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Özcan Erel - One of the best experts on this subject based on the ideXlab platform.
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effect of sulfite treatment on total antioxidant capacity total oxidant status Lipid Hydroperoxide and total free sulfydryl groups contents in normal and sulfite oxidase deficient rat plasma
Cell Biology and Toxicology, 2009Co-Authors: Emine Nur Herken, Özcan Erel, Erdogan Kocamaz, Hakim Celik, Vural KucukatayAbstract:Sulfites, which are commonly used as preservatives, are continuously formed in the body during the metabolism of sulfur-containing amino acids. Sulfite oxidase (SOX) is an essential enzyme in the pathway of the oxidative degradation of sulfite to sulfate protecting cells from sulfite toxicity. This article investigated the effect of sulfite on total antioxidant capacity (TAC), total oxidant status, Lipid Hydroperoxide (LOOH), and total free sulfydryl groups (–SH) levels in normal and SOX-deficient male albino rat plasma. For this purpose, rats were divided into four groups: control, sulfite-treated, SOX-deficient, and sulfite-treated SOX-deficient groups. SOX deficiency was established by feeding rats a low molybdenum diet and adding to their drinking water 200 ppm tungsten. Sulfite (70 mg/kg) was administered to the animals via their drinking water. SOX deficiency together with sulfite treatment caused a significant increase in the plasma LOOH and total oxidant status levels. –SH content of rat plasma significantly decreased by both sulfite treatment and SOX deficiency compared to the control. There was also a significant decrease in plasma TAC level by sulfite treatment. In conclusion, sulfite treatment affects the antioxidant/oxidant balance of the plasma cells of the rats toward oxidants in SOX-deficient groups.
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evaluation of blood oxidant antioxidant balance in dogs with sarcoptic mange
Veterinary Parasitology, 2009Co-Authors: İlker Çamkerten, T Sahin, G Borazan, Anke Gökçen, Özcan ErelAbstract:Abstract The aim of this study was to investigate of oxidant/antioxidant balance in dogs with sarcoptic mange. The study materials consisted of totally 30 cross-breed male dogs; 15 with sarcoptic mange (study group) and 15 healthy as control. Blood samples for analyses were taken from control and study group. In study group, microscopic examination of dermal scrapings of 15 dogs revealed S. scabies . Lipid Hydroperoxide level, total oxidant status and oxidative stress index in dogs with sarcoptic mange were higher ( P P P P
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Evaluation of blood oxidant/antioxidant balance in dogs with sarcoptic mange.
Veterinary parasitology, 2009Co-Authors: İlker Çamkerten, T Sahin, G Borazan, Anke Gökçen, Özcan ErelAbstract:The aim of this study was to investigate of oxidant/antioxidant balance in dogs with sarcoptic mange. The study materials consisted of totally 30 cross-breed male dogs; 15 with sarcoptic mange (study group) and 15 healthy as control. Blood samples for analyses were taken from control and study group. In study group, microscopic examination of dermal scrapings of 15 dogs revealed S. scabies. Lipid Hydroperoxide level, total oxidant status and oxidative stress index in dogs with sarcoptic mange were higher (P
Donald Armstrong - One of the best experts on this subject based on the ideXlab platform.
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a rat model for choroidal neovascularization using subretinal Lipid Hydroperoxide injection
American Journal of Pathology, 2010Co-Authors: Takayuki Baba, Donald Armstrong, Imran A Bhutto, C Merges, Rhonda Grebe, David Emmert, Scott D Mcleod, Gerard A LuttyAbstract:The purpose of this study was to develop and characterize a rat model of choroidal neovascularization (CNV) as occurs in age-related macular degeneration. The Lipid Hydroperoxide 13(S)-hydroperoxy-9Z,11E-octadecadienoic acid (HpODE) is found in submacular Bruch’s membrane in aged humans and has been reported to generate neovascularization in a rabbit model. Three weeks after a single subretinal injection of 30 μg of HpODE, eyes of Sprague-Dawley rats were harvested. Follow-up fluorescein angiography was done on other animals until 5 weeks postinjection. Histological studies, immunohistochemical staining, and flatmount choroids for CNV measurements were performed. In addition, we used murine neuronal, bovine endothelial, and human ARPE19 cells for testing the in vitro effects of HpODE. CNV developed in 85.7% of HpODE-injected eyes. The neovascular areas were significantly greater in HpODE-injected eyes compared with those in control eyes (P = 0.023). The CNV had maximum dye leakage at 3 weeks, which subsided by the 5th week. Histologically, CNV extended from the choriocapillaris into the subretinal space. ED1-positive macrophages were recruited to the site. In vitro assays demonstrated that only 30 ng/ml HpODE induced cell proliferation and migration of endothelial cells. HpODE-induced CNV was highly reproducible, and its natural course seems to be ideal for evaluating therapeutic modalities. Because HpODE has been isolated from aged humans, the HpODE-induced rat model seems to be a relevant experimental model for CNV in age-related macular degeneration.
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protective effect of polyethylene glycol superoxide dismutase on leukocyte dynamics in rat retinal microcirculation under Lipid Hydroperoxide induced oxidative stress
Experimental Eye Research, 2005Co-Authors: Akihisa Matsubara, Kazushi Tamai, Kazuyuki Tomida, Yoshito Matsuda, Hiroshi Morita, Donald Armstrong, Y Niwa, Yuichiro OguraAbstract:Abstract The levels of Lipid Hydroperoxide (LHPs) in vitreous are elevated in a variety of retinal disorders. Recently, we have shown that increased levels of LHPs in the vitreous enhanced leukocyte-endothelium interaction in the retina, which should contribute to the initial disturbance of the retinal microcirculation. Based upon the previous work, the purpose of the present study was to investigate the effect of polyethylene glycol-superoxide dismutase (PEG-SOD), one of the important enzyme antioxidants, on leukocyte-endothelial interaction in the retinal microcirculation under LHP-induced oxidative stress. Male Brown-Norway rats weighing approximately 250 g were used. LHP(18:2) was made from linoleic acid (LA) with lipoxygenase and 10 μg of LHP dissolved in 5 μl of sodium borate buffer (SBB, 0.02 m ) was slowly injected into the vitreous using a 33-gauge needle. PEG-SOD (5000 units/kg) was given intravenously 5 min before LHP injection. At 2, 4, 6, 12, 24 and 48 hr after the vitreous injections, we evaluated the number of rolling leukocytes along the major retinal veins and the number of leukocytes that accumulated in the retinal microvasculature with acridine orange digital fluorography. In LHP-treated rats, leukocyte rolling along the major retinal veins was maximal at 6 hr after LHP injection. The number of rolling leukocytes in the PEG-SOD-treated rats was decreased to 5.5% of those in the LHP-treated rats at 6 hr after LHP injection ( P P P
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Lipid Hydroperoxide stimulates subretinal choroidal neovascularization in the rabbit
Experimental Eye Research, 2002Co-Authors: Kazushi Tamai, Yuichiro Ogura, Richard F Spaide, Ann E Ellis, Shigehiro Iwabuchi, Donald ArmstrongAbstract:Abstract The authors sought to evaluate the effect of linoleic acid Hydroperoxide (18:2/LHP) in promoting choroidal neovascularization (CNV). Albino male rabbits received a subretinal injection of various amounts of LHP (ranging from 5 to 200 μ g) dissolved in 50 μ l of sodium borate buffer. Control eyes received the buffer only. Eyes were examined up to 4 weeks later with indirect ophthalmoscopy, fundus photography and fluorescein angiography. Animals were killed on days 3, 7, 14 or 28, and eyes examined by light and transmission electron microscopy. In eyes injected with LHP of 150–200 μ g, exposed areas turned white as observed ophthalmoscopically and showed both severe retinal and choroidal atrophy histologically. Neither fluorescein leakage nor CNV was found in these eyes or in controls. In 33 eyes injected with LHP of 100 μ g or less, prominent fluorescein leakage was seen in three (9%) and less prominent focal leakage in five (15%). In 11 (46%) of the 24 eyes injected with 12.5–50 μ g LHP, CNV was found histologically. Subretinal injection of LHP is capable of inducing CNV.
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Lipid Hydroperoxide stimulates leukocyte-endothelium interaction in the retinal microcirculation.
Experimental eye research, 2002Co-Authors: Kazushi Tamai, Akihisa Matsubara, Kazuyuki Tomida, Yoshito Matsuda, Hiroshi Morita, Donald Armstrong, Yuichiro OguraAbstract:Leukocyte dynamics were evaluated in vivo in rat retinal microcirculation following exposure to Lipid Hydroperoxide (LHP) in the vitreous. Leukocytes were observed as fluorescent dots in acridine orange digital fluorography.
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Lipid Hydroperoxide stimulates retinal neovascularization in rabbit retina through expression of tumor necrosis factor alpha vascular endothelial growth factor and platelet derived growth factor
Angiogenesis, 1998Co-Authors: Donald Armstrong, Toshihiko Ueda, Takako Ueda, Ahmad Aljada, Richard W Browne, Shohei Fukuda, Robert N Spengler, Richard C Chou, Mary Hartnett, Peter BuchAbstract:To test the hypothesis that oxidative damage associated with tissue hypoxia plays a role in neovascularization, a Lipid Hydroperoxide (LHP) was injected into the vitreous of rabbits. Single injections of LHP (50–600μg) caused a sustained retinal neovascularization visualized clinically by ophthalmoscopy and confirmed by microscopy. Vasodilators, i.e. histamine and nitric oxide, peaked at 6h and 7 days, respectively. The levels of both tumor necrosis factor-α and interleukin-lα peaked at 12h and dropped to basal levels by 24h. Expression of vascular endothelial growth factor (VEGF) and transforming growth factor-β peaked at 24h and were sustained throughout the following 3 weeks, and platelet-derived growth factor was also elevated throughout the same period. Upregulation of these five angiogenic cytokines, but not basic fibroblast growth factor, occurred prior to the appearance of neovascularization. Leakage of fluorescein at the tips of new vessels was demonstrated by fluorescein angiography. Linoleic Hydroperoxide induced neovascularization, but saturated or unsaturated native C-18 fatty acids had no effect. The cascade of multiple, angiogenic cytokines induced by LHP may interact to promote sustained neovascularization.
Yuichiro Ogura - One of the best experts on this subject based on the ideXlab platform.
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protective effect of polyethylene glycol superoxide dismutase on leukocyte dynamics in rat retinal microcirculation under Lipid Hydroperoxide induced oxidative stress
Experimental Eye Research, 2005Co-Authors: Akihisa Matsubara, Kazushi Tamai, Kazuyuki Tomida, Yoshito Matsuda, Hiroshi Morita, Donald Armstrong, Y Niwa, Yuichiro OguraAbstract:Abstract The levels of Lipid Hydroperoxide (LHPs) in vitreous are elevated in a variety of retinal disorders. Recently, we have shown that increased levels of LHPs in the vitreous enhanced leukocyte-endothelium interaction in the retina, which should contribute to the initial disturbance of the retinal microcirculation. Based upon the previous work, the purpose of the present study was to investigate the effect of polyethylene glycol-superoxide dismutase (PEG-SOD), one of the important enzyme antioxidants, on leukocyte-endothelial interaction in the retinal microcirculation under LHP-induced oxidative stress. Male Brown-Norway rats weighing approximately 250 g were used. LHP(18:2) was made from linoleic acid (LA) with lipoxygenase and 10 μg of LHP dissolved in 5 μl of sodium borate buffer (SBB, 0.02 m ) was slowly injected into the vitreous using a 33-gauge needle. PEG-SOD (5000 units/kg) was given intravenously 5 min before LHP injection. At 2, 4, 6, 12, 24 and 48 hr after the vitreous injections, we evaluated the number of rolling leukocytes along the major retinal veins and the number of leukocytes that accumulated in the retinal microvasculature with acridine orange digital fluorography. In LHP-treated rats, leukocyte rolling along the major retinal veins was maximal at 6 hr after LHP injection. The number of rolling leukocytes in the PEG-SOD-treated rats was decreased to 5.5% of those in the LHP-treated rats at 6 hr after LHP injection ( P P P
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Lipid Hydroperoxide stimulates subretinal choroidal neovascularization in the rabbit
Experimental Eye Research, 2002Co-Authors: Kazushi Tamai, Yuichiro Ogura, Richard F Spaide, Ann E Ellis, Shigehiro Iwabuchi, Donald ArmstrongAbstract:Abstract The authors sought to evaluate the effect of linoleic acid Hydroperoxide (18:2/LHP) in promoting choroidal neovascularization (CNV). Albino male rabbits received a subretinal injection of various amounts of LHP (ranging from 5 to 200 μ g) dissolved in 50 μ l of sodium borate buffer. Control eyes received the buffer only. Eyes were examined up to 4 weeks later with indirect ophthalmoscopy, fundus photography and fluorescein angiography. Animals were killed on days 3, 7, 14 or 28, and eyes examined by light and transmission electron microscopy. In eyes injected with LHP of 150–200 μ g, exposed areas turned white as observed ophthalmoscopically and showed both severe retinal and choroidal atrophy histologically. Neither fluorescein leakage nor CNV was found in these eyes or in controls. In 33 eyes injected with LHP of 100 μ g or less, prominent fluorescein leakage was seen in three (9%) and less prominent focal leakage in five (15%). In 11 (46%) of the 24 eyes injected with 12.5–50 μ g LHP, CNV was found histologically. Subretinal injection of LHP is capable of inducing CNV.
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Lipid Hydroperoxide stimulates leukocyte-endothelium interaction in the retinal microcirculation.
Experimental eye research, 2002Co-Authors: Kazushi Tamai, Akihisa Matsubara, Kazuyuki Tomida, Yoshito Matsuda, Hiroshi Morita, Donald Armstrong, Yuichiro OguraAbstract:Leukocyte dynamics were evaluated in vivo in rat retinal microcirculation following exposure to Lipid Hydroperoxide (LHP) in the vitreous. Leukocytes were observed as fluorescent dots in acridine orange digital fluorography.
Kazushi Tamai - One of the best experts on this subject based on the ideXlab platform.
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protective effect of polyethylene glycol superoxide dismutase on leukocyte dynamics in rat retinal microcirculation under Lipid Hydroperoxide induced oxidative stress
Experimental Eye Research, 2005Co-Authors: Akihisa Matsubara, Kazushi Tamai, Kazuyuki Tomida, Yoshito Matsuda, Hiroshi Morita, Donald Armstrong, Y Niwa, Yuichiro OguraAbstract:Abstract The levels of Lipid Hydroperoxide (LHPs) in vitreous are elevated in a variety of retinal disorders. Recently, we have shown that increased levels of LHPs in the vitreous enhanced leukocyte-endothelium interaction in the retina, which should contribute to the initial disturbance of the retinal microcirculation. Based upon the previous work, the purpose of the present study was to investigate the effect of polyethylene glycol-superoxide dismutase (PEG-SOD), one of the important enzyme antioxidants, on leukocyte-endothelial interaction in the retinal microcirculation under LHP-induced oxidative stress. Male Brown-Norway rats weighing approximately 250 g were used. LHP(18:2) was made from linoleic acid (LA) with lipoxygenase and 10 μg of LHP dissolved in 5 μl of sodium borate buffer (SBB, 0.02 m ) was slowly injected into the vitreous using a 33-gauge needle. PEG-SOD (5000 units/kg) was given intravenously 5 min before LHP injection. At 2, 4, 6, 12, 24 and 48 hr after the vitreous injections, we evaluated the number of rolling leukocytes along the major retinal veins and the number of leukocytes that accumulated in the retinal microvasculature with acridine orange digital fluorography. In LHP-treated rats, leukocyte rolling along the major retinal veins was maximal at 6 hr after LHP injection. The number of rolling leukocytes in the PEG-SOD-treated rats was decreased to 5.5% of those in the LHP-treated rats at 6 hr after LHP injection ( P P P
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Lipid Hydroperoxide stimulates subretinal choroidal neovascularization in the rabbit
Experimental Eye Research, 2002Co-Authors: Kazushi Tamai, Yuichiro Ogura, Richard F Spaide, Ann E Ellis, Shigehiro Iwabuchi, Donald ArmstrongAbstract:Abstract The authors sought to evaluate the effect of linoleic acid Hydroperoxide (18:2/LHP) in promoting choroidal neovascularization (CNV). Albino male rabbits received a subretinal injection of various amounts of LHP (ranging from 5 to 200 μ g) dissolved in 50 μ l of sodium borate buffer. Control eyes received the buffer only. Eyes were examined up to 4 weeks later with indirect ophthalmoscopy, fundus photography and fluorescein angiography. Animals were killed on days 3, 7, 14 or 28, and eyes examined by light and transmission electron microscopy. In eyes injected with LHP of 150–200 μ g, exposed areas turned white as observed ophthalmoscopically and showed both severe retinal and choroidal atrophy histologically. Neither fluorescein leakage nor CNV was found in these eyes or in controls. In 33 eyes injected with LHP of 100 μ g or less, prominent fluorescein leakage was seen in three (9%) and less prominent focal leakage in five (15%). In 11 (46%) of the 24 eyes injected with 12.5–50 μ g LHP, CNV was found histologically. Subretinal injection of LHP is capable of inducing CNV.
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Lipid Hydroperoxide stimulates leukocyte-endothelium interaction in the retinal microcirculation.
Experimental eye research, 2002Co-Authors: Kazushi Tamai, Akihisa Matsubara, Kazuyuki Tomida, Yoshito Matsuda, Hiroshi Morita, Donald Armstrong, Yuichiro OguraAbstract:Leukocyte dynamics were evaluated in vivo in rat retinal microcirculation following exposure to Lipid Hydroperoxide (LHP) in the vitreous. Leukocytes were observed as fluorescent dots in acridine orange digital fluorography.
Kazuo Sasaki - One of the best experts on this subject based on the ideXlab platform.
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Brain Lipid Hydroperoxide level increases in senescence-accelerated mice at an early age.
Neuroscience letters, 2003Co-Authors: Fumihiko Yasui, Seiichi Matsugo, Masaru Ishibashi, Yutaka Oomura, Shosuke Kojo, Kazuo SasakiAbstract:We previously reported that the levels of Lipid Hydroperoxides, one of oxidative stress markers, in the brain and peripheral organs such as liver, heart, and lung are significantly higher in senescence accelerated-prone 8 mice (SAMP8) than in their controls, senescence accelerated-resistant mice (SAMR1), at 3, 6, and/or 9 months of age. To ascertain the exact age at which the Lipid Hydroperoxide levels increase in SAMP8, we measured them in the brain and liver of SAMP8 and SAMR1 at both 1 and 2 months of age. At 1 month of age, there was no significant inter-strain difference in the levels in brain or liver. However, in SAMP8 both levels were significantly greater at 2 months of age than at 1 month of age, but no such difference was detected for SAMR1. The present results suggest that SAMP8 are exposed to elevated levels of oxidative stress from an early age (2 months old), and that this may be a cause of the senescence-related impairments and degeneration in the brain and peripheral tissues (such as liver, heart, and lung) seen in this strain.
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effects of chronic acetyl l carnitine treatment on brain Lipid Hydroperoxide level and passive avoidance learning in senescence accelerated mice
Neuroscience Letters, 2002Co-Authors: Fumihiko Yasui, Seiichi Matsugo, Masaru Ishibashi, Takahiro Kajita, Yoshiharu Ezashi, Yutaka Oomura, Shosuke Kojo, Kazuo SasakiAbstract:In the present study, we examined the effects of acetyl-L-carnitine (ALC) on the brain Lipid Hydroperoxide level and on passive avoidance performance in senescence-acceleration-prone 8 mice (SAMP8). Mice were treated intraperitoneally with either saline or ALC (100 or 400 mg/kg) three times a week up to 4 months of age (starting at 3 weeks of age). In 4-month-old SAMP8, the deficit in learning and memory seen in saline-treated controls was significantly ameliorated in 400 mg/kg ALC-treated SAMP8, and the brain Lipid Hydroperoxide level was significantly lower in the 400 mg/kg ALC-treated group than in the saline-treated controls. Administration of 100 mg/kg ALC to SAMP8 did not have significant effect on learning and memory performance or on the brain Lipid Hydroperoxide level (by comparison with the saline-treated controls). These results suggest that ALC has antioxidant activity towards oxidative stress, and that the improvement in cognitive ability seen with ALC may occur through an amelioration of cellular dysfunction via an inhibition of the increase in Lipid hydroperoxidation observed in the brain tissue of untreated SAMP8.