Butylated hydroxyanisole is more than a reactive oxygen species scavenger

The chemotactic peptide N-formyl-methionyl-leucyl-phenylalanine (FMLP) has been shown to constrict both bronchial and coronary vascular smooth muscle through the action of cyclooxygenase or lipoxygenase products. We observed that intravenous FMLP increased pulmonary vascular resistance (PVR) in isolated buffer-perfused rabbit lungs. FMLP increased the PVR (primarily in the middle segment of the pulmonary vascular bed) at concentrations greater than or equal to 10(-7) M. Maximum vasoconstriction occurred at 5 min and then slowly declined to a level that remained above baseline at 30 min. Tachyphylaxis was observed in response to FMLP. When polymorphonuclear leukocytes (PMNs) were added to the perfusate, FMLP caused a greater increase in PVR. PMN depletion with dimethylmyleran significantly reduced the PVR response to FMLP. Pretreatment with two dissimilar cyclooxygenase inhibitors, meclofenamate and ibuprofen, and the leukotriene synthesis blocker MK 886 had no effect on the FMLP-induced vasoconstriction. However, the reactive oxygen species scavenger catalase significantly reduced the vasoconstriction. These results suggest that FMLP induces vasoconstriction that is dependent on PMNs and mediated by reactive oxygen species with no involvement of cyclooxygenase or lipoxygenase products.

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Protection against reactive oxygen species by NAD(P)H:quinone reductase induced by the dietary antioxidant butylated hydroxyanisole (BHA)

FEBS Letters ◽

10.1016/0014-5793(84)80290-2 ◽

1984 ◽

Vol 169 (1) ◽

pp. 63-66 ◽

Cited By ~ 33

Author(s):

Heribert Wefers ◽

Toru Komai ◽

Paul Talalay ◽

Helmut Sies

Keyword(s):

Reactive Oxygen Species ◽

Reactive Oxygen ◽

Butylated Hydroxyanisole ◽

Oxygen Species ◽

Dietary Antioxidant

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Production of reactive oxygen species due to metabolic activation of butylated hydroxyanisole

Toxicology ◽

10.1016/0300-483x(89)90056-5 ◽

1989 ◽

Vol 59 (2) ◽

pp. 179-194 ◽

Cited By ~ 43

Author(s):

Regine Kahl ◽

Sabine Weinke ◽

Hermann Kappus

Keyword(s):

Reactive Oxygen Species ◽

Reactive Oxygen ◽

Metabolic Activation ◽

Butylated Hydroxyanisole ◽

Oxygen Species

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The pH Hypothesis of Postconditioning

Circulation ◽

10.1161/circulationaha.106.675710 ◽

2007 ◽

Vol 115 (14) ◽

pp. 1895-1903 ◽

Cited By ~ 212

Author(s):

Michael V. Cohen ◽

Xi-Ming Yang ◽

James M. Downey

Keyword(s):

Reactive Oxygen Species ◽

Mitochondrial Permeability Transition ◽

Reactive Oxygen ◽

Permeability Transition Pore ◽

Permeability Transition ◽

Oxygen Species ◽

Risk Zone ◽

Kinase C ◽

Protective Signaling ◽

Reactive Oxygen Species Scavenger

Background— It is unclear how reperfusion of infarcting hearts with alternating cycles of coronary reperfusion/occlusion attenuates infarction, but prevention of mitochondrial permeability transition pore (MPTP) formation is crucial. Acidosis also suppresses MPTP formation. We tested whether postconditioning protects by maintaining acidosis during early reoxygenation. Methods and Results— After 30-minute regional ischemia in isolated rabbit hearts, reperfusion with buffer (pH 7.4) caused 34.4±2.2% of the risk zone to infarct, whereas 2 minutes of postconditioning (6 cycles of 10-second reperfusion/10-second occlusion) at reperfusion resulted in 10.7±2.9% infarction. One minute (3 cycles) of postconditioning was not protective. Hypercapnic buffer (pH 6.9) for the first 2 minutes of reperfusion in lieu of postconditioning caused equivalent cardioprotection (15.0±2.6% infarction), whereas 1 minute of acidosis did not protect. Delaying postconditioning (6 cycles) or 2 minutes of acidosis for 1 minute aborted protection. Reperfusion with buffer (pH 7.7) blocked postconditioning protection, but addition of the MPTP closer cyclosporin A restored protection. Reactive oxygen species scavenger N-2-mercaptopropionyl glycine, protein kinase C antagonist chelerythrine, and mitochondrial K ATP channel closer 5-hydroxydecanoate each blocked protection from 2 minutes of acidosis as they did for postconditioning. Conclusion— Thus, postconditioning prevents MPTP formation by maintaining acidosis during the first minutes of reperfusion as reoxygenated myocardium produces reactive oxygen species that activate protective signaling to inhibit MPTP formation after pH normalization.

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