Oxygen-related Damage Research Articles

High-temperature high cycle fatigue performance of laser powder bed fusion fabricated Hastelloy X: Study into the microstructure and oxidation effects

High-temperature fatigue properties are critical for laser powder bed fusion (LPBF) fabricated Nickel-based superalloy Hastelloy-X (HX) used in aero engines. In this study, superior high-temperature high-cycle fatigue properties of LPBF HX were achieved. The detailed investigations show that the grain boundary oxidation promoted by the different deformation modes between neighboring grains, despite the reduced oxygen-related damage in the coarser LPBF HX microstructures, are the potential causes for the inter-granular fatigue crack initiation and the subsequent crack coalescence. In the meantime, the crack propagation could be hindered by the refined carbides and annealing twins with Σ3 misorientation (60°/〈111〉) in LPBF HX. Furthermore, the recrystallized grains formed ahead of the crack tip due to the severe deformation within the plastic zone and high testing temperature have different crystallographic orientations, which leads to the crack propagation path changes and increases the fatigue crack propagation resistance.

Cuminaldehyde induces oxidative stress-mediated physical damage and death of Haemonchus contortus

Cuminaldehyde (CA), a monoterpenoid, preset in many plant sources including cumin, induces reactive oxygen-related damage and death in Haemonchus contortus, a parasitic worm with an LD50, values of 127.3 ± 7.5, 184.5 ± 12.1 and 104.1 ± 7.9 μg/mL for an adult female, adult male worms (12 h) and L3 larvae, respectively (24 h). Fifty percent of inhibition of egg hatching (IC50) was obtained at 142.4 ± 11.4 μg/mL after 48 h of exposure. Scanning electron microscopy revealed physical damage to the anterior and posterior ends, intestinal, ovarian, and esophageal regions of the warms on exposure to ca. The exposure of worms to CA also led to a systemic increase in reactive oxygen species (ROS) within 3 h. The better activity was seen with CA compared to standard antihelminthic drug albendazole (Alb). 74 μg/mL CA showed 2.3 fold more increase of catalase (CAT), 0.61 fold increase of superoxide dismutase (SOD), 3.3 fold increase of glutathione peroxidase (GPx) activity and 17.5 fold increase of glutathione (GSH) activity in comparison with Alb (500 μg/mL) for the same time of exposure (3 h). A firm increase of (2.9 fold) was also observed in nitric oxide synthase (NOS) activity within 12 h of exposure with CA (74 μg/mL) in comparison with Alb. Therefore the preclinical potential of CA is much higher than widely used antihelminthic drug Alb. The results open new opportunities to explore CA as a new active antihelminthic molecule.

Role of oxygen in enhanced fatigue cracking in a PM Ni-based superalloy: Stress assisted grain boundary oxidation or dynamic embrittlment?

The role of oxygen in enhanced fatigue cracking in an advanced Ni-based superalloy for turbine disc application has been evaluated in fatigue crack initiation and propagation stages along with static oxidation tests. It is found that the grain boundary oxide intrusion has a layered structure. The microstructure- and deformation-dependent grain boundary oxidation dominates the fatigue crack initiation and early propagation processes. As the crack propagates, this contribution arising from oxidation damage may gradually be overtaken by dynamic embrittlement processes until the mechanical damage outstrips the oxygen-related damage, resulting in a transition from intergranular to transgranular crack propagation.

Effects of oxygen-related damage on dwell-fatigue crack propagation in a P/M Ni-based superalloy: From 2D to 3D assessment

Effects of oxygen-related damage (i.e. oxidation and dynamic embrittlement) on fatigue crack propagation behavior in an advanced disc alloy have been assessed in air and vacuum under dwell-fatigue conditions at 725°C. The enhanced fatigue crack propagation is closely related to oxygen-related damage at/ahead of the crack tip, which is determined by the testing environment, the dwell period and the crack propagation rate itself based on two dimensional (2D) observation of the crack tip in an optical microscope and scanning electron microscope. X-ray computed tomography has also been employed to examine the differences between three dimension (3D) crack morphology in air and vacuum conditions, and the crack features have been quantified in terms of crack opening displacements, secondary cracks and uncracked bridging ligaments. The results show that the fatigue crack propagation rate is related to the amount of secondary cracks, and the crack length increment in a loading cycle is related to the breaking/cracking of the uncracked bridging ligaments within the discontinuous cracking zone ahead of the crack tip as oxygen-related damage preferentially occurs in these highly deformed regions. By combination of 3D X-ray computed tomography and traditional 2D observation, a deeper understanding is provided of the mechanisms of oxygen-enhanced fatigue crack propagation behavior.

Nitric-oxide-induced reoxygenation injury in the cyanotic immature heart is prevented by controlling oxygen content during initial reoxygenation.

Reintroduction of high levels of molecular oxygen after a hypoxic period is followed by a burst of nitric oxide (NO), peroxynitrite, and oxygen free radicals (OFR), which are highly cytotoxic. This study indicates that hyperoxic reoxygenation of cyanotic immature hearts on cardiopulmonary bypass (CPB) induces a reoxygenation injury and that, by reducing NO and OFR production during institution of CPB with subsequent reoxygenation under blood cardioplegic arrest, this oxygen-related damage can be avoided and biochemical and functional status improved. Of 25 immature piglets (3-5 kg, two to three weeks old), 6 underwent one hour of CPB including thirty minutes of aortic clamping with substrate-enriched modified blood cardioplegia (hypocalcemic, alkalotic, and hyperosmolar; warm induction-cold replenishment-warm reperfusion) without preceding hypoxia (controls). Nineteen others were made hypoxic (arterial [Po2] 20-30 mmHg) for up to two hours by lowering the fraction of inspired oxygen (FIO2) on ventilator. These hypoxic piglets were then reoxygenated on CPB at different Po2 levels (hyperoxic, normoxic, or hypoxic) for five minutes, followed by the aforementioned blood cardioplegic (BCP) arrest regimen. Myocardial conjugated diene (CD) production as a marker of lipid peroxidation, and NO production, determined as its spontaneous oxidation products, nitrite (NO2-) and nitrate (NO3-), were assessed during blood cardioplegic induction, and antioxidant reserve capacity was determined by incubating myocardium in the oxidant t-butylhydroperoxide (t-BHP). Myocardial function was evaluated from end-systolic elastance (Ees, conductance catheter). Blood cardioplegic arrest caused no functional or biochemical changes in normoxic control immature piglets. In contrast, brief reoxygenation at PO2 > 400 mmHg, followed by BCP-arrest (hyperoxic) resulted in marked CD production (42 +/- 4 vs 3 +/- 1 A233 nm/minute/100 g; P < 0.05), and NO production (4500 +/- 500 vs 450 +/- 32 mmol/minute/100 g; P < 0.05) during blood cardioplegic induction, reduced antioxidant reserve capacity (malondialdehyde [MDA] at 4.0 mM of t-BHP: 1342 +/- 59 vs 958 +/- 50 nM/g protein; P < 0.05), and caused profound myocardial dysfunction; Ees recovered only 21 +/- 2% (vs 104 +/- 7; P < 0.05), despite the blood cardioplegic regimen shown to be cardioprotective in control normoxic piglets. Conversely, controlling initial PO2 to normoxic (100 mmHg) or hypoxic (20-30 mmHg) levels reduced lipid peroxidation (CD production 16 +/- 2, 2 +/- 1 A233nm/minute/100 g) and NO production (1264 +/- 736, 270 +/- 182 mmol/minute/100 g), restored antioxidant reserve capacity (MDA at 4.0 mM of t-BHP: 940 +/- 95, 982 +/- 88 nM/g protein), and allowed significant functional recovery (58 +/- 11% and 83 +/- 8%), in a PO2-dependent fashion. The authors conclude that reoxygenation of hypoxemic immature hearts by initiating hyperoxic CPB causes oxidant-related damage characterized by lipid peroxidation, enhanced NO production, and reduced antioxidants, leading to functional depression that nullifies the cardioprotective effects of blood cardioplegia. These detrimental effects can be reduced in a PO2-dependent fashion by controlling initial PO2 on CPB and subsequent reoxygenation during blood cardioplegic arrest.

Protective action of epidermal growth factor and a fraction from Triticum vulgare extract in mouse tail necrosis.

Several peptide growth factors, including EGF, are known to protect endothelium from oxygen-related damage or ischemia-reperfusion, in vitro experiments show that such protective effect involves endogenous endothelium-related factors like nitric oxide and prostanoids. However, in vivo demonstrations of a possible role in related vascular diseases are lacking. In our experiments, human EGF and fraction C, a 3-10 kDa oligosaccharidic fraction from an aqueous extract of Triticum vulgare, known as growth promoters for several cell types including endothelial cells, were found protective against ischemic necrosis of the mouse tail induced by i.v. k-carrageenin plus endothelin-1. After i.p. injection, peak activities were observed at 10 micrograms/kg EGF and 2 mg/kg fraction C. Pretreatment with L-NAME reduced protection in a dose-dependent manner. Addition of indomethacin increased the effect of L-NAME, suggesting that both nitric oxide and eicosanoids are involved in the protective effect of EGF and fraction C.

953-35 Reduction of Nitric Oxide Induced Reoxygenation Injury in the Cyanotic Immature Heart by Controlling Oxygen Content

Abrupt reoxygenation of cyanotic infants on cardiopulmonary bypass (CPB) is followed by a burst of nitric oxide (NO). and oxygen free radicals, leading to impaired myocardial contractility. This oxygen related damage may be reduced by controlling pO 2 during initial reoxygenation. Twenty-five piglets (2–3 weeks) were made hypoxic on Ventilator for 2 hours. Six were not made hypoxic (Control) . Simulating clinical routine, 9 hypoxic piglets were placed on hyperoxic (pO 2 400 mmHg) CPS (Hyperoxic) . Five others were put on normoxic (pO 2 100 mmHg) (Normoxic) , and 5 underwent hypoxic CPS at ambient pO 2 (25 mmHg). delaying reoxygenation until blood cardioplegic (BCP) arrest (Hypoxic). During 30 a min period of SCP-arrest Nitric oxide (pmol/100 g/min) and conjugated diene production (A 233 nm/100 g/min) were measured. Post CPB measurements included % recovery of end-systolic elastance (impedance catheter), and tissue antioxidant reserve capacity (MDA production after exposure to t-BOOH). Ensystolic elastance Anti oxidant reserve capacity Conjugated Diene production Nitric Oxide production Control 102 ± 7 943 ± 88 3.2 ± 1 270 ± 182 Hyperoxic 21 ± 2 # 1342 ± 89 # 420 ± 4.4 # 4767 ± 2455 # Normoxic 56 ± 11 * 939 ± 74 * 15.5 ± 3.1 * 1264 ± 736 * Hypoxic 83 ± 8 * 982 ± 88 * 1.8 ± l.4 * , † 309 ± 88 * , † # P &lt; 0.05 vs. Control. * p &lt; 0.05 vs. Hyperoxic, † = P&lt; 0.05 vs. Normoxic These data document a NO and oxygen free radical related injuryin the hypoxic immature heart after hyperoxic reoxygenation on CPS Inormal clinical routine). Controlling pO 2 during the initial reoxygenation period resulted in dose dependent less NO production, and in improved biochemical and functional status. Clinical application of “controlled reoxygenation” could improve myocardial protection in cyanotic immature hearts on CPB and improve clinical outcome.

The role of free radical-mediated processes in oxygen-related damage in cultured murine myocardial cells.

A new approach to quantifying myocyte cell death utilizing fluorescence-activated sorting of antimyosin antibody-labeled cells was used to study the effects of oxygen-generated free radicals on cell survival. Uptake of antimyosin, reflecting sarcolemmal damage, increased under conditions which promoted elevated free radical formation and decreased in the presence of increased levels of free radical-scavenging agents. Superoxide dismutase decreased antimyosin uptake at pH 6.7 and 7.5. Mannitol decreased antimyosin uptake at pH 6.5 and 6.7 but not at pH 7.5, and dimethyl sulfoxide decreased antimyosin uptake at pH 6.4 but not at pH 7.5. These data suggest that a greater portion of hydroxyl radicals are produced at higher concentrations of hydrogen ion. Mannitol, a scavenger of hydroxyl radicals, was effective in reducing antimyosin uptake at pH 7.5 in the presence of ferrous sulfate, but had no effect on antimyosin uptake in the absence of ferrous sulfate, suggesting possible iron-mediated catalysis of hydroxyl radical formation. The data suggest that oxygen-derived free radicals can cause significant loss of membrane integrity in cultured myocytes, that the species of radical formed is dependent both on pH and the concentration of iron salts, and that this injury is, at least in part, preventable by the administration of exogenous radical scavenging agents.