The Experts below are selected from a list of 294 Experts worldwide ranked by ideXlab platform
Ari D Brooks - One of the best experts on this subject based on the ideXlab platform.
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nonthermal dielectric barrier discharge plasma induced inactivation involves oxidative dna damage and Membrane Lipid peroxidation in escherichia coli
Antimicrobial Agents and Chemotherapy, 2011Co-Authors: Suresh G Joshi, Moogega Cooper, Adam Yost, Michelle Paff, Utku Kursat Ercan, Gregory Fridman, Gary Friedman, Alexander Fridman, Ari D BrooksAbstract:ABSTRACT Oxidative stress leads to Membrane Lipid peroxidation, which yields products causing variable degrees of detrimental oxidative modifications in cells. Reactive oxygen species (ROS) are the key regulators in this process and induce Lipid peroxidation in Escherichia coli . Application of nonthermal (cold) plasma is increasingly used for inactivation of surface contaminants. Recently, we reported a successful application of nonthermal plasma, using a floating-electrode dielectric-barrier discharge (FE-DBD) technique for rapid inactivation of bacterial contaminants in normal atmospheric air (S. G. Joshi et al., Am. J. Infect. Control 38:293-301, 2010). In the present report, we demonstrate that FE-DBD plasma-mediated inactivation involves Membrane Lipid peroxidation in E. coli . Dose-dependent ROS, such as singlet oxygen and hydrogen peroxide-like species generated during plasma-induced oxidative stress, were responsible for Membrane Lipid peroxidation, and ROS scavengers, such as α-tocopherol (vitamin E), were able to significantly inhibit the extent of Lipid peroxidation and oxidative DNA damage. These findings indicate that this is a major mechanism involved in FE-DBD plasma-mediated inactivation of bacteria.
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Nonthermal dielectric-barrier discharge plasma-induced inactivation involves oxidative DNA damage and Membrane Lipid peroxidation in Escherichia coli
Antimicrobial Agents and Chemotherapy, 2011Co-Authors: Suresh G Joshi, Moogega Cooper, Adam Yost, Michelle Paff, Utku Kursat Ercan, Gregory Fridman, Gary Friedman, Alexander Fridman, Ari D BrooksAbstract:Oxidative stress leads to Membrane Lipid peroxidation, which yields products causing variable degrees of detrimental oxidative modifications in cells. Reactive oxygen species (ROS) are the key regulators in this process and induce Lipid peroxidation in Escherichia coli. Application of nonthermal (cold) plasma is increas-ingly used for inactivation of surface contaminants. Recently, we reported a successful application of nonther-mal plasma, using a floating-electrode dielectric-barrier discharge (FE-DBD) technique for rapid inactivation of bacterial contaminants in normal atmospheric air (S. G. Joshi et al., Am. J. Infect. Control 38:293–301, 2010). In the present report, we demonstrate that FE-DBD plasma-mediated inactivation involves Membrane Lipid peroxidation in E. coli. Dose-dependent ROS, such as singlet oxygen and hydrogen peroxide-like species generated during plasma-induced oxidative stress, were responsible for Membrane Lipid peroxidation, and ROS scavengers, such as ␣-tocopherol (vitamin E), were able to significantly inhibit the extent of Lipid peroxidation and oxidative DNA damage. These findings indicate that this is a major mechanism involved in FE-DBD plasma-mediated inactivation of bacteria. Nonthermal (cold) dielectric-barrier discharge (DBD) at-mospheric-pressure plasma is widely under investigation for use as an alternative sterilization and disinfection method in the fields of biology and medicine. Most recently, we demon-strated that Escherichia coli, Staphylococcus aureus, and methi-cillin-resistant Staphylococcus aureus in both their planktonic form and in biofilms are rapidly inactivated by nonthermal DBD plasma using a floating-electrode technique (11). Com-plete inactivation of E. coli was seen in less than 120 s when E. coli was present in its planktonic form, and complete inactiva-tion occurred in about 180 s when it was in the biofilm form, making this technique attractive for sterilization processes. E. coli is one of the most common Gram-negative bacterial con-taminants responsible for hospital-acquired infections (HAI) and one of the most widely studied organisms in the laboratory and therefore is a good choice to track various oxidative-stress pathways. A DBD plasma-generating probe is an apparatus that gen-erates microsecond-long, high-voltage-pulsed cold plasma be-tween the primary electrode covered with a quartz surface and the surface of the biological sample, which serves as a second electrode. The high-voltage electrode is completely covered with a dielectric barrier, which makes it safe for sterilization applications, and the nature of the applied microsecond pulses do not elevate the surface temperature above 28°C. In the floating-electrode DBD (FE-DBD) plasma setup, the second electrode (biological sample) is not grounded and remains at a floating potential. Discharge ignites when the powered elec-trode approaches the surface to be treated at a distance (dis-charge gap) less than about 3 mm, depending on the form, duration, and polarity of the driving voltage, and it is safe to apply to human or animal skin and delicate surfaces which are likely to be damaged by thermal (hot) plasma. In thermal plasma, argon is used, and in this instance, the local tempera-ture is increased significantly. Other DBD plasmas can be generated either in special gas flow or vacuum, and the sample of interest is held between the two electrodes (5, 11) (see reference 5 for details). Thus, the FE-DBD plasma technique offers better potential for diversity, since it works in room air (normal atmospheric pressure) and is cold to touch. Nonthermal plasma at normal atmospheric pressure (room air) generates many physical and chemical active species when applied to biological samples using the floating-electrode (FE) technique. Some of the species being characterized in our laboratories are ozone, hydrogen peroxide, singlet oxygen, su-peroxide, hydroxyl radical, nitric oxide, and UV (5). All or most of these species are capable of causing oxidative damage to bacteria, and if the damage is extensive (beyond the capacity of the cellular repair machinery), it will lead to cell death. There are many speculative reports supporting this mecha-nism, and although the exact changes occurring are not yet known, the involvement of reactive oxygen species (ROS) and oxidative damage specific to proteins, Lipid layers, or DNA have been observed. Furthermore, the FE-DBD plasma appli-cation technique is relatively new, and plasma-generated
Suresh G Joshi - One of the best experts on this subject based on the ideXlab platform.
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nonthermal dielectric barrier discharge plasma induced inactivation involves oxidative dna damage and Membrane Lipid peroxidation in escherichia coli
Antimicrobial Agents and Chemotherapy, 2011Co-Authors: Suresh G Joshi, Moogega Cooper, Adam Yost, Michelle Paff, Utku Kursat Ercan, Gregory Fridman, Gary Friedman, Alexander Fridman, Ari D BrooksAbstract:ABSTRACT Oxidative stress leads to Membrane Lipid peroxidation, which yields products causing variable degrees of detrimental oxidative modifications in cells. Reactive oxygen species (ROS) are the key regulators in this process and induce Lipid peroxidation in Escherichia coli . Application of nonthermal (cold) plasma is increasingly used for inactivation of surface contaminants. Recently, we reported a successful application of nonthermal plasma, using a floating-electrode dielectric-barrier discharge (FE-DBD) technique for rapid inactivation of bacterial contaminants in normal atmospheric air (S. G. Joshi et al., Am. J. Infect. Control 38:293-301, 2010). In the present report, we demonstrate that FE-DBD plasma-mediated inactivation involves Membrane Lipid peroxidation in E. coli . Dose-dependent ROS, such as singlet oxygen and hydrogen peroxide-like species generated during plasma-induced oxidative stress, were responsible for Membrane Lipid peroxidation, and ROS scavengers, such as α-tocopherol (vitamin E), were able to significantly inhibit the extent of Lipid peroxidation and oxidative DNA damage. These findings indicate that this is a major mechanism involved in FE-DBD plasma-mediated inactivation of bacteria.
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Nonthermal dielectric-barrier discharge plasma-induced inactivation involves oxidative DNA damage and Membrane Lipid peroxidation in Escherichia coli
Antimicrobial Agents and Chemotherapy, 2011Co-Authors: Suresh G Joshi, Moogega Cooper, Adam Yost, Michelle Paff, Utku Kursat Ercan, Gregory Fridman, Gary Friedman, Alexander Fridman, Ari D BrooksAbstract:Oxidative stress leads to Membrane Lipid peroxidation, which yields products causing variable degrees of detrimental oxidative modifications in cells. Reactive oxygen species (ROS) are the key regulators in this process and induce Lipid peroxidation in Escherichia coli. Application of nonthermal (cold) plasma is increas-ingly used for inactivation of surface contaminants. Recently, we reported a successful application of nonther-mal plasma, using a floating-electrode dielectric-barrier discharge (FE-DBD) technique for rapid inactivation of bacterial contaminants in normal atmospheric air (S. G. Joshi et al., Am. J. Infect. Control 38:293–301, 2010). In the present report, we demonstrate that FE-DBD plasma-mediated inactivation involves Membrane Lipid peroxidation in E. coli. Dose-dependent ROS, such as singlet oxygen and hydrogen peroxide-like species generated during plasma-induced oxidative stress, were responsible for Membrane Lipid peroxidation, and ROS scavengers, such as ␣-tocopherol (vitamin E), were able to significantly inhibit the extent of Lipid peroxidation and oxidative DNA damage. These findings indicate that this is a major mechanism involved in FE-DBD plasma-mediated inactivation of bacteria. Nonthermal (cold) dielectric-barrier discharge (DBD) at-mospheric-pressure plasma is widely under investigation for use as an alternative sterilization and disinfection method in the fields of biology and medicine. Most recently, we demon-strated that Escherichia coli, Staphylococcus aureus, and methi-cillin-resistant Staphylococcus aureus in both their planktonic form and in biofilms are rapidly inactivated by nonthermal DBD plasma using a floating-electrode technique (11). Com-plete inactivation of E. coli was seen in less than 120 s when E. coli was present in its planktonic form, and complete inactiva-tion occurred in about 180 s when it was in the biofilm form, making this technique attractive for sterilization processes. E. coli is one of the most common Gram-negative bacterial con-taminants responsible for hospital-acquired infections (HAI) and one of the most widely studied organisms in the laboratory and therefore is a good choice to track various oxidative-stress pathways. A DBD plasma-generating probe is an apparatus that gen-erates microsecond-long, high-voltage-pulsed cold plasma be-tween the primary electrode covered with a quartz surface and the surface of the biological sample, which serves as a second electrode. The high-voltage electrode is completely covered with a dielectric barrier, which makes it safe for sterilization applications, and the nature of the applied microsecond pulses do not elevate the surface temperature above 28°C. In the floating-electrode DBD (FE-DBD) plasma setup, the second electrode (biological sample) is not grounded and remains at a floating potential. Discharge ignites when the powered elec-trode approaches the surface to be treated at a distance (dis-charge gap) less than about 3 mm, depending on the form, duration, and polarity of the driving voltage, and it is safe to apply to human or animal skin and delicate surfaces which are likely to be damaged by thermal (hot) plasma. In thermal plasma, argon is used, and in this instance, the local tempera-ture is increased significantly. Other DBD plasmas can be generated either in special gas flow or vacuum, and the sample of interest is held between the two electrodes (5, 11) (see reference 5 for details). Thus, the FE-DBD plasma technique offers better potential for diversity, since it works in room air (normal atmospheric pressure) and is cold to touch. Nonthermal plasma at normal atmospheric pressure (room air) generates many physical and chemical active species when applied to biological samples using the floating-electrode (FE) technique. Some of the species being characterized in our laboratories are ozone, hydrogen peroxide, singlet oxygen, su-peroxide, hydroxyl radical, nitric oxide, and UV (5). All or most of these species are capable of causing oxidative damage to bacteria, and if the damage is extensive (beyond the capacity of the cellular repair machinery), it will lead to cell death. There are many speculative reports supporting this mecha-nism, and although the exact changes occurring are not yet known, the involvement of reactive oxygen species (ROS) and oxidative damage specific to proteins, Lipid layers, or DNA have been observed. Furthermore, the FE-DBD plasma appli-cation technique is relatively new, and plasma-generated
Pablo V Escriba - One of the best experts on this subject based on the ideXlab platform.
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Membrane Lipid Switches: How Membrane Lipid Structure Influences Protein–Lipid Interactions
2020Co-Authors: Manuel Torres, Victoria Llado, Catalina Ana Rosselló, Paula Fernández-garcía, Pablo V EscribaAbstract:Peripheral Membrane proteins are required for signal propagation upon ligand-induced receptor activation at the plasma Membrane. The translocation of this amphitropic peripheral proteins from or to the plasma Membrane enables signal cascade propagation into the cells. This translocation greatly depends on the Membrane’s Lipid composition and, consequently, regulation of the Lipid bilayer emerges as a novel therapeutic strategy. Indeed, relevant changes in Membrane Lipids can induce massive translocation of peripheral signaling proteins from or to the plasma Membrane, which controls how cells behave. We called these changes “Lipid switches”, as they alter the cell’s status (e.g., proliferation, differentiation, death, etc.) in response to the modulation of Membrane Lipids. This discovery enables therapeutic interventions focused on modifying the bilayer’s Lipids, an approach known as Membrane-Lipid therapy (MLT) or melitherapy.
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The Implications for Cells of the Lipid Switches Driven by Protein-Membrane Interactions and the Development of Membrane Lipid Therapy.
International Journal of Molecular Sciences, 2020Co-Authors: Manuel Torres, Victoria Llado, Catalina Ana Rosselló, Paula Fernández-garcía, Or Kakhlon, Pablo V EscribaAbstract:The cell Membrane contains a variety of receptors that interact with signaling molecules. However, agonist–receptor interactions not always activate a signaling cascade. Amphitropic Membrane proteins are required for signal propagation upon ligand-induced receptor activation. These proteins localize to the plasma Membrane or internal compartments; however, they are only activated by ligand-receptor complexes when both come into physical contact in Membranes. These interactions enable signal propagation. Thus, signals may not propagate into the cell if peripheral proteins do not co-localize with receptors even in the presence of messengers. As the translocation of an amphitropic protein greatly depends on the Membrane’s Lipid composition, regulation of the Lipid bilayer emerges as a novel therapeutic strategy. Some of the signals controlled by proteins non-permanently bound to Membranes produce dramatic changes in the cell’s physiology. Indeed, changes in Membrane Lipids induce translocation of dozens of peripheral signaling proteins from or to the plasma Membrane, which controls how cells behave. We called these changes “Lipid switches”, as they alter the cell’s status (e.g., proliferation, differentiation, death, etc.) in response to the modulation of Membrane Lipids. Indeed, this discovery enables therapeutic interventions that modify the bilayer’s Lipids, an approach known as Membrane-Lipid therapy (MLT) or melitherapy.
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Membrane-Lipid therapy: A historical perspective of Membrane-targeted therapies - From Lipid bilayer structure to the pathophysiological regulation of cells.
Biochimica et Biophysica Acta, 2017Co-Authors: Pablo V EscribaAbstract:Abstract Our current understanding of Membrane Lipid composition, structure and functions has led to the investigation of their role in cell signaling, both in healthy and pathological cells. As a consequence, therapies based on the regulation of Membrane Lipid composition and structure have been recently developed. This novel field, known as Membrane Lipid Therapy, is growing and evolving rapidly, providing treatments that are now in use or that are being studied for their application to oncological disorders, Alzheimer's disease, spinal cord injury, stroke, diabetes, obesity, and neuropathic pain. This field has arisen from relevant discoveries on the behavior of Membranes in recent decades, and it paves the way to adopt new approaches in modern pharmacology and nutrition. This innovative area will promote further investigation into Membranes and the development of new therapies with molecules that target the cell Membrane. Due to the prominent roles of Membranes in the cells' physiology and the paucity of therapeutic approaches based on the regulation of the Lipids they contain, it is expected that Membrane Lipid therapy will provide new treatments for numerous pathologies. The first on-purpose rationally designed molecule in this field, minerval, is currently being tested in clinical trials and it is expected to enter the market around 2020. However, it seems feasible that during the next few decades other Membrane regulators will also be marketed for the treatment of human pathologies. This article is part of a Special Issue entitled: Membrane Lipid Therapy: Drugs Targeting BioMembranes edited by Pablo V. Escriba
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Membrane Lipid therapy: Modulation of the cell Membrane composition and structure as a molecular base for drug discovery and new disease treatment
Progress in Lipid Research, 2015Co-Authors: Pablo V Escriba, Zsolt Torok, Xavier Busquets, Ibolya Horváth, John L. Harwood, Jin-ichi Inokuchi, Gábor Balogh, László VíghAbstract:Nowadays we understand cell Membranes not as a simple double Lipid layer but as a collection of complex and dynamic protein–Lipid structures and microdomains that serve as functional platforms for interacting signaling Lipids and proteins. Membrane Lipids and Lipid structures participate directly as messengers or regulators of signal transduction. In addition, protein–Lipid interactions participate in the localization of signaling protein partners to specific Membrane microdomains. Thus, Lipid alterations change cell signaling that are associated with a variety of diseases including cancer, obesity, neurodegenerative disorders, cardiovascular pathologies, etc. This article reviews the newly emerging field of Membrane Lipid therapy which involves the pharmacological regulation of Membrane Lipid composition and structure for the treatment of diseases. Membrane Lipid therapy proposes the use of new molecules specifically designed to modify Membrane Lipid structures and microdomains as pharmaceutical disease-modifying agents by reversing the malfunction or altering the expression of disease-specific protein or Lipid signal cascades. Here, we provide an in-depth analysis of this emerging field, especially its molecular bases and its relevance to the development of innovative therapeutic approaches.
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Membrane Lipid therapy a new approach in molecular medicine
Trends in Molecular Medicine, 2006Co-Authors: Pablo V EscribaAbstract:Although most drugs bind to proteins and regulate their activity, some drugs act through a new therapeutic approach called Membrane-Lipid therapy and bind to Lipids, thus modulating the structure of Membranes. Most cellular functions are highly dependent on the Lipid environment because they are controlled by proteins in or around Membranes. The wide variety of cell and organelle Membranes and the existence of special Lipid regions (e.g. microvilli) and domains (e.g. Lipid rafts) support the possibility of designing specific Lipid therapies. Indeed, recent evidence suggests that Lipid therapy might have potential for the treatment of cancer, cardiovascular pathologies, neurodegenerative processes, obesity, metabolic disorders, inflammation, and infectious and autoimmune diseases.
Moogega Cooper - One of the best experts on this subject based on the ideXlab platform.
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nonthermal dielectric barrier discharge plasma induced inactivation involves oxidative dna damage and Membrane Lipid peroxidation in escherichia coli
Antimicrobial Agents and Chemotherapy, 2011Co-Authors: Suresh G Joshi, Moogega Cooper, Adam Yost, Michelle Paff, Utku Kursat Ercan, Gregory Fridman, Gary Friedman, Alexander Fridman, Ari D BrooksAbstract:ABSTRACT Oxidative stress leads to Membrane Lipid peroxidation, which yields products causing variable degrees of detrimental oxidative modifications in cells. Reactive oxygen species (ROS) are the key regulators in this process and induce Lipid peroxidation in Escherichia coli . Application of nonthermal (cold) plasma is increasingly used for inactivation of surface contaminants. Recently, we reported a successful application of nonthermal plasma, using a floating-electrode dielectric-barrier discharge (FE-DBD) technique for rapid inactivation of bacterial contaminants in normal atmospheric air (S. G. Joshi et al., Am. J. Infect. Control 38:293-301, 2010). In the present report, we demonstrate that FE-DBD plasma-mediated inactivation involves Membrane Lipid peroxidation in E. coli . Dose-dependent ROS, such as singlet oxygen and hydrogen peroxide-like species generated during plasma-induced oxidative stress, were responsible for Membrane Lipid peroxidation, and ROS scavengers, such as α-tocopherol (vitamin E), were able to significantly inhibit the extent of Lipid peroxidation and oxidative DNA damage. These findings indicate that this is a major mechanism involved in FE-DBD plasma-mediated inactivation of bacteria.
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Nonthermal dielectric-barrier discharge plasma-induced inactivation involves oxidative DNA damage and Membrane Lipid peroxidation in Escherichia coli
Antimicrobial Agents and Chemotherapy, 2011Co-Authors: Suresh G Joshi, Moogega Cooper, Adam Yost, Michelle Paff, Utku Kursat Ercan, Gregory Fridman, Gary Friedman, Alexander Fridman, Ari D BrooksAbstract:Oxidative stress leads to Membrane Lipid peroxidation, which yields products causing variable degrees of detrimental oxidative modifications in cells. Reactive oxygen species (ROS) are the key regulators in this process and induce Lipid peroxidation in Escherichia coli. Application of nonthermal (cold) plasma is increas-ingly used for inactivation of surface contaminants. Recently, we reported a successful application of nonther-mal plasma, using a floating-electrode dielectric-barrier discharge (FE-DBD) technique for rapid inactivation of bacterial contaminants in normal atmospheric air (S. G. Joshi et al., Am. J. Infect. Control 38:293–301, 2010). In the present report, we demonstrate that FE-DBD plasma-mediated inactivation involves Membrane Lipid peroxidation in E. coli. Dose-dependent ROS, such as singlet oxygen and hydrogen peroxide-like species generated during plasma-induced oxidative stress, were responsible for Membrane Lipid peroxidation, and ROS scavengers, such as ␣-tocopherol (vitamin E), were able to significantly inhibit the extent of Lipid peroxidation and oxidative DNA damage. These findings indicate that this is a major mechanism involved in FE-DBD plasma-mediated inactivation of bacteria. Nonthermal (cold) dielectric-barrier discharge (DBD) at-mospheric-pressure plasma is widely under investigation for use as an alternative sterilization and disinfection method in the fields of biology and medicine. Most recently, we demon-strated that Escherichia coli, Staphylococcus aureus, and methi-cillin-resistant Staphylococcus aureus in both their planktonic form and in biofilms are rapidly inactivated by nonthermal DBD plasma using a floating-electrode technique (11). Com-plete inactivation of E. coli was seen in less than 120 s when E. coli was present in its planktonic form, and complete inactiva-tion occurred in about 180 s when it was in the biofilm form, making this technique attractive for sterilization processes. E. coli is one of the most common Gram-negative bacterial con-taminants responsible for hospital-acquired infections (HAI) and one of the most widely studied organisms in the laboratory and therefore is a good choice to track various oxidative-stress pathways. A DBD plasma-generating probe is an apparatus that gen-erates microsecond-long, high-voltage-pulsed cold plasma be-tween the primary electrode covered with a quartz surface and the surface of the biological sample, which serves as a second electrode. The high-voltage electrode is completely covered with a dielectric barrier, which makes it safe for sterilization applications, and the nature of the applied microsecond pulses do not elevate the surface temperature above 28°C. In the floating-electrode DBD (FE-DBD) plasma setup, the second electrode (biological sample) is not grounded and remains at a floating potential. Discharge ignites when the powered elec-trode approaches the surface to be treated at a distance (dis-charge gap) less than about 3 mm, depending on the form, duration, and polarity of the driving voltage, and it is safe to apply to human or animal skin and delicate surfaces which are likely to be damaged by thermal (hot) plasma. In thermal plasma, argon is used, and in this instance, the local tempera-ture is increased significantly. Other DBD plasmas can be generated either in special gas flow or vacuum, and the sample of interest is held between the two electrodes (5, 11) (see reference 5 for details). Thus, the FE-DBD plasma technique offers better potential for diversity, since it works in room air (normal atmospheric pressure) and is cold to touch. Nonthermal plasma at normal atmospheric pressure (room air) generates many physical and chemical active species when applied to biological samples using the floating-electrode (FE) technique. Some of the species being characterized in our laboratories are ozone, hydrogen peroxide, singlet oxygen, su-peroxide, hydroxyl radical, nitric oxide, and UV (5). All or most of these species are capable of causing oxidative damage to bacteria, and if the damage is extensive (beyond the capacity of the cellular repair machinery), it will lead to cell death. There are many speculative reports supporting this mecha-nism, and although the exact changes occurring are not yet known, the involvement of reactive oxygen species (ROS) and oxidative damage specific to proteins, Lipid layers, or DNA have been observed. Furthermore, the FE-DBD plasma appli-cation technique is relatively new, and plasma-generated
Adam Yost - One of the best experts on this subject based on the ideXlab platform.
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nonthermal dielectric barrier discharge plasma induced inactivation involves oxidative dna damage and Membrane Lipid peroxidation in escherichia coli
Antimicrobial Agents and Chemotherapy, 2011Co-Authors: Suresh G Joshi, Moogega Cooper, Adam Yost, Michelle Paff, Utku Kursat Ercan, Gregory Fridman, Gary Friedman, Alexander Fridman, Ari D BrooksAbstract:ABSTRACT Oxidative stress leads to Membrane Lipid peroxidation, which yields products causing variable degrees of detrimental oxidative modifications in cells. Reactive oxygen species (ROS) are the key regulators in this process and induce Lipid peroxidation in Escherichia coli . Application of nonthermal (cold) plasma is increasingly used for inactivation of surface contaminants. Recently, we reported a successful application of nonthermal plasma, using a floating-electrode dielectric-barrier discharge (FE-DBD) technique for rapid inactivation of bacterial contaminants in normal atmospheric air (S. G. Joshi et al., Am. J. Infect. Control 38:293-301, 2010). In the present report, we demonstrate that FE-DBD plasma-mediated inactivation involves Membrane Lipid peroxidation in E. coli . Dose-dependent ROS, such as singlet oxygen and hydrogen peroxide-like species generated during plasma-induced oxidative stress, were responsible for Membrane Lipid peroxidation, and ROS scavengers, such as α-tocopherol (vitamin E), were able to significantly inhibit the extent of Lipid peroxidation and oxidative DNA damage. These findings indicate that this is a major mechanism involved in FE-DBD plasma-mediated inactivation of bacteria.
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Nonthermal dielectric-barrier discharge plasma-induced inactivation involves oxidative DNA damage and Membrane Lipid peroxidation in Escherichia coli
Antimicrobial Agents and Chemotherapy, 2011Co-Authors: Suresh G Joshi, Moogega Cooper, Adam Yost, Michelle Paff, Utku Kursat Ercan, Gregory Fridman, Gary Friedman, Alexander Fridman, Ari D BrooksAbstract:Oxidative stress leads to Membrane Lipid peroxidation, which yields products causing variable degrees of detrimental oxidative modifications in cells. Reactive oxygen species (ROS) are the key regulators in this process and induce Lipid peroxidation in Escherichia coli. Application of nonthermal (cold) plasma is increas-ingly used for inactivation of surface contaminants. Recently, we reported a successful application of nonther-mal plasma, using a floating-electrode dielectric-barrier discharge (FE-DBD) technique for rapid inactivation of bacterial contaminants in normal atmospheric air (S. G. Joshi et al., Am. J. Infect. Control 38:293–301, 2010). In the present report, we demonstrate that FE-DBD plasma-mediated inactivation involves Membrane Lipid peroxidation in E. coli. Dose-dependent ROS, such as singlet oxygen and hydrogen peroxide-like species generated during plasma-induced oxidative stress, were responsible for Membrane Lipid peroxidation, and ROS scavengers, such as ␣-tocopherol (vitamin E), were able to significantly inhibit the extent of Lipid peroxidation and oxidative DNA damage. These findings indicate that this is a major mechanism involved in FE-DBD plasma-mediated inactivation of bacteria. Nonthermal (cold) dielectric-barrier discharge (DBD) at-mospheric-pressure plasma is widely under investigation for use as an alternative sterilization and disinfection method in the fields of biology and medicine. Most recently, we demon-strated that Escherichia coli, Staphylococcus aureus, and methi-cillin-resistant Staphylococcus aureus in both their planktonic form and in biofilms are rapidly inactivated by nonthermal DBD plasma using a floating-electrode technique (11). Com-plete inactivation of E. coli was seen in less than 120 s when E. coli was present in its planktonic form, and complete inactiva-tion occurred in about 180 s when it was in the biofilm form, making this technique attractive for sterilization processes. E. coli is one of the most common Gram-negative bacterial con-taminants responsible for hospital-acquired infections (HAI) and one of the most widely studied organisms in the laboratory and therefore is a good choice to track various oxidative-stress pathways. A DBD plasma-generating probe is an apparatus that gen-erates microsecond-long, high-voltage-pulsed cold plasma be-tween the primary electrode covered with a quartz surface and the surface of the biological sample, which serves as a second electrode. The high-voltage electrode is completely covered with a dielectric barrier, which makes it safe for sterilization applications, and the nature of the applied microsecond pulses do not elevate the surface temperature above 28°C. In the floating-electrode DBD (FE-DBD) plasma setup, the second electrode (biological sample) is not grounded and remains at a floating potential. Discharge ignites when the powered elec-trode approaches the surface to be treated at a distance (dis-charge gap) less than about 3 mm, depending on the form, duration, and polarity of the driving voltage, and it is safe to apply to human or animal skin and delicate surfaces which are likely to be damaged by thermal (hot) plasma. In thermal plasma, argon is used, and in this instance, the local tempera-ture is increased significantly. Other DBD plasmas can be generated either in special gas flow or vacuum, and the sample of interest is held between the two electrodes (5, 11) (see reference 5 for details). Thus, the FE-DBD plasma technique offers better potential for diversity, since it works in room air (normal atmospheric pressure) and is cold to touch. Nonthermal plasma at normal atmospheric pressure (room air) generates many physical and chemical active species when applied to biological samples using the floating-electrode (FE) technique. Some of the species being characterized in our laboratories are ozone, hydrogen peroxide, singlet oxygen, su-peroxide, hydroxyl radical, nitric oxide, and UV (5). All or most of these species are capable of causing oxidative damage to bacteria, and if the damage is extensive (beyond the capacity of the cellular repair machinery), it will lead to cell death. There are many speculative reports supporting this mecha-nism, and although the exact changes occurring are not yet known, the involvement of reactive oxygen species (ROS) and oxidative damage specific to proteins, Lipid layers, or DNA have been observed. Furthermore, the FE-DBD plasma appli-cation technique is relatively new, and plasma-generated