Effects of Oxidative Stress in Trabecular Meshwork Cells Are Reduced by Prostaglandin Analogues

Yu, Alice L.; Fuchshofer, Rudolf; Welge–Lüßen, Ulrich

doi:10.1167/iovs.07-0984

Cited by 74 publications

(58 citation statements)

References 49 publications

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“…This observation can be explained not only by the effect of active substances, but also by BAK action. Many other in vitro studies have shown that preservatives are cytotoxic, especially for the cells of the ocular surface: conjunctival and corneal epithelium and keratocytes [7,9,14,[16][17][18][19] but also for the deeper ocular tissues (fibroblast of Tenon's capsule, cells of lens epithelium and trabecular meshwork) [15,20]. Although the cytotoxic effect of BAK is well documented in patients [15] and on cultivated adherent cells, its influence on lymphocytes seems not to have been explored until this study.…”

Section: Discussion Discussion Discussion Discussionmentioning

confidence: 99%

“…Huge differences in these concentrations are probably due to differences in methods of cell treatments by BAK (especially in treatment and recovery time) and sensitivities of assays. Trabecular meshwork cells also seem to be very sensitive to BAK stimulation: in concentrations as low as 0.00015%, it kills about 20% of cells [20].…”

Section: Discussion Discussion Discussion Discussionmentioning

confidence: 99%

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Benzalkonium chloride (BAK) induces apoptosis or necrosis, but has no major influence on the cell cycle of Jurkat cells

Pożarowska¹,

Pożarowski²

2011

Folia Histochem Cytobiol.

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Section: Discussion Discussion Discussion Discussionmentioning

confidence: 99%

Section: Discussion Discussion Discussion Discussionmentioning

confidence: 99%

Benzalkonium chloride (BAK) induces apoptosis or necrosis, but has no major influence on the cell cycle of Jurkat cells

Pożarowska¹,

Pożarowski²

2011

Folia Histochem Cytobiol.

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“…In addition, iodine has proven to significantly decrease malondialdehyde (MDA) in animal models of abdominal aortic I/R (26), induce liver peroxidation (27), and reduce hydrogen peroxide-induced pathological glaucomatous changes in cultured cells (28).…”

Section: Resultsmentioning

confidence: 99%

Effects of Picroside II on Myocardial Ischemia-Reperfusion Injury in Streptozotocin-Induced Diabetic Rats

Polat¹,

Dursun²,

Küçük³

et al. 2017

GMJ

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Objective: Diabates mellitus, is a chronic metabolic disorder accompanied by an increase in oxidative stress. Ischemia-reperfusion injury is a cascade of events initiated by tissue ischemia. The cellular damage produced by reperfusion leads to an active inflammatory response. This study was performed to investigate the effect of picroside II on myocardial ischemiareperfusion injury in rats with streptozotocin-induced diabetes. Methods: Animals were equally (n:6) divided for five groups as follows;, and diabetes+I/R+ picroside II [DIRP]. In DIR group, a left anterior descending artery branch was occluded for 60 minutes, the reperfused for 120 minutes. In DIRP group, picroside II was administrated via 10 mg/kg intraperitoneal route 30 minutes before ligating the left anterior descending artery. At the end of the study, myocardial tissues were taken for total oxidant status and total antioxidant status level determinations. Results: Total oxidant status levels were significantly higher in DIR group, when compared with C, DP, and DIRP groups (p:0.001, p:0.019, and p:0.031, respectively). Total antioxidant status levels were significantly higher in DIR group, when compared with C, DP, and DIRP groups (p:0.006, p:0.024, and p:0.007, respectively). Conclusion: These results indicate that administration of picroside II may have protective effects against I/R injury.

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“…It has been shown to possess a number of biological effects in addition to its well-known vasoactive activity (23). These include cell proliferation, differentiation, and oxidative stress-induced cell death inhibition (24)(25)(26).…”

Section: Discussionmentioning

confidence: 99%

Antioxidative effects of adrenomedullin and vascular endothelial growth factor on lung injury induced by skeletal muscle ischemia-reperfusion

Gl¹,

Kirişçi²,

Dursun³

et al. 2013

BLL

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Abstract:Purpose: The aim of this study was to investigate the effects of adrenomedullin (AM) and vascular endothelial growth factor (VEGF) on lung injury as a remote organ following skeletal muscle ischemia-reperfusion injury in a rat model. Materials and methods: Thirty-six Wistar rats were randomized into six groups (n=6). Laparotomy was performed in all groups under general anesthesia. Nothing else was done in Group S (Sham). Ischemia reperfusion group (Group I/R) underwent ischemia and reperfusion performed by clamping and declamping of the infrarenal abdominal aorta for 120 minutes, respectively. Group VEGF and Group AM received intravenous infusion of VEGF (0.8 μg/kg) or AM (12 μg /kg) respectively, without ischemia and reperfusion. Group IR+VEGF and Group IR+AM received intravenous infusion of VEGF (0.8 μg/kg) or AM (12 μg /kg) respectively immediately after 2 hours period of ischemia. At the end of reperfusion period. Lung tissue samples were taken for biochemical examination. Total oxidant status (TOS) and total antioxidant status (TAS) levels in lung tissue were determined by using a novel automated method. p<0.05 was considered as statistically signifi cant. Results: TOS levels were signifi cantly higher in Group I/R, when compared with groups S, AM and VEGF (p=0.004, p=0.011, p=0.017, respectively) and signifi cantly lower in groups I/R+AM and I/R+VEGF, when compared with Group I/R (p=0.018, p=0.006, respectively). TAS levels were signifi cantly higher in Group I/R, when compared with groups S, AM and VEGF (p=0.006 p=0.016, p=0.016, respectively) and signifi cantly lower in Group I/R+AM, when compared with Group I/R (p=0.016). Conclusion: These fi ndings indicate that AM and VEGF acted effectively on the prevention of lung injury induced by skeletal muscle ischemia-reperfusion injury in a rat model (Fig. 2, Ref. 30). Full Text in PDF www.elis.sk.

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Effects of Oxidative Stress in Trabecular Meshwork Cells Are Reduced by Prostaglandin Analogues

Abstract: Oxidative stress is able to induce characteristic glaucomatous TM changes in vitro, and these oxidative stress-induced TM changes can be minimized by the use of prostaglandin analogues. Thus, prevention of oxidative stress exposure to the TM may help to reduce the progression of POAG.

Cited by 74 publications

References 49 publications

Benzalkonium chloride (BAK) induces apoptosis or necrosis, but has no major influence on the cell cycle of Jurkat cells

Benzalkonium chloride (BAK) induces apoptosis or necrosis, but has no major influence on the cell cycle of Jurkat cells

Effects of Picroside II on Myocardial Ischemia-Reperfusion Injury in Streptozotocin-Induced Diabetic Rats

Antioxidative effects of adrenomedullin and vascular endothelial growth factor on lung injury induced by skeletal muscle ischemia-reperfusion

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