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The effect of air pollution on oxidative stress markers in newborns
Ambrož, Antonín ; Rössner, Pavel (advisor) ; Rubeš, Jiří (referee) ; Gábelová, Alena (referee)
In everyday life, humans are exposed to toxic substances of anthropogenic origin. These substances can also be found in the ambient air and their impact poses a long-term risk for human health. Respirable particulate matter (PM) of aerodynamic diameter < 2.5 µm (PM2.5) is intensively studied, along with carcinogenic polycyclic aromatic hydrocarbons (PAHs), bound to it, such as benzo[a]pyrene (B[a]P), a reference carcinogenic PAH. Owing to small size, PM2.5 can penetrate the human body primarily via the airways and represent an increased health risk compared to larger particles. The negative health impacts of anthropogenic PM2.5, generated e.g. by fossil fuel combustion, are linked with its small size, relatively large surface, as well as with PAHs and other substances adsorbed on PM surface. PAHs, generated by an incomplete combustion of organic matter, can enter organism either via ingestion of contaminated food, water or via inhalation of polluted air. PAHs affect organisms via genotoxic, mutagenic, carcinogenic, embryotoxic and other adverse effects. One of the common denominators of these effects is oxidative stress, which is also considered to be the main mechanism of action caused by PM in the human organism. Oxidative damage induced by reactive oxygen species (ROS) may affect any cellular...
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Oxidative damage to cellular components after oxidative stress induction by specific herbicides
Kramná, Barbara ; Wilhelmová, Naďa (advisor) ; Ryšlavá, Helena (referee)
Oxidative stress is caused by overproduction and overaccumulation of ROS (reactive oxygen species). This state is responsible for cellular damage during unfavorable environmental conditions such as drought, low temperatures, salinity. In order to directly study oxidative stress at tobacco plants (Nicotiana tabacum cv. Xanthi) I used specific herbicides, MV (methyl viologen) and 3-AT (3- aminotriazole). There were several markers used for monitoring oxidative damage to cellular components: DNA damage detected by a comet assay, lipid peroxidation, carbonylated proteins and modification of activities of antioxidant enzymes CAT (catalase) and APX (ascorbate peroxidase). Fluorescent microscopy documented changes in a redox state of tobacco cells and a specific signal for peroxisomes was observed after treatment with higher concentrations of MV and 3-AT. Application of both herbicides caused significant DNA damage, while they worked in a different concentrations, MV in µM and 3-AT in mM. Another convincing oxidative stress marker for MV was protein carbonylation. The inhibition of antioxidant enzymes CAT and APX was less significant when compared to the effects of 3-AT. Decreasing membrane stability proved to be an universal oxidative stress marker for both herbicides. On the other hand, lipid...
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The effect of air pollution on oxidative stress markers in newborns
Ambrož, Antonín
In everyday life, humans are exposed to toxic substances of anthropogenic origin. These substances can also be found in the ambient air and their impact poses a long-term risk for human health. Respirable particulate matter (PM) of aerodynamic diameter < 2.5 µm (PM2.5) is intensively studied, along with carcinogenic polycyclic aromatic hydrocarbons (PAHs), bound to it, such as benzo[a]pyrene (B[a]P), a reference carcinogenic PAH. Owing to small size, PM2.5 can penetrate the human body primarily via the airways and represent an increased health risk compared to larger particles. The negative health impacts of anthropogenic PM2.5, generated e.g. by fossil fuel combustion, are linked with its small size, relatively large surface, as well as with PAHs and other substances adsorbed on PM surface. PAHs, generated by an incomplete combustion of organic matter, can enter organism either via ingestion of contaminated food, water or via inhalation of polluted air. PAHs affect organisms via genotoxic, mutagenic, carcinogenic, embryotoxic and other adverse effects. One of the common denominators of these effects is oxidative stress, which is also considered to be the main mechanism of action caused by PM in the human organism. Oxidative damage induced by reactive oxygen species (ROS) may affect any cellular...
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The effect of air pollution on oxidative stress markers in newborns
Ambrož, Antonín
In everyday life, humans are exposed to toxic substances of anthropogenic origin. These substances can also be found in the ambient air and their impact poses a long-term risk for human health. Respirable particulate matter (PM) of aerodynamic diameter < 2.5 µm (PM2.5) is intensively studied, along with carcinogenic polycyclic aromatic hydrocarbons (PAHs), bound to it, such as benzo[a]pyrene (B[a]P), a reference carcinogenic PAH. Owing to small size, PM2.5 can penetrate the human body primarily via the airways and represent an increased health risk compared to larger particles. The negative health impacts of anthropogenic PM2.5, generated e.g. by fossil fuel combustion, are linked with its small size, relatively large surface, as well as with PAHs and other substances adsorbed on PM surface. PAHs, generated by an incomplete combustion of organic matter, can enter organism either via ingestion of contaminated food, water or via inhalation of polluted air. PAHs affect organisms via genotoxic, mutagenic, carcinogenic, embryotoxic and other adverse effects. One of the common denominators of these effects is oxidative stress, which is also considered to be the main mechanism of action caused by PM in the human organism. Oxidative damage induced by reactive oxygen species (ROS) may affect any cellular...
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The effect of air pollution on oxidative stress markers in newborns
Ambrož, Antonín ; Rössner, Pavel (advisor) ; Rubeš, Jiří (referee) ; Gábelová, Alena (referee)
In everyday life, humans are exposed to toxic substances of anthropogenic origin. These substances can also be found in the ambient air and their impact poses a long-term risk for human health. Respirable particulate matter (PM) of aerodynamic diameter < 2.5 µm (PM2.5) is intensively studied, along with carcinogenic polycyclic aromatic hydrocarbons (PAHs), bound to it, such as benzo[a]pyrene (B[a]P), a reference carcinogenic PAH. Owing to small size, PM2.5 can penetrate the human body primarily via the airways and represent an increased health risk compared to larger particles. The negative health impacts of anthropogenic PM2.5, generated e.g. by fossil fuel combustion, are linked with its small size, relatively large surface, as well as with PAHs and other substances adsorbed on PM surface. PAHs, generated by an incomplete combustion of organic matter, can enter organism either via ingestion of contaminated food, water or via inhalation of polluted air. PAHs affect organisms via genotoxic, mutagenic, carcinogenic, embryotoxic and other adverse effects. One of the common denominators of these effects is oxidative stress, which is also considered to be the main mechanism of action caused by PM in the human organism. Oxidative damage induced by reactive oxygen species (ROS) may affect any cellular...
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Oxidative damage to cellular components after oxidative stress induction by specific herbicides
Kramná, Barbara ; Wilhelmová, Naďa (advisor) ; Ryšlavá, Helena (referee)
Oxidative stress is caused by overproduction and overaccumulation of ROS (reactive oxygen species). This state is responsible for cellular damage during unfavorable environmental conditions such as drought, low temperatures, salinity. In order to directly study oxidative stress at tobacco plants (Nicotiana tabacum cv. Xanthi) I used specific herbicides, MV (methyl viologen) and 3-AT (3- aminotriazole). There were several markers used for monitoring oxidative damage to cellular components: DNA damage detected by a comet assay, lipid peroxidation, carbonylated proteins and modification of activities of antioxidant enzymes CAT (catalase) and APX (ascorbate peroxidase). Fluorescent microscopy documented changes in a redox state of tobacco cells and a specific signal for peroxisomes was observed after treatment with higher concentrations of MV and 3-AT. Application of both herbicides caused significant DNA damage, while they worked in a different concentrations, MV in µM and 3-AT in mM. Another convincing oxidative stress marker for MV was protein carbonylation. The inhibition of antioxidant enzymes CAT and APX was less significant when compared to the effects of 3-AT. Decreasing membrane stability proved to be an universal oxidative stress marker for both herbicides. On the other hand, lipid...
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Effect of CO2 on free-radical damage
Dušková, Eliška ; Kalous, Martin (referee) ; Wilhelm, Jiří (advisor)
CO2, known for its role in acid-base regulations, is a mediator of peroxynitrite-induced oxidative damage and it also enhances Cu,Zn-SOD's antioxidant activity. These two means, by which CO₂ affects free-radical damage, are well-explored, but there are many other mechanisms. When CO2 joins in free radical reactions, carbonate radical is often produced. The carbonate radical specifically damages substrates, but it is not possible to generalize, if the effect is pro-oxidant or antioxidant. A protective role of CO2 has been observed during lipid peroxidation and during peroxynitrite-induced oxidation of DNA, when the carbonate radical caused injury to specific bases, but in the same time it prevented DNA strand breaks. Similarly, CO2 prevented peroxynitrite- induced protein fragmentation as well as it caused injury to specific aminoacids. These observations are mostly based on experiments in a chemical system, which means under simplified conditions. In vivo, CO2 exerts much more mechanisms to affect free radical reactions. Under more complex conditions, as cell culture is, there was an increase of oxidative stress after CO2 exposure. Increased concentration of CO2 causes a change in erythrocyte's function and an increase of oxidative stress on the organism's level.
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