scholarly journals The effect of carbon monoxide on meiotic maturation of porcine oocytes

PeerJ ◽  
2021 ◽  
Vol 9 ◽  
pp. e10636
Author(s):  
David Němeček ◽  
Eva Chmelikova ◽  
Jaroslav Petr ◽  
Tomas Kott ◽  
Markéta Sedmíková
Keyword(s):  
Oxidative Stress ◽  
Carbon Monoxide ◽  
Heme Oxygenase ◽  
Protein Localization ◽  
Somatic Cells ◽  
Antioxidant Properties ◽  
Protoporphyrin Ix ◽  
Antioxidant Effect ◽  
Meiotic Maturation

Oxidative stress impairs the correct course of meiotic maturation, and it is known that the oocytes are exposed to increased oxidative stress during meiotic maturation in in vitro conditions. Thus, reduction of oxidative stress can lead to improved quality of cultured oocytes. The gasotransmitter carbon monoxide (CO) has a cytoprotective effect in somatic cells. The CO is produced in cells by the enzyme heme oxygenase (HO) and the heme oxygenase/carbon monoxide (HO/CO) pathway has been shown to have an antioxidant effect in somatic cells. It has not yet been investigated whether the CO has an antioxidant effect in oocytes as well. We assessed the level of expression of HO mRNA, using reverse transcription polymerase chain reaction. The HO protein localization was evaluated by the immunocytochemical method. The influence of CO or HO inhibition on meiotic maturation was evaluated in oocytes cultured in a culture medium containing CO donor (CORM-2 or CORM-A1) or HO inhibitor Zn-protoporphyrin IX (Zn-PP IX). Detection of reactive oxygen species (ROS) was performed using the oxidant-sensing probe 2′,7′-dichlorodihydrofluorescein diacetate. We demonstrated the expression of mRNA and proteins of both HO isoforms in porcine oocytes during meiotic maturation. The inhibition of HO enzymes by Zn-PP IX did not affect meiotic maturation. CO delivered by CORM-2 or CORM-A1 donors led to a reduction in the level of ROS in the oocytes during meiotic maturation. However, exogenously delivered CO also inhibited meiotic maturation, especially at higher concentrations. In summary, the CO signaling molecule has antioxidant properties in porcine oocytes and may also be involved in the regulation of meiotic maturation.

scholarly journals Antioxidant Roles of Heme Oxygenase, Carbon Monoxide, and Bilirubin in Cerebral Circulation during Seizures

2012 ◽  
Vol 32 (6) ◽  
pp. 1024-1034 ◽  
Author(s):  
Helena Parfenova ◽  
Charles W Leffler ◽  
Shyamali Basuroy ◽  
Jianxiong Liu ◽  
Alexander L Fedinec
Keyword(s):  
Oxidative Stress ◽  
Carbon Monoxide ◽  
Heme Oxygenase ◽  
Vascular Dysfunction ◽  
Antioxidant Properties ◽  
Cerebrovascular Function ◽  
Cerebrovascular Dysfunction ◽  
Cobalt Protoporphyrin ◽  
Endogenous Antioxidant ◽  
The Brain

Postictal cerebrovascular dysfunction is an adverse effect of seizures in newborn piglets. The brain heme oxygenase (HO) provides protection against cerebrovascular dysfunction. We investigated the contribution of reactive oxygen species (ROS) to seizure-induced vascular damage and the mechanism of HO vasoprotection. In a bicuculline model of seizures, we addressed the hypotheses: (1) seizures increase brain ROS; (2) ROS contribute to cerebral vascular dysfunction; (3) ROS initiate a vasoprotective mechanisms by activating endogenous HO; and (4) HO products have antioxidant properties. As assessed by dihydroethidium oxidation (ox-DHE), seizures increased ROS in cerebral vessels and cortical astrocytes; ox-DHE elevation was prevented by tiron and apocynin. An HO inhibitor, tin protoporphyrin, potentiated, whereas an HO-1 inducer, cobalt protoporphyrin, blocked seizure-induced increase in DHE oxidation. Heme oxygenase products carbon monoxide (CO) (CORM-A1) and bilirubin attenuated ox-DHE elevation during seizures. Antioxidants tiron and bilirubin prevented the loss of postictal cerebrovascular dilations to bradykinin, glutamate, and sodium nitroprusside. Tiron and apocynin abrogated activation of the brain HO during seizures. Overall, these data suggest that long-term adverse cerebrovascular effects of seizures are attributed to oxidative stress. On the other hand, seizure-induced ROS are required for activation of the endogenous antioxidant HO/CO/bilirubin system that alleviates oxidative stress-induced loss of postictal cerebrovascular function in piglets.

Upregulation of heme oxygenase-1 potentiates EDH-type relaxations in the mesenteric artery of the spontaneously hypertensive rat

2013 ◽  
Vol 305 (10) ◽  
pp. H1471-H1483 ◽  
Author(s):  
Zhuoming Li ◽  
Yu Wang ◽  
Ricky Y. K. Man ◽  
Paul M. Vanhoutte
Keyword(s):  
Carbon Monoxide ◽  
Heme Oxygenase ◽  
Spontaneously Hypertensive Rat ◽  
Combined Treatment ◽  
Antioxidant Properties ◽  
Mesenteric Arteries ◽  
Heme Oxygenase 1 ◽  
Zinc Protoporphyrin ◽  
Spontaneously Hypertensive

Heme oxygenase (HO) converts heme to carbon monoxide, bilirubin, and free iron. The present study investigated whether or not HO-1 induction improves vascular relaxations attributable to endothelium-dependent hyperpolarization (EDH). Thirty-six-week-old spontaneously hypertensive rats were treated with the HO-1 inducer hemin, the HO inhibitor zinc protoporphyrin IX (II) (ZnPP), the antioxidant apocynin, or combinations of these compounds. Isolated mesenteric arteries were prepared for measurement of isometric tension, protein presence, and production of reactive oxygen species (ROS). Hemin potentiated acetylcholine-evoked EDH-type relaxations in the presence of Nω-nitro-l-arginine methyl ester (l-NAME) and indomethacin, while the combined treatment with ZnPP plus hemin prevented these improvements. The intermediate conductance Ca2+-activated K+ channel (IKCa) blocker TRAM-34 and the Na+-K+-ATPase blocker ouabain significantly impaired these hemin-potentiated relaxations. NS309-induced TRAM-34- and ouabain-sensitive relaxations were enhanced by hemin. K+-induced ouabain-sensitive relaxations and the expression of Na+-K+-ATPase were increased by hemin. Thus HO-1 induction improves EDH-type relaxations by augmented activation of IKCa and the downstream Na+-K+-ATPase. Treatment with apocynin showed a similar effect as hemin in impairing ROS production, enhancing K+-induced relaxations, and increasing Na+-K+-ATPase expression, without affecting the expression of HO-1. The effects of hemin and apocynin were not additive. These observations suggest that the effect of HO-1 induction on EDH-type relaxations is possibly due to its antioxidant properties. In vitro treatment with bilirubin, but not carbon monoxide, enhanced EDH-type relaxations and K+-induced ouabain-sensitive relaxations, suggesting that the production of bilirubin may be also involved. The present findings reveal that HO-1 may be a potential vascular-specific therapeutic strategy for endothelial dysfunction in hypertension.

scholarly journals Anti-apoptotic properties of carbon monoxide in porcine oocyte duringin vitroaging

PeerJ ◽  
2017 ◽  
Vol 5 ◽  
pp. e3876 ◽  
Author(s):  
David Němeček ◽  
Markéta Dvořáková ◽  
Ivona Heroutová ◽  
Eva Chmelíková ◽  
Markéta Sedmíková
Keyword(s):  
Carbon Monoxide ◽  
Heme Oxygenase ◽  
Caspase 3 ◽  
Protoporphyrin Ix ◽  
Signal Molecule ◽  
Oocyte Aging ◽  
Porcine Oocyte ◽  
Apoptotic Effects ◽  
Matured Oocyte

If fertilization of matured oocyte does not occur, unfertilized oocyte undergoes aging, resulting in a time-dependent reduction of the oocyte’s quality. The aging of porcine oocytes can lead to apoptosis. Carbon monoxide (CO), a signal molecule produced by the heme oxygenase (HO), possesses cytoprotective and anti-apoptotic effects that have been described in somatic cells. However, the effects of CO in oocytes have yet to be investigated. By immunocytochemistry method we detected that both isoforms of heme oxygenase (HO-1 and HO-2) are present in the porcine oocytes. Based on the morphological signs of oocyte aging, it was found that the inhibition of both HO isoforms by Zn-protoporphyrin IX (Zn-PP IX) leads to an increase in the number of apoptotic oocytes and decrease in the number of intact oocytes during aging. Contrarily, the presence of CO donors (CORM-2 or CORM-A1) significantly decrease the number of apoptotic oocytes while increasing the number of intact oocytes. We also determined that CO donors significantly decrease the caspase-3 (CAS-3) activity. Our results suggest that HO/CO contributes to the sustaining viability through regulation of apoptosis duringin vitroaging of porcine oocytes.

scholarly journals Heme Oxygenase-1 Deficiency and Oxidative Stress: A Review of 9 Independent Human Cases and Animal Models

2021 ◽  
Vol 22 (4) ◽  
pp. 1514 ◽  
Author(s):  
Akihiro Yachie
Keyword(s):  
Oxidative Stress ◽  
Animal Models ◽  
Heme Oxygenase ◽  
Inflammatory Diseases ◽  
Cell Types ◽  
Pharmacological Intervention ◽  
Heme Oxygenase 1 ◽  
Inflammatory Reactions

Since Yachie et al. reported the first description of human heme oxygenase (HO)-1 deficiency more than 20 years ago, few additional human cases have been reported in the literature. A detailed analysis of the first human case of HO-1 deficiency revealed that HO-1 is involved in the protection of multiple tissues and organs from oxidative stress and excessive inflammatory reactions, through the release of multiple molecules with anti-oxidative stress and anti-inflammatory functions. HO-1 production is induced in vivo within selected cell types, including renal tubular epithelium, hepatic Kupffer cells, vascular endothelium, and monocytes/macrophages, suggesting that HO-1 plays critical roles in these cells. In vivo and in vitro studies have indicated that impaired HO-1 production results in progressive monocyte dysfunction, unregulated macrophage activation and endothelial cell dysfunction, leading to catastrophic systemic inflammatory response syndrome. Data from reported human cases of HO-1 deficiency and numerous studies using animal models suggest that HO-1 plays critical roles in various clinical settings involving excessive oxidative stress and inflammation. In this regard, therapy to induce HO-1 production by pharmacological intervention represents a promising novel strategy to control inflammatory diseases.

scholarly journals Antioxidant properties of antiepileptic drugs levetiracetam and clonazepam in mice brain after in vitro-induced oxidative stress

2016 ◽  
Vol 10 (14) ◽  
pp. 278-288 ◽  
Author(s):  
de Albuquerque Oliveira Aline ◽  
Isabel Linhares Maria ◽  
Jos eacute Maia Chaves Filho Adriano ◽  
Ricardo Vasconcelos Rios Emiliano ◽  
Nayane de Carvalho Lima Camila ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Antiepileptic Drugs ◽  
Antioxidant Properties ◽  
Mice Brain

scholarly journals Aminoguanidine Protects Boar Spermatozoa against the Deleterious Effects of Oxidative Stress

Pharmaceutics ◽  
2018 ◽  
Vol 10 (4) ◽  
pp. 212 ◽  
Author(s):  
Eliana Pintus ◽  
Martin Kadlec ◽  
Marija Jovičić ◽  
Markéta Sedmíková ◽  
José Ros-Santaella
Keyword(s):  
Oxidative Stress ◽  
Therapeutic Agent ◽  
Antioxidant Properties ◽  
In Vitro Effects ◽  
Oxide Synthase ◽  
Boar Spermatozoa ◽  
Generating System ◽  
Control Samples ◽  
Inducible Nitric Oxide

Aminoguanidine is a selective inhibitor of the inducible nitric oxide synthase (iNOS) and a scavenger of reactive oxygen species (ROS). Numerous studies have shown the antioxidant properties of aminoguanidine in several cell lines, but the in vitro effects of this compound on spermatozoa under oxidative stress are unknown. In this study, we tested the hypothesis that aminoguanidine may protect against the detrimental effects of oxidative stress in boar spermatozoa. For this purpose, sperm samples were incubated with a ROS generating system (Fe2+/ascorbate) with or without aminoguanidine supplementation (10, 1, and 0.1 mM). Our results show that aminoguanidine has powerful antioxidant capacity and protects boar spermatozoa against the deleterious effects of oxidative stress. After 2 h and 3.5 h of sperm incubation, the samples treated with aminoguanidine showed a significant increase in sperm velocity, plasma membrane and acrosome integrity together with a reduced lipid peroxidation in comparison with control samples (p < 0.001). Interestingly, except for the levels of malondialdehyde, the samples treated with 1 mM aminoguanidine did not differ or showed better performance than control samples without Fe2+/ascorbate. The results from this study provide new insights into the application of aminoguanidine as an in vitro therapeutic agent against the detrimental effects of oxidative stress in semen samples.

The protective properties of synthetic porphyrin tin complexes in toxic hyperbilirubinemia

2000 ◽  
Vol 04 (03) ◽  
pp. 243-247 ◽  
Author(s):  
T. O. PHILIPPOVA ◽  
B. N. GALKIN ◽  
N. YA. GOLOVENKO ◽  
Z. I. ZHILINA ◽  
S. V. VODZINSKII
Keyword(s):  
Heme Oxygenase ◽  
Serum Bilirubin ◽  
Protoporphyrin Ix ◽  
Serum Bilirubin Level ◽  
Oxygenase Activity ◽  
Tetraphenyl Porphyrin ◽  
Tin Complexes ◽  
Cytochrome P 450

Tin complexes of meso-substituted synthetic porphyrins, namely Sn 4+-meso-tetraphenyl- porphyrin ( Sn - TPP ) and Sn 4+-meso-tetrakis(N-methyl-3-pyridyl)porphyrin tetratosylate ( Sn - TMe -3- PyP ), efficiently decrease the serum bilirubin level when injected subcutaneously at a dose of 100 μM kg−1 body weight into mice. These compounds are active during hyperbilirubinemia, induced by phenylhydrazine, hemin and tetrachloromethane, and also during autoimmune hemolytic anemia. In the latter case a decrease in serum bilirubin content was observed, as well as a decrease in the amount of blood reticulocytes which reflects a milder course of the disease. The Sn complexes under study induce, in vivo, cytochrome P-450, inhibit microsomal heme oxygenase and decrease the intensity of lipid peroxidation. At the same time, in vitro the hepatic and splenic heme oxygenase activity is blocked only when a 0.1 μM concentration of Sn - TMe -3- PyP or Sn -protoporphyrin IX is added to the incubation mixture. Sn - TPP does not affect the activity of this enzyme in vitro.

Heme oxygenase-1 induction by hemin prevents oxidative stress-induced acute cholestasis in the rat

2019 ◽  
Vol 133 (1) ◽  
pp. 117-134 ◽  
Author(s):  
Pamela L. Martín ◽  
Paula Ceccatto ◽  
María V. Razori ◽  
Daniel E.A. Francés ◽  
Sandra M.M. Arriaga ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heme Oxygenase ◽  
Bile Flow ◽  
Driving Forces ◽  
Membrane Lipids ◽  
Ex Vivo ◽  
Heme Oxygenase 1 ◽  
Canalicular Transporters

Abstract We previously demonstrated in in vitro and ex vivo models that physiological concentrations of unconjugated bilirubin (BR) prevent oxidative stress (OS)-induced hepatocanalicular dysfunction and cholestasis. Here, we aimed to ascertain, in the whole rat, whether a similar cholestatic OS injury can be counteracted by heme oxygenase-1 (HO-1) induction that consequently elevates endogenous BR levels. This was achieved through the administration of hemin, an inducer of HO-1, the rate-limiting step in BR generation. We found that BR peaked between 6 and 8 h after hemin administration. During this time period, HO-1 induction fully prevented the pro-oxidant tert-butylhydroperoxide (tBuOOH)-induced drop in bile flow, and in the biliary excretion of bile salts and glutathione, the two main driving forces of bile flow; this was associated with preservation of the membrane localization of their respective canalicular transporters, bile salt export pump (Bsep) and multidrug resistance-associated protein 2 (Mrp2), which are otherwise endocytosed by OS. HO-1 induction counteracted the oxidation of intracellular proteins and membrane lipids induced by tBuOOH, and fully prevented the increase in the oxidized-to-total glutathione (GSHt) ratio, a sensitive parameter of hepatocellular OS. Compensatory elevations of the activity of the antioxidant enzymes catalase (CAT) and superoxide dismutase (SOD) were also prevented. We conclude that in vivo HO-1 induction protects the liver from acute oxidative injury, thus preventing consequent cholestasis. This reveals an important role for the induction of HO-1 and the consequently elevated levels of BR in preserving biliary secretory function under OS conditions, thus representing a novel therapeutic tool to limit the cholestatic injury that bears an oxidative background.

scholarly journals Protection of the vascular endothelium in experimental situations

2011 ◽  
Vol 4 (1) ◽  
pp. 20-26 ◽  
Author(s):  
Ružena Sotníková ◽  
Jana Nedelčevová ◽  
Jana Navarová ◽  
Viera Nosáľová ◽  
Katarína Drábiková ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Vascular Endothelium ◽  
Vascular Dysfunction ◽  
Antioxidant Properties ◽  
Pharmacological Intervention ◽  
Ros Production ◽  
Nitric Oxide Radical ◽  
Endothelium Dependent Relaxation

Protection of the vascular endothelium in experimental situationsOne of the factors proposed as mediators of vascular dysfunction observed in diabetes is the increased generation of reactive oxygen species (ROS). This provides support for the use of antioxidants as early and appropriate pharmacological intervention in the development of late diabetic complications. In streptozotocin (STZ)-induced diabetes in rats we observed endothelial dysfuction manifested by reduced endothelium-dependent response to acetylcholine of the superior mesenteric artery (SMA) and aorta, as well as by increased endothelaemia. Changes in endothelium-dependent relaxation of SMA were induced by injury of the nitric oxide radical (·NO)-signalling pathway since the endothelium-derived hyperpolarising factor (EDHF)-component of relaxation was not impaired by diabetes. The endothelial dysfunction was accompanied by decreased ·NO bioavailabity as a consequence of reduced activity of eNOS rather than its reduced expression. The results obtained using the chemiluminiscence method (CL) argue for increased oxidative stress and increased ROS production. The enzyme NAD(P)H-oxidase problably participates in ROS production in the later phases of diabetes. Oxidative stress was also connected with decreased levels of reduced glutathione (GSH) in the early phase of diabetes. After 10 weeks of diabetes, adaptational mechanisms probably took place because GSH levels were not changed compared to controls. Antioxidant properties of SMe1EC2 foundin vitrowere partly confirmedin vivo.Administration of SMe1EC2 protected endothelial function. It significantly decreased endothelaemia of diabetic rats and improved endothelium-dependent relaxation of arteries, slightly decreased ROS-production and increased bioavailability of ·NO in the aorta. Further studies with higher doses of SMe1EC2 may clarify the mechanism of its endothelium-protective effectin vivo.

In Vitro Study of Antioxidant Activity of Serum and Plasma Samples As Well As Glutathione Exposed to Various Exogenous Stress Factors

2021 ◽  
Author(s):  
Małgorzata Olszowy-Tomczyk ◽  
Łukasz Paprotny ◽  
Agnieszka Celejewska ◽  
Dorota Szewczak ◽  
Dorota Wianowska
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Activity ◽  
Antioxidant Properties ◽  
In Vitro Study ◽  
Stress Factors ◽  
Plasma Samples ◽  
Serum Samples ◽  
Exogenous Stress

Abstract The imbalance between the production of Reactive Oxygen Species (ROS) and their sequestration promotes the formation of so-called oxidative stress conditions which are considered crucial in the aging process and development of many human diseases. Glutathione plays an essential role in the antioxidative barricade against ROS. Its role in the detoxification process of xenobiotics and carcinogen is also known. However, there are no comparative studies on the antioxidant properties of both biological samples and glutathione as well as the change in these properties as a result of exposure to various stress factors. This paper fills this gap comparing the antioxidant activity of serum and plasma samples of the known glutathione content with the activity of glutathione itself assessed by the different methods. In addition, it reveals a significant role of environmental xenobiotics in oxidative stress and differentiates the stress induced by different groups of drugs, among which the greatest one has been demonstrated for antiarrhythmic drugs and cytostatics. More importantly, it proves that human plasma is more resistant to stress factors and N-acetylcysteine clearly promotes the extension of antioxidant properties of both the plasma and serum samples. The latter conclusion is consistent with the implied preventive and/or supportive action of this drug against SARS-CoV-2.

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