Toxicity of hydrogen peroxide produced by electroplated coatings to pathogenic bacteria

Four incremental protocols of knee extension exercise of different stage durations were compared to study the effect of the protocol upon power output at the last stage (Ppeak). Previous studies of knee extension have found very different power outputs with similar ergometers and these large differences have been interpreted as being the result of the fatigue due to the durations of the protocols. The knee extension device used in previous studies was modified to avoid the action of the knee and hip flexors: the subjects pushing on a lever instead of pulling a rod. In the present study five subjects performed four incremental knee extension exercises which differed with regard to stage duration (60, 90, 180 or 360 s) on this ergometer. The Ppeak, peak oxygen uptake (VO2peak) and peak heart rate (HRpeak) were measured at the end of each of these four incremental protocols. In eight subjects, the reliability of the protocols with the two shortest increments (60 and 90-s stages) was verified by measuring Ppeak at 60 s and 90 s (Ppeak60, Ppeak90) twice. The knee ergometer proposed in the present paper was easy to use without any special training and should improve the measurement of Ppeak. The Ppeak60 [49.4 (SD 5.6) W] was higher than at 180 s [Ppeak180), 43.6 (SD 5.8) W, P < 0.05] and at 360 s [Ppeak360, 43.4 (SD 5.3) W, P < 0.05]. All the other differences in Ppeak, VO2 peak and HRpeak were not significant. All correlations between Ppeak60, Ppeak90, Ppeak180 and Ppeak360 were significant, except those between Ppeak360 and Ppeak90 or Ppeak180. The effect of the stage duration on power output and oxygen uptake at the end of the knee extension exercises was not great. Consequently, the large differences in power output and oxygen uptake observed in previous studies cannot be explained by the protocol only. The significant difference between Ppeak 60 and Ppeak90 was of the order of 10% in agreement with findings in the literature using cycle ergometry. The reliability of Ppeak60 and Ppeak90 was high and the use of these protocols can be recommended if further studies show that the measurement of Ppeak, is useful in the evaluation of local endurance.     

Prostaglandins attenuate cardiac contractile dysfunction produced by free radical generation but not by hydrogen peroxide

Both fast neutron radiotherapy and boron neutron capture therapy have been investigated as new radiation treatment techniques for patients with malignant gliomas. While each of these techniques individually has shown the potential for pathological eradication of malignant glioma, to date neither has evolved into an accepted, improved method of treatment. We have recently begun a research program investigating the feasibility of combining the benefits of both types of therapy. As a fast neutron beam penetrates tissue some of the particles are degraded to thermal energies. These can be captured by 10B or other suitable isotopes resulting in a highly-localized release of additional energy during a course of fast neutron radiotherapy. In this article we will review the rationale for such an approach, and review the underlying physics as well as in vitro, in vivo, and early human studies testing its feasibility. If appropriate carrier agents can be found that preferentially-localize in tumor cells, this approach ena be applied to many different tumor systems.     

Oxidative DNA damage induced by Cu(II)-oligopeptide complexes and hydrogen peroxide

At physiological pH values, Cu(II)-tetraglycine and Cu(II) complexes with peptides containing a histidyl residue at the N-terminal caused DNA strand breakage in the presence of H2O2, whereas Cu(II) complexes with peptides containing histidyl residue in the second or third position did not. Because of the correlation between the generation of hydroxyl radical and DNA strand scission, a mechanism for the reaction is proposed.     

Effects of N-methyl hexanoylhydroxamic acid (NMHH) and myoglobin on endothelial damage by hydrogen peroxide

OBJECTIVE: The aim was to investigate the interaction of the novel antioxidant N-methyl hexanoylhydroxamic acid (NMHH) with myoglobin in protecting endothelial cells against H2O2 mediated damage. METHODS: Cultured bovine aortic endothelial cells were exposed to 50-100 microM H2O2 for 10-60 min with and without NMHH and/or myoglobin, and immediate or delayed damage was assessed by lactate dehydrogenase release, 3H adenine uptake, a tetrazolium reduction assay, and microscopy. RESULTS: Brief exposure to low concentrations of H2O2 caused cell damage, for which the tetrazolium reduction assay was the most sensitive assay, and inhibited subsequent cell division. NMHH in concentrations from 50 to 200 microM protected against damage provided it was present at the time of adding H2O2, and the effect was markedly potentiated by 10 microM oxymyoglobin, which had little protective effect alone. CONCLUSIONS: NMHH is an effective antioxidant which is markedly potentiated by low concentrations of oxymyoglobin. Oxymyoglobin may potentiate NMHH by scavenging H2O2 through the rapid formation of ferrylmyoglobin, which is then reduced by NMHH. This synergism may be particularly relevant to the protection of myoglobin-rich cells such as myocytes.     

铜催化过氧化氢氧化纳米银-原子吸收光谱法测定过氧化氢

以柠檬酸三钠作还原剂,微波高压法制备了纳米银,采用高速离心法纯化除去柠檬酸三钠获得了纯纳米银。将H2O2-Cu2+-纳米银催化反应与离心技术结合,用原子吸收光谱法做检测技术,建立了一个灵敏度高、选择性较好的测定痕量H2O2的新方法。在pH 3.8的HAc-NaAc缓冲溶液中,Cu2+催化H2O2氧化银纳米微粒生成Ag+,以原子吸收光谱法测定Ag+从而间接测定H2O2含量。随着H2O2浓度增大,氧化产生的Ag+越多,其吸光度值随之增加,H2O2浓度在5.8~63.4μmol/L范围内与离心液中Ag+的吸收值ΔA呈良好线性关系,回归方程为ΔA=0.007 7c+0.014,相关系数为0.994 1,方法检出限为2.0μmol/L。本方法用于废水中H2O2的测定,回收率在96.4%~108.3%之间,RSD为3.6%,与光度法结果相吻合。     

Effect of sodium metabisulfite on hydrogen peroxide production in light-exposed pediatric parenteral amino acid solutions

The effect of sodium metabisulfite (MBS) on hydrogen peroxide (HP) production in model and commercial amino acid solutions exposed to phototherapy light was studied. Model and commercial pediatric amino acid solutions were prepared such that the amino acid concentration was 1%. MBS concentration, riboflavin concentration, and duration of exposure to phototherapy light were varied to determine the effect on HP production. Control solutions were kept in the dark. HP production was assayed in the model amino acid solutions by using potassium iodide in the presence of ammonium molybdate. In all experiments, HP production was measured at 360 nm in the presence and absence of catalase. In light-exposed solutions, HP production increased linearly for several hours and reached a plateau by eight hours. A mean maximum of 940 microM was produced (data pooled for all solutions). No detectable HP was generated in the solutions kept in the dark. After two hours of light exposure, it was necessary to add at least 10 times more MBS than is typically found in commercial total parenteral nutrient solutions to scavenge all the HP produced. An average of up to 940 microM of HP was produced in model and commercial pediatric parenteral 1% amino acid solutions in the presence of phototherapy light and clinically relevant concentrations of riboflavin and MBS. Light exposure decreased the antioxidant effect of MBS.     

过氧化氢分光光度法测定湿法提钒工艺中钒

为了提高湿法提钒工艺过程控制效率,采用以过氧钒离子(VO(O₂)⁺)显色特性为基础的过氧化氢分光光度法测定钒含量,实现了样品中钒含量的现场快速测定。首先通过在试样溶液中加入适量氢氧化钠溶液,调整溶液pH值至9～10,然后加入过氧化氢将低价态钒全部氧化至钒(V),再加入硫酸调整溶液至酸性,钒(V)与过氧化氢在室温下形成稳定的红棕色过氧钒离子(VO(O₂)⁺),于450 nm处测定吸光度。钒质量浓度在2.0~400 mg/L内与吸光度值符合比尔定律。采用实验方法测定3种湿法冶金提钒液体试样(包括钒浸取溶液、钒盐沉淀后溶液以及废水等)中钒,结果的相对标准偏差(RSD,n=10)分别为0.38%、3.5%和7.6%;与高锰酸钾氧化-硫酸亚铁铵滴定法结果相一致。     

Internal hydrogen supersaturation produced by dislocation transport

A quantitative model is presented for the generation of internal supersaturations of hydrogen by kinetic rather than thermodynamic means. The maximum brittleness and slow strain rate limit is treated. The process invoked assumes hydrogen transport to deposition sites by dislocation drag, and reemission of the hydrogen by diffusion. The kinetic supersaturation is calculated from a balance between hydrogen arrival and departure rates, for internal and external hydrogen sources, and for smooth section and crack geometries. When applied to ferritic and austenitic steels, the model predicts that the kinetic supersaturations are extremely small in all realistic situations.     

Internal hydrogen supersaturation produced by dislocation transport

A quantitative model is presented for the generation of internal supersaturations of hydrogen by kinetic rather than thermodynamic means. The maximum brittleness and slow strain rate limit is treated. The process invoked assumes hydrogen transport to deposition sites by dislocation drag, and reemission of the hydrogen by diffusion. The kinetic supersaturation is calculated from a balance between hydrogen arrival and departure rates, for internal and external hydrogen sources, and for smooth section and crack geometries. When applied to ferritic and austenitic steels, the model predicts that the kinetic supersaturations are extremely small in all realistic situations.     

Lipoxygenase-catalyzed oxidation of chlorpromazine by hydrogen peroxide at acidic pH

The hydroperoxidase activity of soybean lipoxygenase, a non-heme protein, oxidizes chlorpromazine using H2O2 at acidic pHs ranging from 3.0 to 4.0. The enzyme is assayed at pH 3.5, at which the half-life is 2 h (lower pHs cause higher inactivation rates). This oxidation is enzymatical since boiled enzyme or even iron ions both with H2O2 failed to produce any increase in absorbance. In addition, the concentration of CPZ radical cation formed and the concomitant enzyme activity directly depends on the enzyme concentration up to 0.23 microM. The Vmax value is 125 mumol/min per mg protein and the Km for chlorpromazine and H2O2 are 2.1 mM and 0.25 mM, respectively. Similar results were obtained when linoleic acid hydroperoxide was used instead of H2O2 with a Km value of 95 microM. The radical cation obtained in the oxidation of chlorpromazine by lipoxygenase decays by a disproportionation reaction. This permits to consider the overall reaction as a sum of an enzymatic reaction coupled with a chemical second order reaction with substrate regeneration, similar to those produced by peroxidases from different sources.     

Ionizing radiation and hydrogen peroxide induced oxidative DNA base damage in two L5178Y cell lines

Seven oxidized DNA bases were quantified, by gas GC/MS-SIM, in chromatin from gamma-rays and H2O2 treated mouse lymphoma L5178Y (LY) cells, inversely cross-sensitive to these agents. In H2O2 treated cells (2 mM, 1 h, 37 degrees C) we found more damage in LY-R cells than in LY-S cells. On the contrary, in gamma-rays (400 Gy) treated cells we found more damaged DNA bases in LY-S cells. The yield of damaged bases in control cells was similar in both cell lines, with the exception of 8OHAde and FapyGua that were found at a much higher level in LY-S cells. The yields of damaged bases were related to cellular sensitivity to damaging agent; this observation points to a relationship between DNA base damage induction, antioxidant defense system in the intracellular milieu and cell sensitivity.     

The importance of immunological markers in the diagnosis of central nervous system infections produced by mycobacteria

More than 40 different oral diseases and conditions have been described in patients infected with human immunodeficiency virus (HIV). The recognition of the oral manifestations of HIV disease is of great significance because they may represent the first signs of the disease and have been shown to be highly predictive markers of severe immune deterioration and disease progression. Although some oral diseases and conditions have a weak association with HIV disease, others are strongly linked with the disorder, and a few are acquired immune deficiency syndrome (AIDS)-defining in nature. The spectrum of oral manifestations of HIV disease is reviewed with emphasis on clinical recognition, diagnosis, and treatment.     

The importance of measured intake in assessing exposure of breast-fed infants to organochlorines

OBJECTIVES: To estimate infants' intake of organochlorines (OCs) from their measured intake of breast milk; to compare these with the acceptable daily intakes (ADIs) set by the World Health Organization (WHO). DESIGN: Primiparous nursing mothers were recruited from either an industrial or rural area between January and November 1992. SETTING: Mothers volunteered in response to information displayed at their Infant Welfare Centre. All sampling was undertaken in the subject's home. SUBJECTS: The sole entry criterion was primiparity. Three breast milk samples were collected at one month intervals from each mother. OC levels were measured on a milk fat basis by gas chromatograph-mass spectrometer and individual milk intakes were used to determine the infant's daily OC intake. Of the 23 mothers who entered the study, 17 finished, resulting in 57 samples for intake determination. RESULTS: Some intakes of hexachlorobenzene (HCB), chlordane, dieldrin and heptachlor epoxide (HE) exceeded the ADI. High OC levels in breast milk did not necessarily result in a high intake for the infant. CONCLUSIONS: Assessment of the exposure of infants to OC contaminants in breast milk requires an accurate estimate of OC intake. Intakes estimated using inferred rather than measured values for milk fat and milk intake are not reliable indicators of actual intakes.     

Nitric oxide formation from hydroxylamine by myoglobin and hydrogen peroxide

Hydroxylamine (HA), which is a natural product of mammalian cells, has been shown to possess vasodilatory properties in several model systems. In this study, HA and methyl-substituted hydroxylamines, N-methylhydroxylamine (NMHA) and N,N-dimethylhydroxylamine (NDMHA), have been tested for their ability to generate free diffusible nitric oxide (NO) in the presence of myoglobin (Mb) and hydrogen peroxide. A NO-specific conversion of 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (carboxy-PTIO) to 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl (carboxy-PTI), measured by electron spin resonance (ESR) spectroscopy, along with nitrite and nitrate production, was observed for HA but not for NMHA and NDMHA. ESR measurements at 77 K showed the formation of the ferrous nitrosyl myoglobin, Mb-NO, in the reaction mixtures containing Mb, H2O2 and HA. Our data also demonstrate that Mb-NO is an end product of the reaction pathway involving Mb, H2O2 and HA, rather than a reaction intermediate in the formation of NO. In summary, our results demonstrate a possible pathway of NO formation from HA, however, the significance of this mechanism for bioactivation of HA in vivo is unknown at the present time.     

DNA damage produced by povidone-iodine in cultured human diploid cells

Povidone-iodine is capable of selective altering the DNA of human diploid cells growing in culture. This finding extends to eukaryotic cells, the previously reported DNA-modifying activity of this agent for bacteria. In view of the known relationship between DNA-modifying activity and potential carcinogenicity, the results suggest that the potential hazards posed by the widespread use of this agent be evaluated.     

Spread of damage produced by electrolytic lesions in the hypothalamus.

Demonstrated, in 2 experiments with 13 female albino Sprague-Dawley rats, the progressive and systematic expansion of behavioral deficits caused by electrolytic lesions in the hypothalamus. The effects continued to develop over several hours of testing after lesioning. The expansion affected electrical brain stimulation. Thresholds for positive and aversive brain stimulation rose and the intensity-response functions for self-stimulation changed progressively. The effects appear unrelated to general debility since contralateral stimulation was unaffected. Exp II showed systematically developing deficits in ingestive behavior. Immediate or quickly developing deficits in water drinking were followed by rejection of liquid food and less palatable solid food. Motor coordination progressively deteriorated. The phenomena provide a tool for systematic analysis of deficits and perhaps prediction of the course of recovery. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Transformation in vitro of a nontumorigenic rat urothelial cell line by hydrogen peroxide

Chronic infection/inflammation of the urinary tract is a significant risk factor for the development of bladder cancer. The present study examined the hypothesis that hydrogen peroxide (H202) and cytokines released during inflammation are involved in the enhancement of bladder carcinogenesis. Using growth in soft agar and tumorigenicity in athymic nude mice as indices of transformation, we examined the effect of H202 and cytokines on the enhancement of N-methyl-N-nitrosourea (MNU)-initiated transformation of MYP3 cells, an anchorage-dependent nontumorigenic rat bladder epithelial cell line. MYP3 cells pretreated with or without MNU were exposed to H202 (0.001 to 0.1 mM) daily for 1 week in monolayer culture and were then tested for growth in soft agar. A marked increase in colony numbers was observed in the cells that were MNU-initiated and exposed to H202 (P < 0.01). Furthermore, H202 exposure alone at 0.01 mM or 0.1 mM caused colony formation in soft agar. The transformants induced by MNU plus H202 or H202 alone formed high-grade transitional cell carcinomas when injected into nude mice. The growth of these transformants was stimulated by several cytokines (interleukin 1alpha, interleukin 6, and tumor necrosis factor-alpha) better than the parental cells both on a plastic surface and in soft agar. Our results indicate that H202 causes genetic change(s) to induce tumorigenic conversion in urothelial cells and that the transformants are stimulated to grow because of their selective response to several cytokines. We suggest that these mechanisms may be involved in the in vivo carcinogenesis associated with chronic urinary tract infection.     

Differential role of hydrogen peroxide and organic peroxides in augmenting asbestos-mediated DNA damage: implications for asbestos induced carcinogenesis

The incubation of asbestos with DNA in presence of peroxides augmented DNA damage several fold as compared to the damage caused by individual treatments. Asbestos in presence of hydrogen peroxide causes DNA double strand breaks, damage to its deoxyribose sugar moiety and enhanced DNA fidelity. However, only DNA double strand breaks and enhanced DNA fidelity could be recorded in presence of organic hydroperoxide/peroxide but no DNA sugar damage could be observed. Further, the extent of DNA damage could be correlated to the carcinogenic potential of asbestos fibre. Crocidolite, the most carcinogenic variety of asbestos, produces maximum damage to DNA in presence of both hydrogen peroxide and organic hydroperoxide/peroxide while chrysolite which is only a co-carcinogen produces significantly less DNA damage. The observed differences in DNA damage by hydrogen peroxide and organic hydroperoxide/peroxide have been ascribed to the differential reactivity of DNA with hydroxyl and alkoxy/aryloxy free radicals produced respectively from these inorganic and organic peroxides.