Disease relevance of BONGKREKIC ACID

• In purified mitochondria, two ligands of ANT, bongkrekic acid and the protein vMIA from cytomegalovirus, failed to prevent MMP induced by BaxBH3 or Bcl2BH3 [1].
• An isomer of bongkrekic acid, designated as isobongkrekic acid, has been isolated from ethereal extracts of Pseudomonas cocovenenans grown on defatted coconut [2].
• Bongkrekic acid causes fatal food poisoning which is associated with hyperglycaemia [3].
• Betanodavirus induces phosphatidylserine exposure and loss of mitochondrial membrane potential in secondary necrotic cells, both of which are blocked by bongkrekic acid [4].
• The objective of this study was to determine whether bongkrekic acid (BKA) ameliorates ischemic neuronal damage by inhibiting the release of cyt-c. These results showed that a 10min period of global ischemia caused neuronal death, increased the release of cyt-c and activated astrocytes in the cortex and CA1 [5].

High impact information on BONGKREKIC ACID

• We tested the effect of a specific inhibitor of PT, bongkrekic acid (BA), a ligand of the mitochondrial adenine nucleotide translocator, on a prototypic model of apoptosis glucocorticoid-induced thymocyte death [6].
• Inhibition of the mitochondrial ANT with bongkrekic acid (BA) prevented NMDA receptor-mediated apoptosis of cerebrocortical neurons [7].
• Treatment with oligomycin and/or bongkrekic acid indicated that the maintenance of Deltapsi(m) during exposure to NO is caused by reversal of the ATP synthase and other electrogenic pumps [8].
• All of these changes were dependent on Ca2+ and were prevented by cyclosporin A (CsA) and bongkrekic acid, both of which close the PT pores (megachannels), indicating that Bax- and Bak-induced mitochondrial changes were mediated through the opening of these pores [9].
• The PT pore inhibitors cyclosporin A and bongkrekic acid blocked mitochondrial dysregulation and cell death [10].

Chemical compound and disease context of BONGKREKIC ACID

• In contrast, inhibitors of the mitochondrial permeability transition (MPT), cyclosporin A and bongkrekic acid, did not alter [Ca(2+)](m) accumulation during ischemia, but markedly suppressed the surge in rhod-2 fluorescence during reperfusion [11].

Biological context of BONGKREKIC ACID

• An inhibitor of lipid peroxidation, trolox, significantly suppressed NO-mediated apoptosis in APO-S Jurkat cells, whereas bongkrekic acid (BA), which blocks mitochondrial permeability transition, provided only a moderate antiapoptotic effect [12].
• Bongkrekic acid prevents all PPIX-induced phenomena, including superoxide anion generation, chromatinolysis, and oligonucleosomal DNA fragmentation [13].
• Inhibition of this mitochondrial transmembrane potential loss by Bcl-2 or by specific inhibitors acting on the mitochondrial permeability transition pore (bongkrekic acid, cyclosporin A) prevents K+ leakage [14].
• Bongkrekic acid completely inhibited any appearance of cell death, whereas inhibitors of autophagy, caspases-9 or -3, prevented only TUNEL-positive cell death [15].
• Bongkrekic acid, a specific adenine nucleotide translocator (ANT) inhibitor, also reduced rho degrees cell growth and mitochondrial membrane potential [16].

Anatomical context of BONGKREKIC ACID

• Specific antioxidants, as well as two inhibitors of mitochondria permeability transition, bongkrekic acid and cyclosporin A, significantly blocked the DNA degradation induced in Jurkat T cells by SCCHN cells [17].
• Apoptosis induced by both drugs was inhibited by Bcl-2 or Bcl-X(L) overexpression or by bongkrekic acid, an agent that stabilizes mitochondrial membrane barrier function, suggesting a critical role for mitochondria [18].
• The role of the mitochondrial permeability transition (MPT) in the killing of HeLa cells by staurosporine (STR) was assessed with the use of bongkrekic acid (BK), an inhibitor of the MPT [19].
• This stimulation is completely inhibited by atractyloside and bongkrekic acid, two different specific inhibitors of the mitochondrial adenine nucleotide translocase. cAMP directly mobilizes Mg2+ efflux from isolated rat liver mitochondria [20].
• Reversible inhibition of adenine nucleotide translocation by long chain acyl-CoA esters in bovine heart mitochondria and inverted submitochondrial particles. Comparison with atractylate and bongkrekic acid [21].

Associations of BONGKREKIC ACID with other chemical compounds

• PS-341-induced mitochondrial depolarization was attenuated by Z-VDVAD-FMK, tiron, and an inhibitor of the mitochondrial permeability transition pore (bongkrekic acid) [22].
• Despite these observations, treatment with the mitochondrial stabilizer, bongkrekic acid, or with catalase, known to degrade H(2)O(2), fails to reverse VAA-I-induced apoptosis [23].
• Furthermore, the pre-treatment of tobacco cells with bongkrekic acid, a known inhibitor of the mitochondrial permeability transition pore in animal cells, was found to completely block gene induction when AA, H2O2 or SA were subsequently added [24].
• We found that moderately low doses of tributyltin decrease mitochondrial membrane potential and induce cytochrome c release by a mechanism inhibited by cyclosporine A and bongkrekic acid [25].
• Cyclosporin A, bongkrekic acid, and N-ethylmaleimide completely abolish all the above-described effects, suggesting that Cbx can be considered an inducer of mitochondrial permeability transition by means of oxidative stress [26].

Gene context of BONGKREKIC ACID

• Eosinophil incubation with bongkrekic acid, an inhibitor of the mitochondrial permeability transition pore (MPTP) opening, failed to modify Fas-mediated loss in DeltaPsi(m), caspase activation, and apoptosis [27].
• Bongkrekic acid, an inhibitor of Delta Psi(m) disruption, blocked the cytochrome c release from mitochondria and the following caspase-3-mediated cell death [28].
• Inhibition of the mitochondrial permeability transition by bongkrekic acid impaired TNF-alpha-induced cell death without affecting the activity of NF-kappaB [29].
• Moreover, the apoptosis produced by ANT3 was inhibited by bongkrekic acid and by cyclosporin A [30].
• MMD inhibition by Bongkrekic acid prevents high-glucose-induced loss of UCP3 and apoptosis [31].

Analytical, diagnostic and therapeutic context of BONGKREKIC ACID

• 5. (i) Microinjection of atractyloside or bongkrekic acid caused a substantial fall in the resting Na efflux [32].
• Employing the double silicone oil layer filtering centrifugation method, we examined the kinetic properties of the uptake of various adenylates as well as the inhibitory effects exerted by carboxyatractyloside, atractyloside and bongkrekic acid, known specific inhibitors of the mitochondrial adenylate translocator [33].
• The dRCM with added lipid was inoculated with B. cocovenenans, incubated at 30 degrees C for 5 days and the amount of bongkrekic acid formed quantified by HPLC [34].
• 3H- or 35S-labeled atractyloside and carboxyatractyloside, atractyloside derivatives used for affinity chromatography, photoaffinity labeling, and spin labeling, and 3H- or 14C-labeled bongkrekic acid [35].

References