Nano zinc oxide for UV protection of textiles

This paper describes the effect on the fading of dyed polyester fabrics in artificial sunlight, when the Ultra Violet (UV) component of the radiation was blocked by coating the fabric with zinc oxide nanoparticles, dispersed in an acrylic polymer. Zinc oxide is photoactive and generates superoxide and hydroxyl radicals (Reactive Oxygen Species; ROS) when irradiated with UV in the presence of oxygen and water. The results for the four dyes studied show that different dye chromophores interact differently with ROS. Selection of dyes with anti oxidant properties or addition of other anti oxidants may reduce the adverse effects of ROS

Antioxidant treatment with N-acetylcysteine regulates mammalian skeletal muscle Na+-K+-ATPase ∝ gene expression during repeated contractions

Exercise increases Na+–K+ pump isoform gene expression and elevates muscle reactive oxygen species (ROS). We investigated whether enhanced ROS scavenging induced with the antioxidant N-acetylcysteine (NAC) blunted the increase in Na+–K+ pump mRNA during repeated contractions in human and rat muscle. In experiment 1, well-trained subjects received saline or NAC intravenously prior to and during 45 min cycling. Vastus lateralis muscle biopsies were taken pre-infusion and following exercise. In experiment 2, isolated rat extensor digitorum longus muscles were pre-incubated without or with 10 mm NAC and then rested or stimulated electrically at 60 Hz for 90 s. After 3 h recovery, muscles were frozen. In both experiments, the muscles were analysed for Na+–K+ pump α1, α2, α3, β1, β2 and β3 mRNA. In experiment 1, exercise increased α2 mRNA by 1.0-fold (P = 0.03), but α2 mRNA was reduced by 0.40-fold with NAC (P = 0.03). Exercise increased α3, β1 and β2 mRNA by 2.0- to 3.4-fold (P < 0.05), but these were not affected by NAC (P > 0.32). Neither exercise nor NAC altered α1 or β3 mRNA (P > 0.31). In experiment 2, electrical stimulation increased α1, α2 and α3 mRNA by 2.3- to 17.4-fold (P < 0.05), but these changes were abolished by NAC (P > 0.07). Electrical stimulation almost completely reduced β1 mRNA but only in the presence of NAC (P < 0.01). Neither electrical stimulation nor NAC altered β2 or β3 mRNA (P > 0.09). In conclusion, NAC attenuated the increase in Na+–K+ pump α2 mRNA with exercise in human muscle and all α isoforms with electrical stimulation in rat muscle. This indicates a regulatory role for ROS in Na+–K+ pump α isoform mRNA in mammalian muscle during repeated contractions.

Potential role of nitric oxide in contraction-stimulated glucose uptake and mitochondrial biogenesis in skeletal muscle

• 1. The present review discusses the potential role of nitric oxide (NO) in the: (i) regulation of skeletal muscle glucose uptake during exercise; and (ii) activation of mitochondrial biogenesis after exercise.
• 2. We have shown in humans that local infusion of an NO synthase inhibitor during exercise attenuates increases in skeletal muscle glucose uptake without affecting blood flow. Recent studies from our laboratory in rodents support these findings in humans, although rodent studies from other laboratories have yielded conflicting results.
• 3. There is clear evidence that NO increases mitochondrial biogenesis in non-contracting cells and that NO influences basal skeletal muscle mitochondrial biogenesis. However, there have been few studies examining the potential role of NO in the activation of mitochondrial biogenesis following an acute bout of exercise or in response to exercise training. Early indications are that NO is not involved in regulating the increase in mitochondrial biogenesis that occurs in response to exercise.
• 4. Exercise is considered the best prevention and treatment option for diabetes, but unfortunately many people with diabetes do not or cannot exercise regularly. Alternative therapies are therefore critical to effectively manage diabetes. If skeletal muscle NO is found to play an important role in regulating glucose uptake and/or mitochondrial biogenesis, pharmaceutical agents designed to mimic these effects of exercise may improve glycaemic control.

Dimerisation of N-acetyl-L-tyrosine ethyl ester and Aß peptides via formation of dityrosine

Alzheimer's disease (AD) is characterised by the formation of amyloid deposits composed primarily of the amyloid β-peptide (Aβ). This peptide has been shown to bind redox active metals ions such as copper and iron, leading to the production of reactive oxygen species (ROS) and formation of hydrogen peroxide (H2O2). The generation of H2O2 has been linked with Aβ neurotoxicity and neurodegeneration in AD. Because of the relative stability of a tyrosyl radical, the tyrosine residue (Tyr-10) is believed to be critical to the neurotoxicity of Aβ. This residue has also been shown to be important to Aβ aggregation and amyloid formation. It is possible that the formation of an Aβ tyrosyl radical leads to increased aggregation via the formation of dityrosine as an early aggregation step, which is supported by the identification of dityrosine in amyloid plaque. The role of dityrosine formation in Aβ aggregation and neurotoxicity is as yet undetermined, partly because there are no facile methods for the synthesis of Aβ dimers containing dityrosine. Here we report the use of horseradish peroxidase and H2O2 to dimerise N-acetyl-l-tyrosine ethyl ester and apply the optimised conditions for dityrosine formation to fully unprotected Aβ peptides. We also report a simple fluorescent plate reader method for monitoring Aβ dimerisation via dityrosine formation.

Effects of undoped and manganese-doped zinc oxide nanoparticles on the colour fading of dyed polyester fabrics

This paper describes the effects of applying coatings of an acrylic polymer containing nanoparticles of zinc oxide (ZnO) on the fading rate in artificial sunlight of polyester fabrics dyed with disperse dyes containing anthraquinone and benzopyran chromophores. Factors affecting the transparency and UV absorbance of the coatings are discussed. Removing the UV component of sunlight with ZnO nanoparticles markedly decreased the fading rate of the dyes, provided the polymer/ZnO film was not in direct contact with the fabric. When the treatment was applied directly to the fabrics, however, the protection against colour fading was different for the two dyes studied. Whereas the rate of colour fading of a benzopyran dye, of relatively low lightfastness, was decreased by the polymer-ZnO film, the treatment increased the fading rate of the dye of higher lightfastness, based on anthraquinone. This effect has been attributed to the generation of reactive oxygen species (ROS) when ZnO is exposed to UV. The effect of decreasing the photoactivity of ZnO by doping with manganese has been examined. For the benzopyran dye, the UV protection was greatly increased, whereas a much smaller improvement was found for the anthraquinone-based dye.

Metal catalyzed oxidation of tyrosine residues by different oxidation systems of copper/hydrogen peroxide

Metal-catalysed oxidation (MCO) reactions result in the formation of reactive oxygen species (ROS) in biological systems. These ROS cause oxidative stress that contributes to a number of pathological processes leading to a variety of diseases. Tyrosine is one residue that is very susceptible to oxidative modification and the formation of dityrosine (DT) and 3,4-dihydroxyphenylalanine (DOPA) have been widely reported in a number of diseases. However, the mechanisms of MCO of tyrosine in biological systems are poorly understood and require further investigation. In this study we investigated the mechanism of DT and DOPA formation by MCO using N-acetyl tyrosine ethyl ester as a model for tyrosine in proteins and peptides. The results showed that DT formation could be observed upon Cu²⁺/H₂O₂ oxidation at pH 7.4. Our results indicate that it is unlikely to be via Fenton chemistry since Cu⁺/H₂O₂ oxidative conditions did not lead to the formation of DT.

Metal-catalyzed oxidative damage and oligomerization of the amyloid-β peptide of Alzheimer’s disease

The most common form of dementia in old age is Alzheimer’s disease (AD). The presence in the brain of senile plaque is the major pathological marker of AD. The plaques are primarily composed of aggregated amyloid-β peptide (Aβ). Aβ is a 40–42 amino acid peptide that is a proteolytic product derived from the β-amyloid precursor protein. The function of Aβ and the exact mechanism of Aβ aggregation and neurotoxicity are unclear. However, metal coordination by Aβ plays an important role in inducing aggregation and the generation of reactive oxygen species, which appears to be at least partially responsible for Aβ neurotoxicity. In this review we examine the role of copper and zinc ions in Aβ neurotoxicity, especially with regards to the generation of free radicals. We discuss the role of copper or zinc ions in oxidative damage and Aβ conformational changes and the relationship of these metals to AD.

Polymer coatings containing nano particles of zinc oxide for the UV protection of dyed polyester fabrics

The useful life of many outdoor textile products is limited by degradation caused by exposure to sunlight, in particular by the ultra violet component (below 400 nm). The degradation results in fading of colours and also loss of physical properties, such as tear strength and abrasion resistance. Degradation can be decreased with UV absorbers, often used in conjunction with antioxidants or free radical quenchers. The protection afforded by these organic compounds is, however, limited as they are ultimately destroyed by the UV radiation they absorb.
An alternative approach is to coat fabrics with a polymer containing an inorganic UV absorber, such as zinc oxide. The inherent stability of zinc oxide would be expected to provide a protective effect over a much longer period than can be achieved with an organic UV absorber. A possible disadvantage of zinc oxide when applied in a polymer film is that absorption and scattering of visible light can produce hazy films and, hence, an unacceptable change in fabric appearance.
This poster paper examines the possibility of using nano particles of zinc oxide dispersed in acrylic polymers for protecting dyed polyester fabrics against sunlight fading. Factors affecting both UV absorbance and film clarity will be discussed. The possibility will also be examined that the protective effect may be reduced in some circumstances by reactive oxygen species, generated by the interaction of UV with zinc oxide in the presence of air and water.

N-Acetylcysteine infusion does not affect glucose disposal during prolonged moderate-intensity exercise in humans

There is evidence that reactive oxygen species (ROS) signalling is required for normal increases in glucose uptake during contraction of isolated mouse skeletal muscle, and that AMP-activated protein kinase (AMPK) is involved. The aim of this study was to determine whether ROS signalling is involved in the regulation of glucose disposal and AMPK activation during moderate-intensity exercise in humans. Nine healthy males completed 80 min of cycle ergometry at 62 ± 1 of peak oxygen consumption ( . A 6,6-2H-glucose tracer was infused at rest and during exercise, and in a double-blind randomised cross-over design, N-acetylcysteine (NAC) or saline (CON) was co-infused. NAC was infused at 125 mg kg?1h?1for 15 min and then at 25 mg kg?1h?1for 20 min before and throughout exercise. NAC infusion elevated plasma NAC and cysteine, and muscle NAC and cysteine concentrations during exercise. Although neither NAC infusion nor exercise significantly affected muscle reduced or oxidised glutathione (GSH or GSSG) concentration (P> 0.05), S-glutathionylation (an indicator of oxidative stress) of a protein band of ?270 kDa was increased ?3-fold with contraction and this increase was prevented by NAC infusion. Despite this, exercised-induced increases in tracer determined glucose disposal, plasma lactate, plasma non-esterified fatty acids (NEFAs), and decreases in plasma insulin were not affected by NAC infusion. In addition, skeletal muscle AMPK? and acetyl-CoA carboxylase-? (ACC?) phosphorylation increased during exercise by ?3- and ?6-fold (P< 0.05), respectively, and this was not affected by NAC infusion. Unlike findings in mouse muscle ex vivo, NAC does not attenuate skeletal muscle glucose disposal or AMPK activation during moderate-intensity exercise in humans.

Regulation of skeletal muscle oxidative capacity and insulin signaling by the Mitochondrial Rhomboid Protease PARL

Type 2 diabetes mellitus (T2DM) and aging are characterized by insulin resistance and impaired mitochondrial energetics. In lower organisms, remodeling by the protease pcp1 (PARL ortholog) maintains the function and lifecycle of mitochondria. We examined whether variation in PARL protein content is associated with mitochondrial abnormalities and insulin resistance. PARL mRNA and mitochondrial mass were both reduced in elderly subjects and in subjects with T2DM. Muscle knockdown of PARL in mice resulted in malformed mitochondrial cristae, lower mitochondrial content, decreased PGC1α protein levels, and impaired insulin signaling. Suppression of PARL protein in healthy myotubes lowered mitochondrial mass and insulin-stimulated glycogen synthesis and increased reactive oxygen species production. We propose that lower PARL expression may contribute to the mitochondrial abnormalities seen in aging and T2DM.

Age and exposure to arsenic alter base excision repair transcript levels in mice

Arsenic (As) induces DNA-damaging reactive oxygen species. Most oxidative DNA damage is countered by base excision repair (BER), the capacity for which may be reduced in older animals. We examined whether age and consumption of As in lactational milk or drinking water influences BER gene transcript levels in mice. Lactating mothers and 24-week-old mice were exposed (24 h or 2 weeks) to As (2 or 50 p.p.m.) in drinking water. Lung tissue was harvested from adults, neonates (initially 1 week old) feeding from lactating mothers and untreated animals 1– 26 weeks old. Transcripts encoding BER proteins were quantified. BER transcript levels decreased precipitously with age in untreated mice but increased in neonates whose mothers were exposed to 50 p.p.m. As for 24 h or 2 weeks. Treatment of 24-week-old mice with 2 or 50 p.p.m. As for 2 weeks decreased all transcript levels measured. Exposure to As attenuated the age-related transcript level decline for only one BER gene. We conclude that aging is associated with a rapid reduction of BER transcript levels in mice, which may contribute to decreased BER activity in older animals. Levels of As that can alter gene expression are transmitted to neonatal mice in lactational milk produced by mothers drinking water containing As, raising concerns about breastfeeding in countries having As-contaminated groundwater. Reduction of BER transcript levels in 24- week-old mice exposed to As for 2 weeks suggests As may potentiate sensitivity to itself in older animals.

From bivalves to birds : oxidative stress and longevity

1. The oxidative stress theory of ageing predicts that animals living longer will have less cumulative oxidative damage together with structural characteristics that make them more resistant to oxidative damage itself.
2. Although a general relationship between body size, metabolism and longevity does not exist in marine invertebrates, they are generally characterized by low rates of metabolism and reactive oxygen species (ROS) formation associated with lower antioxidant enzyme activities compared to vertebrates.
3. Birds and mammals have very similar size-affected metabolic rates and their metabolic intensity explains only some of the variation in maximum lifespan potential (MLSP).Within each class, smaller animals have higher rates of metabolism and ROS production and membranes that are more susceptible to oxidative damage and autocatalytic propagation of free radicals than larger ones.
4. Although the high variation in life-history strategies is accompanied by substantial variation in MLSP, there is a consistent positive correlation between rates of ROS formation and antioxidant levels among most animals examined so far for these traits. The consensus of these studies is that ROS and antioxidant levels are inversely related to MLSP.
5. The lack of a clear stoichiometric relation between variables contributing to oxidative stress limits our capacity to infer longevity consequences from measures of pro-oxidant or antioxidant status among or within species

A role for glutathione in the pathophysiology of bipolar disorder and schizophrenia? Animal models and relevance to clinical practice.

The tripeptide, glutathione (glutamylcysteinylglycine) is the primary endogenous free radical scavenger in the human body. When glutathione (GSH) levels are reduced there is an increased potential for cellular oxidative stress, characterised by an increase and accruement of reactive oxygen species (ROS). Oxidative stress has been implicated in the pathology of schizophrenia and bipolar disorder. This could partly be caused by alterations in dopaminergic and glutamatergic activity that are implicated in these illnesses. Glutamate and dopamine are highly redox reactive molecules and produce ROS during normal neurotransmission. Alterations to these neurotransmitter pathways may therefore increase the oxidative burden in the brain. Furthermore, mitochondrial dysfunction, as a source of oxidative stress, has been documented in both schizophrenia and bipolar disorder. The combination of altered neurotransmission and this mitochondrial dysfunction leading to oxidative damage may ultimately contribute to illness symptoms. Animal models have been established to investigate the involvement of glutathione depletion in aspects of schizophrenia and bipolar disorder to further characterise the role of oxidative stress in psychopathology. Stemming from preclinical evidence, clinical studies have recently shown antioxidant precursor treatment to be effective in schizophrenia and bipolar disorder, providing a novel clinical angle to augment often suboptimal conventional treatments.

Determination of intracellular glutathione and glutathione disulfide using high performance liquid chromatography with acidic potassium permanganate chemiluminescence detection

Measurement of glutathione (GSH) and glutathione disulfide (GSSG) is a crucial tool to assess cellular redox state. Herein we report a direct approach to determine intracellular GSH based on a rapid chromatographic separation coupled with acidic potassium permanganate chemiluminescence detection, which was extended to GSSG by incorporating thiol blocking and disulfide bond reduction. Importantly, this simple procedure avoids derivatisation of GSH (thus minimising auto-oxidation) and overcomes problems encountered when deriving the concentration of GSSG from ‘total GSH’. The linear range and limit of detection for both analytes were 7.5 × 10−7 to 1 × 10−5 M, and 5 × 10−7 M, respectively. GSH and GSSG were determined in cultured muscle cells treated for 24 h with glucose oxidase (0, 15, 30, 100, 250 and 500 mU mL−1), which exposed them to a continuous source of reactive oxygen species (ROS). Both analyte concentrations were greater in myotubes treated with 100 or 250 mU mL−1 glucose oxidase (compared to untreated controls), but were significantly lower in myotubes treated with 500 mU mL−1 (p < 0.05), which was rationalised by considering measurements of H2O2 and cell viability. However, the GSH/GSSG ratio in myotubes treated with 100, 250 and 500 mU mL−1 glucose oxidase exhibited a dose-dependent decrease that reflected the increase in intracellular ROS.

The long life of birds : the rat-pigeon comparison revisited

The most studied comparison of aging and maximum lifespan potential (MLSP) among endotherms involves the 7-fold longevity difference between rats (MLSP 5y) and pigeons (MLSP 35y). A widely accepted theory explaining MLSP differences between species is the oxidative stress theory, which purports that reactive oxygen species (ROS) produced during mitochondrial respiration damage bio-molecules and eventually lead to the breakdown of regulatory systems and consequent death. Previous rat-pigeon studies compared only aspects of the oxidative stress theory and most concluded that the lower mitochondrial superoxide production of pigeons compared to rats was responsible for their much greater longevity. This conclusion is based mainly on data from one tissue (the heart) using one mitochondrial substrate (succinate). Studies on heart mitochondria using pyruvate as a mitochondrial substrate gave contradictory results. We believe the conclusion that birds produce less mitochondrial superoxide than mammals is unwarranted. We have revisited the rat-pigeon comparison in the most comprehensive manner to date. We have measured superoxide production (by heart, skeletal muscle and liver mitochondria), five different antioxidants in plasma, three tissues and mitochondria, membrane fatty acid composition (in seven tissues and three mitochondria), and biomarkers of oxidative damage. The only substantial and consistent difference that we have observed between rats and pigeons is their membrane fatty acid composition, with rats having membranes that are more susceptible to damage. This suggests that, although there was no difference in superoxide production, there is likely a much greater production of lipid-based ROS in the rat. We conclude that the differences in superoxide production reported previously were due to the arbitrary selection of heart muscle to source mitochondria and the provision of succinate. Had mitochondria been harvested from other tissues or other relevant mitochondrial metabolic substrates been used, then very different conclusions regarding differences in oxidative stress would have been reached. ©