Reactive Oxygen Species Output Research Articles

Dynamic Production of Hydroxyl Radicals during the Flooding-Drainage Process of Paddy Soil: An In Situ Column Study.

Frequent cycles of flooding and drainage in paddy soils lead to the reductive dissolution of iron (Fe) minerals and the reoxidation of Fe(II) species, all while generating a robust and consistent output of reactive oxygen species (ROS). In this study, we present a comprehensive assessment of the temporal and spatial variations in Fe species and ROS during the flooding-drainage process in a representative paddy soil. Our laboratory column experiments showed that a decrease in dissolved O2 concentration led to rapid Fe reduction below the water-soil interface, and aqueous Fe(II) was transformed into solid Fe(II) phases over an extended flooding time. As a result, the •OH production capacity of liquid phases was reduced while that of solid phases improved. The •OH production capacity of solid phases increased from 227-271 μmol kg-1 (within 1-11 cm depth) to 500-577 to 499-902 μmol kg-1 after 50 day, 3 month, and 1 year incubation, respectively. During drainage, dynamic •OH production was triggered by O2 consumption and Fe(II) oxidation. ROS-trapping film and in situ capture revealed that the soil surface was the active zone for intense H2O2 and •OH production, while limited ROS production was observed in the deeper soil layers (>5 cm) due to the limited oxygen penetration. These findings provide more insights into the complex interplay between dynamic Fe cycling and ROS production in the redox transition zones of paddy fields.

Potential implementation of trees to remediate contaminated soil in Egypt.

Soil and water in Egypt have become contaminated with multiple pollutants. These contaminants arise from diverse sources, including misuse of fertilizers, industrial effluent discharged into irrigation water, discharge of wastewater in rural areas, and mining activities discharging wet and dry atmospheric deposits and heavy metal contamination. The pollutants can directly affect the quality of air, water, and food and have an adverse effect on human health. About 33% of the cultivated lands in Egypt are salinized due to extreme conditions like high temperatures and aridity. The presence of elevated salt levels in the soil leads to grave consequences for seed germination, plant biochemical processes, development, and reproduction, all of which result in the output of reactive oxygen species and eventually plant death. Despite the possibility of thermal, chemical, or a combination of the two to remediate contaminated soils, their applications are complicated and costly. Some plants, called hyperaccumulators, exhibit the potential to clean up pollutants safely from the soil and water at a low cost. All the technologies used in soil decontamination are called phytoremediation. Some physiological (e.g., phytoextraction, phytostabilization, phytotransformation, rhizofiltration, phytostimulation, phytovolatilization, phytodegradation, and phytodesalination) and molecular parameters (e.g., genes, peptides, and proteins) are involved in heavy metals accumulation of these plants. Although trees are not classified as hyperaccumulators, they have recently proved higher phytoremediation potential than herbaceous plants due to their deeper root system and greater biomass growth. Indeed, this review sheds the light on the application of trees for the phytoremediation of salts and heavy metals in Egypt.

Telomeres, atherosclerosis, and human longevity: a causal hypothesis.

Human telomere length, as expressed in leukocytes, is strongly fashioned by heritability.1–5 A number of genes that explain some of the inter-individual variation in leukocyte telomere length have already been identified.6–9 Leukocyte telomere length is longer in women than in men3,10,11 and in African Americans than in whites of European descent.12,13 In addition, offspring of older fathers display a longer leukocyte telomere length, a finding that may reflect longer telomeres in sperm of older men.14–17 In contrast to the male germline, telomeres in replicative somatic tissues, including the hematopoietic system, display age-dependent shortening. A shorter leukocyte telomere length is associated with aging-related diseases, principally atherosclerosis18,19 and reduced longevity.20,21 The prevailing interpretation is that a shorter leukocyte telomere length is the outcome of processes, mainly the age-dependent accruing burden of oxidative stress and inflammation22 that ultimately shorten the human lifespan. As such, leukocyte telomere length is considered to be a non-causal biomarker, ie, a telomeric “clock,” of human aging. We propose that telomere length is not only associated with atherosclerosis and longevity but is also a causal determinant of both. This hypothesis is based on a model of leukocyte telomere length dynamics (leukocyte telomere length and its attrition rate) that incorporates two key features. First, the model differentiates the findings of studies of telomere length dynamics in vitro from those in vivo. Second, the model distinguishes two phases of human leukocyte telomere length dynamics in vivo: growth and adulthood.

Activated Immune System and Inflammation in Healthy Ageing: Relevance for Tryptophan and Neopterin Metabolism

Immune activation not only accompanies inflammation in various disorders including infections, autoimmune syndromes and cancer, but it also represents a characteristic feature of ageing. Immune deviations which are most widely expressed in the elderly include increased neopterin production and tryptophan breakdown. These biochemical events result from the activation of the immune system and are preferentially triggered by pro-inflammatory stimuli, such as the Th1-type cytokine interferon-γ. They seem to play a role in the development of several age-related disorders and might be involved in the pathogenesis of common symptoms, including neurobehavioral disorders (e.g., cognitive and mood disturbances), anemia, cachexia, weight-loss but also immunodeficiency. Concentrations of the biomarkers neopterin and Kyn/Trp were found to be predictive of overall disease specific mortality in coronary artery disease, infections and various types of cancer. Immune activation and inflammation are also accompanied by high output of reactive oxygen species and thereby may lead to the development of oxidative stress and contribute to the vitamin deficiency which is often observed in the elderly. Accordingly, increases in neopterin were found to correlate with a substantial decline in key vitamins, including folate and vitamin-B6, - B12, -C, -D and -E.

Immune changes and neurotransmitters: Possible interactions in depression?

A disturbed metabolism of catecholamines and other neurotransmitters appears to play a major role in the pathogenesis of neurospychiatric symptoms, such as changes in mood and depression. This symptomatology is common in patients with chronic inflammatory disorders such as infections, autoimmune diseases, or cancer. The pathogenesis of these symptoms is still unclear. Pro-inflammatory stimuli interfere not only with the neural circuits and neurotransmitters of the serotonergic system but also with those of the adrenergic system. The pro-inflammatory cytokine interferon-γ stimulates the biosynthesis of 5,6,7,8-tetrahydrobiopterin (BH4), which is a co-factor for several aromatic amino acid mono-oxygenases and is rate-limiting for the biosynthesis of the neurotransmitter serotonin and the catecholamines dopamine, epinephrine (adrenaline) and norepinephrine (noradrenaline). Interferon-γ triggers the high output of reactive oxygen species in macrophages, which can destroy the oxidation-labile BH4. Recent data suggests that oxidative loss of BH4 in chronic inflammatory conditions can reduce the biosynthesis of catecholamines, which may relate to disturbed adrenergic neurotransmitter pathways in patients.

Chronic Immune Stimulation Correlates with Reduced Phenylalanine Turnover

Neuropsychiatric symptoms like mood changes and depression are common in patients with chronic inflammatory disorders such as infections, autoimmune diseases or cancer. The pathogenesis of these symptoms is still unclear. Pro-inflammatory stimuli interfere not only with the neural circuits and neurotransmitters of the serotonergic, but also with those of the adrenergic system. The pro-inflammatory cytokine interferon-gamma stimulates the biosynthesis of 5,6,7,8-tetrahydrobiopterin (BH4), which is cofactor for several aromatic amino acid monooxygenases and thus is strongly involved in the biosynthesis of the neurotransmitter serotonin and the catecholamines dopamine, epinephrine (adrenaline) and norepinephrine (noradrenaline). In macrophages, interferon-gamma also triggers the high output of reactive oxygen species, which can destroy the oxidation-labile BH4. Recent data suggest that oxidative loss of BH4 in chronic inflammatory conditions can reduce the biosynthesis of catecholamines, which may relate to disturbed adrenergic neurotransmitter pathways in patients.