Assisted oocyte activation Current understanding, practice, and future perspectives
David K. Gardner, Ariel Weissman, Colin M. Howles, Zeev Shoham in Textbook of Assisted Reproductive Techniques, 2017
Ca2+ ionophores are usually lipid-soluble molecules that transport Ca2+ across cell membranes by increas- ing Ca2+ permeability. They can cause extracellular Ca2+ influx and also act on intracellular Ca2+ stores to release stored Ca2+ (82, 83). Such agents have been shown to acti- vate oocytes from all animals examined in studies dating back to the 1970s. Examples of well-used Ca2+ ionophores include ionomycin and A23187 (Figure 14.3). Ionomycin is the most specific Ca2+ ionophore and has value for some experimental studies in that it is non-fluorescent. However, A23187 is the most commonly used ionophore to artificially activate oocytes. These agents both result in a similar and single prolonged Ca2+ rise, and they do not elicit Ca2+ oscillations (40, 83). Figure 14.4 shows an exam- ple of a Ca2+ increase in a mouse oocyte exposed to the Ca2+ ionophore ionomycin (84).
Role of Mitochondrial Injury During Oxidative Injury to Hepatocytes: Evidence of a Mitochondrial Permeability Transition by Laser Scanning Confocal Microscopy
John J. Lemasters, Constance Oliver in Cell Biology of Trauma, 2020
We also investigated the ability of fructose to protect against hepatocellular injury by Br-A23187. Br-A23187 and its parent compound, A23187, are calcium ionophores whose cytotoxicity is sometimes used as a model of Ca2+-dependent cell killing.10 Br-A23187 caused time-dependent killing of isolated hepatocytes, and virtually all cells were nonviable after 2 h of exposure (Figure 4). Fructose alone only slightly improved cell survival, but fructose in combination with oligomycin virtually eliminated cell killing. Cell killing by CCCP showed the same pattern of oligomycin and fructose-dependent protection (Figure 4). These observations indicated that mitochondrial uncoupling and accelerated ATP hydrolysis were causing lethal cell injury from Br-A23187, rather than increases of intracellular Ca2+ per se. This is consistent with observations in isolated mitochondria, where A23187 is well known to be an uncoupler.11
Cerebral Metabolic Impairments
Zaven S. Khachaturian, Teresa S. Radebaugh in Alzheimer’s Disease, 2019
Recent studies indicate that one of the triggers for apoptosis is excess influx of calcium due to overstimulation of NMDA receptors. Impairments of oxidative metabolism lead to impairments of cellular calcium homeostasis,6 and cellular calcium homeostasis is impaired in AD.46,87 Intracellular calcium exists in pharmacologically definable pools, and AD cells have an exaggerated bradykinin-insensitive, A23187-sensitive calcium pool.88 As discussed above, in pathological situations mitochondria act as important “sinks” to take up excess calcium from the cytoplasm, and it is reasonable to propose that impairments of mitochondrial oxidative metabolism might therefore sensitize cells to damage from influx of excess calcium. In vitro experiments with cultured AD cells are consistent with this proposal, but direct demonstration of it in neurons in autopsy brain is difficult.89,90
Host-directed therapies for malaria and tuberculosis: common infection strategies and repurposed drugs
Published in Expert Review of Anti-infective Therapy, 2022
Piyush Baindara, Sonali Agrawal, O. L. Franco
Baicalin is a flavone glycoside and is reported to enhance autophagic flux and Mtb clearance in infected macrophages by inhibiting the PI3K/Akt/mTOR signaling pathway [184]. Calcimycin is a polyether antibiotic from Streptomyces chartreusensis and was recently reported to inhibit intracellular Mtb through autophagy induction via eliciting the upregulation of intracellular calcium levels by binding to P2RX7 receptor [185]. Another autophagy inducer is Ambroxol, which is a mucoactive drug, and interestingly, mucokinetic activity of ambroxol is found to induce the autophagic flux by activation of TFEB nuclear translocation in the murine tuberculosis model [186]. Psychotropic drugs like nortriptyline are also reported to induce the autophagic flux by increasing the rate of phagosome formation in Mtb-infected macrophages [111].
Artificial oocyte activation: physiological, pathophysiological and ethical aspects
Published in Systems Biology in Reproductive Medicine, 2019
George Anifandis, Alexandros Michopoulos, Alexandros Daponte, Katerina Chatzimeletiou, Mara Simopoulou, Christina I. Messini, Nikolas P. Polyzos, Katerina Vassiou, Konstantinos Dafopoulos, Dimitrios G. Goulis
Intra-cytoplasmic sperm injection (ICSI) has established its role as an effective infertility treatment. Nevertheless, multiple ICSI failures can be encountered in infertile couples with low oocyte yield in combination with abnormal semen parameters. One of the factors associated with ICSI failure is oocyte activation deficiency (AOD). The latter is considered a result of sperm-derived molecules, such as phospholipase C-zeta (PLCζ), that is not capable of producing adequate Ca+2 oscillations for oocyte activation. Apart from these natural activators, other stimulants, such as Ca+2 ionophore A23187 (calcimycin), ionomycin and strontium chloride have been applied to overcome AOD and ICSI failure. The present narrative review aims to discuss and critically appraise the literature on the role of Ca+2 oscillations in oocyte activation and summarize the evidence concerning the use of natural and artificial factors, as agents for artificial oocyte activation (AOA) in both animals and humans. Physiological, pathophysiological and ethical aspects of AOA will be discussed as well.
Anti-inflammatory effects of Artemisia scoparia and its active constituent, 3,5-dicaffeoyl-epi-quinic acid against activated mast cells
Published in Immunopharmacology and Immunotoxicology, 2018
Sun-Young Nam, Na-Ra Han, So-Young Rah, Youngwan Seo, Hyung-Min Kim, Hyun-Ja Jeong
Fetal bovine serum (FBS) and Isocove’s modified Dulbecco’s medium (IMDM) were purchased from Gibco BRL (Grand Island, NY). Dimethyl sulfoxide (DMSO) and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), phorbol myristate acetate (PMA), A23187 (calcimycin; C29H37N3O6) and bicinchoninic acid (BCA) were obtained from Sigma Chemical Co (St. Louis, MO). TSLP, TNF-α, IL-1β and IL-6 antibodies were procured from R&D Systems Inc. (Minneapolis, MN). Caspase-1, NF-κB, poly-ADP-ribose polymerase, phosphorylated (p)-c-Jun N-terminal kinases (JNK), JNK, p-p38, p38, p-extracellular signal-regulated kinases (ERK), ERK, p-IκBα and tubulin antibodies were obtained from Santa Cruz Biotechnology (Dallas, TX).
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