Oxygen Toxicity: Role of Hydrogen Peroxide and Iron

Asbeck, B. S. Van

doi:10.1007/978-1-4684-5730-8_38

Cited by 12 publications

(13 citation statements)

References 51 publications

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“…This is consistent with another in vitro study performed on human endothelial cells, which reported that DFO did not increase cell susceptibility to exogenous oxidants after 48 h (Fratti et al, 1998). Furthermore, DFO has been shown to be protective in various models of ROS-induced cellular injury as reviewed by van Asbeck (1990). Additionally, DFO was found to react with oxygen products released by PMN following PMA activation (Soriani et al, 1993).…”

Section: Discussionsupporting

confidence: 89%

“…Although these ROS are harmful to bacteria, they also have the potential to destroy host cells. Several studies on the inflammation process have shown that oxidants released by PMN induce tissue damage (Weiss, 1989;van Asbeck, 1990). Oxidants are known to be cytotoxic through many different mechanisms such as protein and amino acid oxidation, lipid peroxidation, and DNA damage.…”

Section: Introductionmentioning

confidence: 99%

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Antioxidants to Prevent Bovine Neutrophil-Induced Mammary Epithelial Cell Damage

Lauzon

Zhao

Bouétard

et al. 2005

Journal of Dairy Science

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Activated neutrophils are able to produce a large quantity of bactericidal molecules such as reactive oxygen species that have been associated with tissue damage in several inflammation models. The protective effects of antioxidants in a context of neutrophil-induced damage to mammary epithelial cells were first evaluated in vitro using a coculture model of activated bovine neutrophils and a bovine mammary epithelial cell line (MAC-T cells). Cell damage was determined by quantifying the release of lactate dehydrogenase by MAC-T cells in culture medium. Morphological observation of cells stained with acridine orange was used to visualize the extent of cell damage. When incubated with neutrophils activated by lipopolysaccharides and phorbol 12-myristate 13-acetate, MAC-T cells released large amounts of lactate dehydrogenase indicating significant cell damage. The addition of dimethylthiourea or bathocuproine disulfonic acid did not reduce the damage whereas catechin, deferoxamine or glutathione ethyl ester significantly reduced neutrophil-induced cytotoxicity in a dose-dependent manner. The effect of deferoxamine, an iron chelator, on the growth of Escherichia coli and the ability of bovine neutrophils to phagocytose these bacteria were then assessed in vitro. Our data showed that deferoxamine did not interfere with the phagocytic activity of neutrophils but inhibited growth of the bacteria. Overall, our results suggest that antioxidants may be effective tools for protecting mammary tissue against neutrophil-induced oxidative stress during bovine mastitis.

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Section: Discussionsupporting

confidence: 89%

Section: Introductionmentioning

confidence: 99%

Antioxidants to Prevent Bovine Neutrophil-Induced Mammary Epithelial Cell Damage

Lauzon

Zhao

Bouétard

et al. 2005

Journal of Dairy Science

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“…In addition to being generated by the divalent reduction of O 2 and protonation during electron transports (reaction 4) O 2 + 2e- + → H 2 O 2 and through the above reaction (2), H 2 O 2 is the primary product of many microsomal and peroxisomal oxidases. This non-radical ROS, with an intermediate reactivity between those of O 2 •- and OH•, is involved in thiol groups oxidation/inactivation and in redox potential imbalance [20]. Moreover, through the reaction (5), the “Fenton reaction” H 2 O 2 + Me n+ → Me (n+1)+ + OH- + OH• transition metal ions can catalyze the H 2 O 2 reduction to OH- plus OH• and oxidized metal ion.…”

Section: Generation Of Ronsmentioning

confidence: 99%

Oxidative Stress and HPV Carcinogenesis

Marco¹

2013

Viruses

107

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Extensive experimental work has conclusively demonstrated that infection with certain types of human papillomaviruses, the so-called high-risk human papillomavirus (HR-HPV), represent a most powerful human carcinogen. However, neoplastic growth is a rare and inappropriate outcome in the natural history of HPV, and a number of other events have to concur in order to induce the viral infection into the (very rare) neoplastic transformation. From this perspective, a number of putative viral, host, and environmental co-factors have been proposed as potential candidates. Among them oxidative stress (OS) is an interesting candidate, yet comparatively underexplored. OS is a constant threat to aerobic organisms being generated during mitochondrial oxidative phosphorylation, as well as during inflammation, infections, ionizing irradiation, UV exposure, mechanical and chemical stresses. Epithelial tissues, the elective target for HPV infection, are heavily exposed to all named sources of OS. Two different types of cooperative mechanisms are presumed to occur between OS and HPV: I) The OS genotoxic activity and the HPV-induced genomic instability concur independently to the generation of the molecular damage necessary for the emergence of neoplastic clones. This first mode is merely a particular form of co-carcinogenesis; and II) OS specifically interacts with one or more molecular stages of neoplastic initiation and/or progression induced by the HPV infection. This manuscript was designed to summarize available data on this latter hypothesis. Experimental data and indirect evidences on promoting the activity of OS in viral infection and viral integration will be reviewed. The anti-apoptotic and pro-angiogenetic role of NO (nitric oxide) and iNOS (inducible nitric oxide synthase) will be discussed together with the OS/HPV cooperation in inducing cancer metabolism adaptation. Unexplored/underexplored aspects of the OS interplay with the HPV-driven carcinogenesis will be highlighted. The aim of this paper is to stimulate new areas of study and innovative approaches.

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“…Ultimately, conjugated fatty acid dienes and lipid hydroperoxides are cleaved into shorter, saturated fatty acids and a series of aldehydes [Bondy and Marwah, 1995;Porter et al, 1995]. Oxygen radicals and hydroxyl radicals can be generated by Fe +2 and other transitional ions by the Fenton reaction [Van Albert, 1990;Sadrzadeh et al, 1984;Lalonde et al, 1994]. Because Sertoli cells secrete transferrin, which then delivers Fe +2 to developing spermatids [Skinner and Griswold, 1980], the peroxidation of PUFAs in spermatozoa membranes is possible.…”

Section: Discussionmentioning

confidence: 99%

A postcryogenic comparison of membrane fatty acids of elephant spermatozoa

Swain

Miller

2000

Zoo Biol.

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Cryogenic protocols have been successful in storing spermatozoa collected from African elephants (Loxodonta africana). However, these same protocols and modifications of these protocols have failed to preserve spermatozoa collected from Asian elephants (Elephas maximus) [Buice et al., 1995, Proceedings of the Association of Zoo Veterinary Technicians, Baltimore, MD; O’Brien et al., 1997, Second International Elephant Research Symposium, Springfield, MO]. Because the success or failure of cryogenic freezing may rely on differences in membrane composition, a postcryogenic comparison of the membrane fatty acid composition of spermatozoa isolated from African and Asian elephants was studied. The spermatozoa of African elephants possessed significantly higher levels of docosahexaenoic acid (22:6, n‐3) and docosapentaenoic acid (22:5, n‐6) as compared to the spermatozoa of Asian elephants. Meanwhile, the spermatozoa of Asian elephants had higher levels of myristic acid (14:0), arachidonic acid (20:4, n‐6), and docosatetraenoic acid (22:4, n‐6) as compared to the spermatozoa of African elephants. The most abundant membrane fatty acid was docosahexaenoic acid (22:6, n‐3). The percentage of membrane docosahexaenoic acid (22:6, n‐3) in the spermatozoa of African elephants was 68.13 ± 0.52 as compared to 42.88 ± 0.87 in the spermatozoa of Asian elephants (t = 31.48, P ≤ 0.0001). Zoo Biol 19:461–473, 2000. © 2000 Wiley‐Liss, Inc.

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Oxygen Toxicity: Role of Hydrogen Peroxide and Iron

Cited by 12 publications

References 51 publications

Antioxidants to Prevent Bovine Neutrophil-Induced Mammary Epithelial Cell Damage

Antioxidants to Prevent Bovine Neutrophil-Induced Mammary Epithelial Cell Damage

Oxidative Stress and HPV Carcinogenesis

A postcryogenic comparison of membrane fatty acids of elephant spermatozoa

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