Disease relevance of tert-Butylhydroperoxide

• Furthermore, diminished CBS levels are associated with reduced cell viability in hepatoma cells challenged with tert-butyl hydroperoxide [1].
• We previously showed that tert-butyl hydroperoxide (TBH) induced apoptosis in naïve rat pheochromocytoma (nPC12) cells that correlated with cellular redox imbalance and mitochondrial apoptotic signaling [2].
• Gene expression after treatment with hydrogen peroxide, menadione, or t-butyl hydroperoxide in breast cancer cells [3].
• The induction of cx43 was observed by mean alpha-particle doses as low as 0.16 cGy, and also in cells exposed to gamma-rays, t-butyl hydroperoxide, and hyperthermia [4].
• AT fibroblasts exhibit, in comparison to NHFs, increased sensitivity to the toxicity of t-butyl hydroperoxide, as measured by colony-forming efficiency assays [5].

Psychiatry related information on tert-Butylhydroperoxide

• Intraperitoneal administration of t-butyl hydroperoxide (BPO) to mice decreased spontaneous locomotor activity in a dose-dependent manner, and the effect was competitively antagonized by caffeine, suggesting a similar receptor [6].
• Peroxidation was induced with tert-butylhydroperoxide and FeCl(2) at 35 degrees C. The decrease of SAPC versus DPPC, or N-palmitoyl SM, or N-stearoyl SM, was monitored by matrix-assisted laser desorption ionization time-of-flight mass spectrometry (MALDI-TOF MS) at various reaction times [7].
• DESIGN: The determinations made include the plasma total antioxidant capacity (TRAP) and tert-butyl hydroperoxide-initiated chemiluminescence and catalase activity in erythrocytes from 18 patients with probable Alzheimer's disease and 18 matched control subjects with normal cognitive function [8].

High impact information on tert-Butylhydroperoxide

• Leukocyte rolling and adhesion were investigated while monitoring venular wall shear rates in the mesenteric microcirculation stimulated with histamine or tert-butyl hydroperoxide in the two strains [9].
• The regulation of intestinal metabolism of t-butylhydroperoxide by glucose was examined in isolated enterocytes from proximal rat intestine [10].
• On a molar basis, these compounds generated much more GSSG than a direct substrate for glutathione peroxidase such as t-butyl hydroperoxide, indicating that the compounds undergo redox-cycling with concomitant production of hydrogen peroxide [11].
• RESULTS: Expression of core/cytochrome P450 2E1 synergistically enhanced cell death induced by either tertiary butyl hydroperoxide or tumor necrosis factor alpha [12].
• Furthermore, TBHP, which is known to increase hepatocyte mitochondrial ROS production, also increased UCP-2 messenger RNA levels [13].

Chemical compound and disease context of tert-Butylhydroperoxide

• The presence of 50 microM t-butyl hydroperoxide induces the oxidation of intramitochondrial pyridine nucleotides and release of accumulated Ca2+ from rat liver but not AS-30D hepatoma mitochondria in the presence of succinate (plus rotenone) as a respiratory substrate [14].
• Cumene hydroperoxide but not t-butyl hydroperoxide closely models the toxicity of hydrogen peroxide [15].
• Nitric oxide prevents oxidative damage produced by tert-butyl hydroperoxide in erythroleukemia cells via nitrosylation of heme and non-heme iron. Electron paramagnetic resonance evidence [16].
• To test this possibility we examined the effects of nigericin on the toxicity and metabolism of a model peroxide, tert-butylhydroperoxide (tert-BOOH), in A549 cells, a cell line in which the GSH redox cycle is known to be the principal pathway for reduction and detoxification of tert-BOOH [17].
• Antimycin A at levels that abolish oxygen consumption had a slight, although statistically significant, inhibitory effect on the toxicity elicited by t-butylhydroperoxide in U937 cells [18].

Biological context of tert-Butylhydroperoxide

• The protease inhibitor Cbz-Leu-Leu-Tyr-CHN2 also delayed the onset of mitochondrial depolarization and cell necrosis during treatment of rat hepatocytes with tert-butyl hydroperoxide, a model of oxidative stress relevant to human disease [19].
• Functional heterogeneity of mitochondria in single cells was observed with respect to membrane potential, sequestration of hormonally evoked cytosolic calcium signals and timing of permeability transition pore opening in response to tert-butyl hydroperoxide [20].
• To examine the bioavailability of membrane iron, we admixed membranes and t-butylhydroperoxide and found that sickle membranes show a tenfold greater peroxidation response than do normal membranes [21].
• 2,3-Epoxy-4-hydroxynonanal was produced with tert-butyl hydroperoxide by epoxidation of trans-4-hydroxy-2-nonenal, a lipid peroxidation product [22].
• The linkage between oxidant-mediated apoptosis and the induction of cellular redox was examined in PC-12 cells using the oxidant, tert-butylhydroperoxide (TBH) [23].

Anatomical context of tert-Butylhydroperoxide

• RESULTS: tert-Butyl hydroperoxide induced a sustained increase in intracellular calciu, bleb formation, and, ultimately, hepatocyte death [24].
• Glutathione oxidants such as tertiary butyl hydroperoxide were shown previously to prevent microtubule assembly and cause breakdown of preassembled cytoplasmic microtubules in human polymorphonuclear leukocytes [25].
• Subtle peroxidative perturbation of normal red blood cells (RBC) using t-butylhydroperoxide creates a leak pathway for monovalent cations that is reversibly activated by cell deformation [26].
• To model the specific hypothesis that oxidatively perturbed RBC membranes would be abnormally susceptible to this potentially adverse effect of deformation, we treated normal RBC with the lipid peroxidant t-butylhydroperoxide [27].
• Increased susceptibility of the sickle cell membrane Ca2+ + Mg(2+)-ATPase to t-butylhydroperoxide: protective effects of ascorbate and desferal [28].

Associations of tert-Butylhydroperoxide with other chemical compounds

• When PGE1 or 16,16'-dimethyl PGE2 was added to the medium of primary cultured rat hepatocytes, lipid peroxidation-dependent killing of the cells by tert-butyl hydroperoxide was significantly attenuated without affecting the extent of malondialdehyde accumulation compared with controls [29].
• When NADPH oxidation was prevented by selective inactivation of glutathione reductase, t-butyl hydroperoxide metabolism was without effect on the mitochondrial Ca2+ pool, whereas the loss from the extramitochondrial pool was accelerated [30].
• We used real-time quantitative PCR to analyze mtDNA integrity, damage repair, and induced mutations after exposure of human adult retinal pigment epithelial (ARPE)-19 cells to 4-nitroquinoline 1-oxide, a UV-mimetic and adduct-forming carcinogen, and tert-butyl hydroperoxide, an oxidant [31].
• Normal and sickle cell erythrocyte membranes were examined for significant differences in their ATPase activities, thiobarbituric acid reactive products formed (measured relative to malondialdehyde), membrane protein polymerization, and number of protein-free sulfhydryl groups when treated with 0.5 mmol/L t-butylhydroperoxide (tBHP) for 30 minutes [28].
• Catalase, thiourea, and conjugated linoleic acid decreased the rate of NNK oxidation by 47, 20, and 45%, respectively. tert-Butyl-hydroperoxide, cumene hydroperoxide, and hydrogen peroxide increased the rate of formation of keto aldehyde and keto alcohol by 210, 40, and 50%, respectively [32].

Gene context of tert-Butylhydroperoxide

• Although the redox state of Gpx2 was not affected by Ca2+, the Gpx2 level was markedly increased in the presence of both tert-butyl hydroperoxide and Ca2+ [33].
• To isolate new antioxidant genes, we have searched for activities that would rescue the tert-butyl hydroperoxide (t-BOOH)-hypersensitive phenotype of a Saccharomyces cerevisiae strain deleted for the gene encoding the oxidative stress response regulator Skn7 [34].
• SDS-polyacrylamide gel electrophoresis shows that glyceraldehyde-3-phosphate dehydrogenase (GAPDH) is the major target for modification following treatment with hydroperoxides (hydrogen peroxide or tert-butylhydroperoxide), whereas this enzyme is unaffected following cellular exposure to the thiol oxidant diamide [35].
• Incubation of 0.05 microM TR with 0.25 microM GSH-Px, in a system free from GSH, resulted in reduction of t-butyl hydroperoxide [36].
• In contrast to a strain deleted for GSH1, which lacks both GSH and gamma-Glu-Cys, the strain deleted for GSH2 was found to be unaffected in mitochondrial function as well as resistance to oxidative stress induced by hydrogen peroxide, tert-butyl hydroperoxide, and the superoxide anion [37].

Analytical, diagnostic and therapeutic context of tert-Butylhydroperoxide

• Furthermore, Bcl-2 enhanced H+ efflux but not K+ flux after treatment of mitochondria with Ca2+ or tert-butyl hydroperoxide [38].
• Perfusion with t-butyl hydroperoxide led to an increase in GSSG release associated with an elevated level of intracellular GSSG [39].
• When 4-hydroxy-2,2,6,6-tetramethylpiperidinoxy radical was administered to cell cultures in combination with t-butyl hydroperoxide, it increased prostaglandin synthesis while inhibiting arachidonate release by the hydroperoxide [40].
• EPR spin-trapping evidence for the direct, one-electron reduction of tert-butylhydroperoxide to the tert-butoxyl radical by copper(II): paradigm for a previously overlooked reaction in the initiation of lipid peroxidation [41].
• Northern blotting results indicated a correlation between concentrations of tert-butyl hydroperoxide used in the treatment and the induction of ohr (an OhrR-regulated gene) expression [42].

References