP coacervates and chemically cross-linked ELP hydrogels that will find useful applications in drug delivery and tissue engineering.

The effects of light on bleaching and tooth sensitivity during in-office vital bleaching: A systematic review and meta-analysis

ObjectiveTo evaluate the influence of light on bleaching efficacy and tooth sensitivity during in-office vital bleaching. Data sourcesWe performed a literature search using Medline, EMBASE and Cochrane Central up to September 2011. Study selectionAll randomised controlled trials (RCTs) or quasi-RCTs comparing the light-activated bleaching system with non-activation bleaching system were included. Reports without clinical data concerning bleaching efficacy or tooth sensitivity were excluded. ResultsEleven studies were included in the meta-analysis. A light-activated system produced better immediate bleaching effects than a non-light system when lower concentrations of hydrogen peroxide (15–20% HP) were used (mean difference [MD], −1.78; 95% confidence interval [CI]: [−2.30, −1.26]; P<0.00001). When high concentrations of HP (25–35%) were employed, there was no difference in the immediate bleaching effect (MD, −0.39; 95% CI: [−1.15, 0.37]; P=0.32) or short-term bleaching effect (MD, 0.25; 95% CI: [−0.47, 0.96]; P=0.50) between the light-activated system and the non-light system. However, the light-activated system produced a higher percentage of tooth sensitivity (odds ratio [OR], 3.53; 95% CI: [1.37, 9.10]; P=0.009) than the non-light system during in-office bleaching. ConclusionsLight increases the risk of tooth sensitivity during in-office bleaching, and light may not improve the bleaching effect when high concentrations of HP (25–35%) are employed. Therefore, dentists should use the light-activated system with great caution or avoid its use altogether. Further rigorous studies are, however, needed to explore the advantages of this light-activated system when lower concentrations of HP (15–20%) are used.

DNA damage by X-rays and their impact on replication processes

BackgroundReplication-dependent radiosensitization of tumors ranks among the most promising tools for future improvements in tumor therapy. However, cell cycle checkpoint signaling during S phase is a key for maintaining genomic stability after ionizing irradiation allowing DNA damage repair by stabilizing replication forks, inhibiting new origin firing and recruiting DNA repair proteins. As the impact of the different types of DNA damage induced by ionizing radiation on replication fork functionality has not been investigated, this study was performed in tumor cells treated with various agents that induce specific DNA lesions. MethodsU2OS cells were exposed to methyl methanesulfonate (MMS) to induce base damage, low or high concentrations of hydrogen peroxide for the induction of SSBs, Topotecan to induce DSBs at replication, Mitomycin C (MMC) to induce interstrand cross-links or ionizing irradiation to analyze all damages. Chk1 phosphorylation, origin firing and replication fork progression, and cell cycle distribution were analyzed. ResultsIn our system, the extent of Chk1 phosphorylation was dependent on the type of damage induced and prolonged Chk1 phosphorylation correlated with the inhibition of replication initiation. Ionizing radiation, high concentrations of hydrogen peroxide, and Topotecan affected replication elongation much more strongly that the other agents. Almost all agents induced a slight increase in the S phase population but subsequent G2 arrest was only observed in response to those agents that strongly inhibited replication elongation and caused prolonged Chk1 phosphorylation. ConclusionsOur data suggest that to improve radiotherapy, radiosensitivity in S phase could be increased by combining irradiation with agents that induce secondary DSB or inhibit checkpoint signaling, such as inhibitors of PARP or Chk1.

Kinetics of the iodate reduction by hydrogen peroxide and relation with the Briggs–Rauscher and Bray–Liebhafsky oscillating reactions

The iodate reduction by hydrogen peroxide in acidic solutions is part of the Bray-Liebhafsky and Briggs-Rauscher oscillating reactions. At low hydrogen peroxide concentrations, typical of the Bray-Liebhafsky reaction, its rate law is -d[IO(-)(3)]/dt = (k'(R) + k"(R)[H(+)])[IO(-)(3)][H(2)O(2)] with k'(R) = 1.3 × 10(-7)(20°), 7.8 × 10(-7) (39°), 1.4 × 10(-5) M(-1) s(-1) (60°) and k"(R) = 1.5 × 10(-5) (25°), 6.2 × 10(-5) (39°), 6.3 × 10(-4) M(-2) s(-1) (60°). It is explained by a non-radical mechanism. At high hydrogen peroxide concentrations, typical of the Briggs-Rauscher reaction, a new reaction pathway appears with a rate more than proportional to [H(2)O(2)](2) and nearly independent of [IO(3)(-)] > 0.01 M. This pathway is inhibited by scavengers of free radicals. We suggest that it has a radical mechanism starting with IOH + H(2)O(2)⇌ IOOH + H(2)O and IOOH+H(2)O(2)→ IO˙ + H(2)O+HOO˙.

Chemical equilibria in the binary and ternary uranyl(vi)–hydroxide–peroxide systems

The composition and equilibrium constants of the complexes formed in the binary U(VI)-hydroxide and the ternary U(VI)-hydroxide-peroxide systems have been studied using potentiometric and spectrophotometric data at 25 °C in a 0.100 M tetramethylammonium nitrate medium. The data for the binary U(VI) hydroxide complexes were in good agreement with previous studies. In the ternary system two complexes were identified, [UO(2)(OH)(O(2))](-) and [(UO(2))(2)(OH)(O(2))(2)](-). Under our experimental conditions the former is predominant over a broad p[H(+)] region from 9.5 to 11.5, while the second is found in significant amounts at p[H(+)] < 10.5. The formation of the ternary peroxide complexes results in a strong increase in the molar absorptivity of the test solutions. The absorption spectrum for [(UO(2))(2)(OH)(O(2))(2)](-) was resolved into two components with peaks at 353 and 308 nm with molar absorptivity of 16200 and 20300 M(-1) cm(-1), respectively, suggesting that the electronic transitions are dipole allowed. The molar absorptivity of [(UO(2))(OH)(O(2))](-) at the same wave lengths are significantly lower, but still about one to two orders of magnitude larger than the values for UO(2)(2+)(aq) and the binary uranyl(VI) hydroxide complexes. It is of interest to note that [(UO(2))(OH)(O(2))](-) might be the building block in cluster compounds such as [UO(2)(OH)(O(2))](60)(60-) studied by Burns et al. (P. C. Burns, K. A. Kubatko, G. Sigmon, B. J. Fryer, J. E. Gagnon, M. R. Antonio and L. Soderholm, Angew. Chem. 2005, 117, 2173-2177). Speciation calculations using the known equilibrium constants for the U(vi) hydroxide and peroxide complexes show that the latter are important in alkaline solutions even at very low total concentrations of peroxide, suggesting that they may be involved when the uranium minerals Studtite and meta-Studtite are formed by α-radiolysis of water. Radiolysis will be much larger in repositories for spent nuclear fuel where hydrogen peroxide might contribute both to the corrosion of the fuel and to transport of uranium in a ground water system.

Crystal Structure of Reduced and of Oxidized Peroxiredoxin IV Enzyme Reveals a Stable Oxidized Decamer and a Non-disulfide-bonded Intermediate in the Catalytic Cycle

Peroxiredoxin IV (PrxIV) is an endoplasmic reticulum-localized enzyme that metabolizes the hydrogen peroxide produced by endoplasmic reticulum oxidase 1 (Ero1). It has been shown to play a role in de novo disulfide formation, oxidizing members of the protein disulfide isomerase family of enzymes, and is a member of the typical 2-Cys peroxiredoxin family. We have determined the crystal structure of both reduced and disulfide-bonded, as well as a resolving cysteine mutant of human PrxIV. We show that PrxIV has a similar structure to other typical 2-Cys peroxiredoxins and undergoes a conformational change from a fully folded to a locally unfolded form following the formation of a disulfide between the peroxidatic and resolving cysteine residues. Unlike other mammalian typical 2-Cys peroxiredoxins, we show that human PrxIV forms a stable decameric structure even in its disulfide-bonded state. In addition, the structure of a resolving cysteine mutant reveals an intermediate in the reaction cycle that adopts the locally unfolded conformation. Interestingly the peroxidatic cysteine in the crystal structure is sulfenylated rather than sulfinylated or sulfonylated. In addition, the peroxidatic cysteine in the resolving cysteine mutant is resistant to hyper-oxidation following incubation with high concentrations of hydrogen peroxide. These results highlight some unique properties of PrxIV and suggest that the equilibrium between the fully folded and locally unfolded forms favors the locally unfolded conformation upon sulfenylation of the peroxidatic cysteine residue.

Copper Quantum Clusters in Protein Matrix: Potential Sensor of Pb2+ Ion

A one-pot synthesis of extremely stable, water-soluble Cu quantum clusters (QCs) capped with a model protein, bovine serum albumin (BSA), is reported. From matrix-assisted laser desorption ionization time-of-flight (MALDI-TOF) mass spectrometry, we assign the clusters to be composed of Cu(5) and Cu(13) cores. The QCs also show luminescence properties having excitation and emission maxima at 325 and 410 nm, respectively, with a quantum yield of 0.15, which are found to be different from that of protein alone in similar experimental conditions. The quenching of luminescence of the protein-capped Cu QCs in the presence of very low hydrogen peroxide concentration (approximately nanomolar, or less than part-per-billion) reflects the efficacy of the QCs as a potential sensing material in biological environments. Moreover, as-prepared Cu QCs can detect highly toxic Pb(2+) ions in water, even at the part-per-million level, without suffering any interference from other metal ions.

Treatment of municipal leachate of landfill by Fenton-like heterogeneous catalytic wet peroxide oxidation using an Al/Fe-pillared montmorillonite as active catalyst

Catalytic wet peroxide oxidation (CWPO) with an Al/Fe-pillared clay catalyst was assessed in the treatment of stabilized leachate of landfill (COD = 5000–7000 mg O 2/dm 3; BOD 5 ∼ 800 mg O 2/dm 3; pH = 8.0; BOD 5/COD = 0.11–0.16). The effects of catalyst loading ( 0.5 – 2.0 g catalyst / 100 c m leachate 3 ), added peroxide concentration (2.34–4.68 mol/dm 3) and its rate of stepwise addition (7.5–30 cm 3/h) in a semi-batch reactor, were studied with COD removal and biodegradability index (BI) 1 1 BI here denotes the biodegradability index as a commonly used name for the leachate's BOD 5/COD ratio. as response parameters. COD removals up to 50% and BI output values exceeding 0.3 were achieved in 4 h of reaction at very mild conditions of room temperature and atmospheric pressure (291 K; 72 kPa). High catalyst loadings together with low peroxide concentrations and dosages (below stoichiometric for total mineralization) and low peroxide addition rates were found to provide better use of the oxidizing agent in terms of both, BI enhancement and COD removal. The clay catalyst resulted quite stable against the chemical leaching of the active iron along the catalytic reactions.

Erosion and abrasion on dental structures undergoing at-home bleaching

Erosion and abrasion on dental structures undergoing at-home bleaching Fl&aacute;vio Fernando Demarco1, S&ocirc;nia Saeger Meireles2, Hugo Ramalho Sarmento1, Raquel Ven&acirc;ncio Fernandes Dantas1, Tatiana Botero3, Sandra Beatriz Chaves Tarquinio11Graduate Program in Dentistry, School of Dentistry, Federal University of Pelotas, Brazil; 2Department of Operative Dentistry, Federal University of Para&iacute;ba, Brazil; 3Cariology, Restorative Science, and Endodontics Department, School of Dentistry, University of Michigan, MI, USAAbstract: This review investigates erosion and abrasion in dental structures undergoing at-home bleaching. Dental erosion is a multifactorial condition that may be idiopathic or caused by a known acid source. Some bleaching agents have a pH lower than the critical level, which can cause changes in the enamel mineral content. Investigations have shown that at-home tooth bleaching with low concentrations of hydrogen or carbamide peroxide have no significant damaging effects on enamel and dentin surface properties. Most studies where erosion was observed were in vitro. Even though the treatment may cause side effects like sensitivity and gingival irritation, these usually disappear at the end of treatment. Considering the literature reviewed, we conclude that tooth bleaching agents based on hydrogen or carbamide peroxide have no clinically significant influence on enamel/dentin mineral loss caused by erosion or abrasion. Furthermore, the treatment is tolerable and safe, and any adverse effects can be easily reversed and controlled.Keywords: peroxide, tooth bleaching, enamel, dentin, erosion, abrasion

Erosion and abrasion on dental structures undergoing at-home bleaching

This review investigates erosion and abrasion in dental structures undergoing at- home bleaching. Dental erosion is a multifactorial condition that may be idiopathic or caused by a known acid source. Some bleaching agents have a pH lower than the critical level, which can cause changes in the enamel mineral content. Investigations have shown that at-home tooth bleaching with low concentrations of hydrogen or carbamide peroxide have no significant damaging effects on enamel and dentin surface properties. Most studies where erosion was observed were in vitro. Even though the treatment may cause side effects like sensitivity and gingival irritation, these usually disappear at the end of treatment. Considering the literature reviewed, we conclude that tooth bleaching agents based on hydrogen or carbamide peroxide have no clinically significant influence on enamel/dentin mineral loss caused by erosion or abrasion. Furthermore, the treatment is tolerable and safe, and any adverse effects can be easily reversed and controlled.

Encapsulation and Enzyme-Mediated Release of Molecular Cargo in Polysulfide Nanoparticles

Poly(propylene sulfide) nanoparticles (<150 nm) have been synthesized by an anionic, ring-opening emulsion polymerization. Upon exposure to parts per million (ppm) levels of oxidizing agent (NaOCl), hydrophobic polysulfide particles are oxidized to hydrophilic polysulfoxides and polysulfones. Utilizing this mechanism, the encapsulation of hydrophobic molecular cargo, including Nile red and Reichardt's dye, within polysulfide nanoparticles has been characterized by a variety of microscopic and spectroscopic methods and its release demonstrated via chemical oxidation. Moreover, release of cargo has been enzymatically driven by oxidoreductase enzymes such as chloroperoxidase and myeloperoxidase in the presence of low concentrations of sodium chloride (200 mM) and hydrogen peroxide (500 μM). This oxidation-driven mechanism holds promise for controlled encapsulation and release of a variety of hydrophobic cargos.

Inhibition of lipid peroxidation by methylated analogues of uric acid

The effects of purines and methylated purine analogues on hydrogen peroxide- and ozone-induced lipid peroxidation in human erythrocyte membranes were studied in-vitro. Many purines and purine analogues showed a suppressive effect on the formation of thiobarbituric acid reactive materials. 1,3-Dimethyluric acid and 1,3,7-trimethyluric acid showed high potency in prevention of lipid peroxidation. These effects were shown to be concentration dependent and were more potent at low concentrations of hydrogen peroxide and ozone. 1,3-Dimethyluric acid and 1,3,7-trimethyluric acid may be useful as antioxidants.

Hydrogen peroxide induces neurite degeneration: Prevention by tocotrienols

Reactive oxygen species (ROS) may attack several types of tissues and chronic exposure to ROS may attenuate various biological functions and increase the risk of several types of serious disorders. It is known that treatments with ROS attack neurons and induce cell death. However, the mechanisms of neuronal change by ROS prior to induction of cell death are not yet understood. Here, it was found that treatment of neurons with low concentrations of hydrogen peroxide induced neurite injury, but not cell death. Unusual bands located above the original collapsin response mediator protein (CRMP)-2 protein were detected by western blotting. Treatment with tocopherol or tocotrienols significantly inhibited these changes in neuro2a cells and cerebellar granule neurons (CGCs). Furthermore, prevention by tocotrienols of hydrogen peroxide-induced neurite degeneration was stronger than that by tocopherol. These findings indicate that neurite beading is one of the early events of neuronal degeneration prior to induction of death of hydrogen peroxide-treated neurons. Treatment with tocotrienols may protect neurite function through its neuroprotective function.

Solar disinfection of fungal spores in water aided by low concentrations of hydrogen peroxide

Our previous contribution showed that Fusarium solani spores are inactivated by low amounts of hydrogen peroxide (lower than 50 mg L(-1)) together with solar irradiation in bottles. The purpose of the current study was to evaluate the effectiveness of solar H(2)O(2)/UV-Vis in distilled water and simulated municipal wastewater treatment plant effluent (SE) contaminated with chlamydospores of Fusarium equiseti in a 60 L solar CPC photo-reactor under solar irradiation. This study showed that F. equiseti chlamydospores in distilled and simulated municipal wastewater effluent were inactivated with 10 mg L(-1) of H(2)O(2) in a 60 L CPC photoreactor. F. equiseti chlamysdospore concentration decreased from 325 (±70) CFU mL(-1) to below the detection limit (DL=2 CFU mL(-1)) within five hours of solar exposure in a solar bottle reactor and from 180 (±53) CFU mL(-1) to below the detection limit in distilled water within two hours of solar irradiation in the solar CPC reactor. These results demonstrate that the use of low concentrations of hydrogen peroxide and CPC systems may be a good alternative for disinfection of resistant microorganisms in water.