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51.
Treatment of bovine pulmonary artery endothelial cells with the calcium ionophore, A23187, stimulates the cell membrane associated protease activity, phospholipase A2 (PLA2) activity, and arachidonic acid (AA) release from the cells. Pretreatment of the cells with arachidonyl-trifluomethylketone (AACOCF3), a cPLA2 inhibitor, but not bromoenollactone (BEL), a iPLA2 inhibitor, prevents A23187 stimulated PLA2 activity and AA release without producing an appreciable alteration of the protease activity. Pretreatment of the cells with aprotinin, an ambient protease inhibitor, prevents the increase in the protease activity and cPLA2 activity in the membrane and AA release from the cells caused by both low and high doses of A23187, and also inhibits protein kinase C (PKC) activity caused by high doses of A23187. Immunoblot study of the endothelial cell membrane isolated from A23187 (10 microM)-treated cells with polyclonal PKCalpha antibody elicited an increase in the 80 kDa immunoreactive protein band along with an additional 47 kDa immunoreactive fragment. Pretreatment of the cells with aprotinin abolished the 47 kDa immunoreactive fragment in the immunoblot. Immunoblot study of the endothelial membrane with polyclonal cPLA2 antibody revealed that treatment of the cells with A23187 dose-dependently increases cPLA2 immunoreactive protein profile in the membrane. It therefore appears from the present study that treatment of the cells with a low dose of A23187 (1 microM) causes a small increase in an aprotinin-sensitive protease activity and that stimulates cPLA2 activity in the cell membrane without an involvement of PKC. By contrast, treatment of the cells with a high dose of 10 microM of A23187 causes optimum increase in the protease activity and that plays an important role in activating PKCalpha, which subsequently stimulates cPLA2 activity in the cell membrane. Although pretreatment of the cells with pertussis toxin caused ADP ribosylation of a 41 kDa protein in the cell membrane, it did not inhibit the cPLA2 activity and AA release caused by both low and high doses of A23187. 相似文献
52.
Ashok?AgarwalEmail author Sajal?Gupta Rakesh?K?Sharma 《Reproductive biology and endocrinology : RB&E》2005,3(1):28
In a healthy body, ROS (reactive oxygen species) and antioxidants remain in balance. When the balance is disrupted towards
an overabundance of ROS, oxidative stress (OS) occurs. OS influences the entire reproductive lifespan of a woman and even
thereafter (i.e. menopause). OS results from an imbalance between prooxidants (free radical species) and the body's scavenging
ability (antioxidants). ROS are a double-edged sword – they serve as key signal molecules in physiological processes but also
have a role in pathological processes involving the female reproductive tract. ROS affect multiple physiological processes
from oocyte maturation to fertilization, embryo development and pregnancy. It has been suggested that OS modulates the age-related
decline in fertility. It plays a role during pregnancy and normal parturition and in initiation of preterm labor. Most ovarian
cancers appear in the surface epithelium, and repetitive ovulation has been thought to be a causative factor. Ovulation-induced
oxidative base damage and damage to DNA of the ovarian epithelium can be prevented by antioxidants. There is growing literature
on the effects of OS in female reproduction with involvement in the pathophsiology of preeclampsia, hydatidiform mole, free
radical-induced birth defects and other situations such as abortions. Numerous studies have shown that OS plays a role in
the pathoysiology of infertility and assisted fertility. There is some evidence of its role in endometriosis, tubal and peritoneal
factor infertility and unexplained infertility. This article reviews the role OS plays in normal cycling ovaries, follicular
development and cyclical endometrial changes. It also discusses OS-related female infertility and how it influences the outcomes
of assisted reproductive techniques. The review comprehensively explores the literature for evidence of the role of oxidative
stress in conditions such as abortions, preeclampsia, hydatidiform mole, fetal embryopathies, preterm labour and preeclampsia
and gestational diabetes. The review also addresses the growing literature on the role of nitric oxide species in female reproduction.
The involvement of nitric oxide species in regulation of endometrial and ovarian function, etiopathogenesis of endometriosis,
and maintenance of uterine quiescence, initiation of labour and ripening of cervix at parturition is discussed. Complex interplay
between cytokines and oxidative stress in the etiology of female reproductive disorders is discussed. Oxidant status of the
cell modulates angiogenesis, which is critical for follicular growth, corpus luteum formation endometrial differentiation
and embryonic growth is also highlighted in the review. Strategies to overcome oxidative stress and enhance fertility, both
natural and assisted are delineated. Early interventions being investigated for prevention of preeclampsia are enumerated.
Trials investigating combination intervention strategy of vitamin E and vitamin C supplementation in preventing preeclampsia
are highlighted. Antioxidants are powerful and there are few trials investigating antioxidant supplementation in female reproduction.
However, before clinicians recommend antioxidants, randomized controlled trials with sufficient power are necessary to prove
the efficacy of antioxidant supplementation in disorders of female reproduction. Serial measurement of oxidative stress biomarkers
in longitudinal studies may help delineate the etiology of some of the diosorders in female reproduction such as preeclampsia. 相似文献
53.
Sujata Roychoudhury Sahl K Ghosh Tapati Chakraborti Sajal Chakraborti 《Molecular and cellular biochemistry》1996,159(2):95-103
We sought to investigate the mechanism(s) by which the oxidant H2O2 stimulates Ca2+ release from mitochondria of bovine pulmonary vascular smooth muscle tissue and to test the hypothesis that hydroxyl radical is involved in this phenomenon. Treatment of the smooth muscle tissue with 1 mM H2O2 dramatically stimulated hydroxyl radical generation as measured by methane (CH4) production by GLC using dimethylsulfoxide (DMSO) as the substrate. Pretreatment of the mitochondria with the hydroxyl radical scavanger dimethylthiourea (DMTU) prevented the increase in CH4 production caused by H2O2. In the absence of EGTA, H2O2 caused stimulation of Ca2+ release from mitochondria occurred with a lag time of about 4 min. Addition of EGTA to Ca2+ loaded mitochondria resulted an immediate loss of Ca2+ and that has been found to be augmented by H2O2. The release of Ca2+ by H2O2 did not appear to occur with concommitant increase in sucrose entry into, K+ release from, and swelling of mitochondria when the Ca2+ cycling was prevented by EGTA. These observations suggested that H2O2-mediated Ca2+ release from bovine pulmonary vascular smooth muscle tissue mitochondria occurred (i) through the involvement of hydroxyl radical; (ii) via specific pathway(s); and (iii) did not appear to happen primarily via nonspecific pore formation.Abbreviations H2O2
hydrogen peroxide
- OH·
hydroxyl radical
- t-buOOH
tert-butyl hydroperoxide
- CH4
methane
- GLC
gas liquid chromatography
- DMTU
dimethylthiourea
- EGTA
ethylene glycol bis(-aminoethyl ether)
- N
Ntetraacetic acid
- DMSO
dimethyl sulfoxide
- CH4
methane
- HBPS
Hank's buffered physiological saline
- HEPES
N-2-hydroxyethylpiperazine-N-2-ethane sulfonic acid
- MOPS
3-(N-morpholino)propane sulfonic acid
- Tris
tris (hydroxymethyl aminomethane) 相似文献
54.
Calcium signaling phenomena in heart diseases: a perspective 总被引:2,自引:0,他引:2
Chakraborti S Das S Kar P Ghosh B Samanta K Kolley S Ghosh S Roy S Chakraborti T 《Molecular and cellular biochemistry》2007,298(1-2):1-40
Ca2+ is a major intracellular messenger and nature has evolved multiple mechanisms to regulate free intracellular (Ca2+)i level in situ. The Ca2+ signal inducing contraction in cardiac muscle originates from two sources. Ca2+ enters the cell through voltage dependent Ca2+ channels. This Ca2+ binds to and activates Ca2+ release channels (ryanodine receptors) of the sarcoplasmic reticulum (SR) through a Ca2+ induced Ca2+ release (CICR) process. Entry of Ca2+ with each contraction requires an equal amount of Ca2+ extrusion within a single heartbeat to maintain Ca2+ homeostasis and to ensure relaxation. Cardiac Ca2+ extrusion mechanisms are mainly contributed by Na+/Ca2+ exchanger and ATP dependent Ca2+ pump (Ca2+-ATPase). These transport systems are important determinants of (Ca2+)i level and cardiac contractility. Altered intracellular Ca2+ handling importantly contributes to impaired contractility in heart failure. Chronic hyperactivity of the β-adrenergic signaling
pathway results in PKA-hyperphosphorylation of the cardiac RyR/intracellular Ca2+ release channels. Numerous signaling molecules have been implicated in the development of hypertrophy and failure, including
the β-adrenergic receptor, protein kinase C, Gq, and the down stream effectors such as mitogen activated protein kinases pathways,
and the Ca2+ regulated phosphatase calcineurin. A number of signaling pathways have now been identified that may be key regulators of
changes in myocardial structure and function in response to mutations in structural components of the cardiomyocytes. Myocardial
structure and signal transduction are now merging into a common field of research that will lead to a more complete understanding
of the molecular mechanisms that underlie heart diseases. Recent progress in molecular cardiology makes it possible to envision
a new therapeutic approach to heart failure (HF), targeting key molecules involved in intracellular Ca2+ handling such as RyR, SERCA2a, and PLN. Controlling these molecular functions by different agents have been found to be beneficial
in some experimental conditions. 相似文献
55.
Glass transition temperature is a unique thermal characteristic of amorphous systems and is associated with changes in physical properties such as heat capacity, viscosity, electrical resistance, and molecular mobility. Glass transition temperature for amorphous solids is referred as (T g), whereas for maximally freeze concentrated solution, the notation is (T g′). This article is focused on the factors affecting determination of T g′ for application to lyophilization process design and frozen storage stability. Also, this review provides a perspective on use of various types of solutes in protein formulation and their effect on T g′. Although various analytical techniques are used for determination of T g′ based on the changes in physical properties associated with glass transition, the differential scanning calorimetry (DSC) is the most commonly used technique. In this article, an overview of DSC technique is provided along with brief discussion on the alternate analytical techniques for T g′ determination. Additionally, challenges associated with T g′ determination, using DSC for protein formulations, are discussed. The purpose of this review is to provide a practical industry perspective on determination of T g′ for protein formulations as it relates to design and development of lyophilization process and/or for frozen storage; however, a comprehensive review of glass transition temperature (T g, T g′), in general, is outside the scope of this work. 相似文献
56.
Animesh Chowdhury Jaganmay Sarkar Pijush Kanti Pramanik Tapati Chakraborti Sajal Chakraborti 《Cell biology international》2020,44(5):1142-1155
We sought to determine the mechanism by which angiotensin II (AngII) inhibits isoproterenol induced increase in adenylate cyclase (AC) activity and cyclic adenosine monophosphate (cAMP) production in bovine pulmonary artery smooth muscle cells (BPASMCs). Treatment with AngII stimulates protein kinase C‐ζ (PKC‐ζ), nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, and PKC‐α activities, and also inhibits isoproterenol induced increase in AC activity and cAMP production in the cells. Pertussis toxin pretreatment eliminates AngII caused inhibition of isoproterenol induced increase in AC activity without a discernible change in PKC‐ζ, NADPH oxidase, and PKC‐α activities. Treatment of the cells with AngII increases α2 isoform of Gi (Giα2) phosphorylation; while pretreatment with chemical and genetic inhibitors of PKC‐ζ and NADPH oxidase attenuate AngII induced increase in PKC‐α activity and Giα2 phosphorylation, and also reverse AngII caused inhibition of isoproterenol induced increase in AC activity. Pretreatment of the cells with chemical and genetic inhibitors of PKC‐α attenuate AngII induced increase in Giα2 phosphorylation and inhibits isoproterenol induced increase in AC activity without a discernible change in PKC‐ζ and NADPH oxidase activities. Overall, PKCζ‐NADPH oxidase‐PKCα signaling axis plays a crucial role in Giα2 phosphorylation resulting in AngII‐mediated inhibition of isoproterenol induced increase in AC activity in BPASMCs. 相似文献
57.
Emerging Freeze-Drying Process Development and Scale-up Issues 总被引:1,自引:0,他引:1
Although several guidelines do exist for freeze-drying process development and scale-up, there are still a number of issues
that require additional attention. The objective of this review article is to discuss some emerging process development and
scale-up issue with emphasis on effect of load condition and freeze-drying in novel container systems such as syringes, Lyoguard
trays, ampoules, and 96-well plates. Understanding the heat and mass transfer under different load conditions and for freeze-drying
in these novel container systems will help in developing a robust freeze-drying process which is also easier to scale-up.
Further research and development needs in these emerging areas have also been addressed. 相似文献
58.
The freshwater wetland systems of India is a complex habitat that supports a broad range of diverse species including molluscs, which play an important role in supplementing third world countries. In the arsenic affected flood plains of West Bengal, a huge amount of arsenic laden groundwater is raised for the purpose of irrigation. Agricultural runoffs and flood water movement during monsoon may cause accumulation of arsenic in the adjacent freshwater aquifers, the common habitat of Lamellidens marginalis (Mollusca; Bivalvia; Eulamellibranchiata), a filter feeder, sensitive to altered environmental conditions. To examine the nature of toxicity induced by inorganic arsenic on both the haemocytes and tissues of the invertebrate heart, the animals were exposed to five different sublethal concentrations of sodium arsenite for a maximum time span of 30 days in vitro. Significant differences were recorded in the total haemocyte count, biochemical and histopathological parameters of the heart of L. marginalis under the arsenic induced stress. Our observations indicate the development of profound haematopoietic and cardiac stress under the sublethal inorganic arsenite exposure and it also implies the nature of risk imposed on the freshwater aquatic ecosystem under potential arsenic contamination. 相似文献
59.
We sought to determine the mechanism by which angiotensin II (ANGII) stimulates NADPH oxidase‐mediated superoxide (O2.?) production in bovine pulmonary artery smooth muscle cells (BPASMCs). ANGII‐induced increase in phospholipase D (PLD) and NADPH oxidase activities were inhibited upon pretreatment of the cells with chemical and genetic inhibitors of PLD2, but not PLD1. Immunoblot study revealed that ANGII treatment of the cells markedly increases protein kinase C‐α (PKC‐α), ‐δ, ‐ε, and ‐ζ levels in the cell membrane. Pretreatment of the cells with chemical and genetic inhibitors of PKC‐ζ, but not PKC‐α, ‐δ, and ‐ε, attenuated ANGII‐induced increase in NADPH oxidase activity without a discernible change in PLD activity. Transfection of the cells with p47phox small interfering RNA inhibited ANGII‐induced increase in NADPH oxidase activity without a significant change in PLD activity. Pretreatment of the cells with the chemical and genetic inhibitors of PLD2 and PKC‐ζ inhibited ANGII‐induced p47phox phosphorylation and subsequently translocation from cytosol to the cell membrane, and also inhibited its association with p22phox (a component of membrane‐associated NADPH oxidase). Overall, PLD?PKCζ?p47phox signaling axis plays a crucial role in ANGII‐induced increase in NADPH oxidase‐mediated O2.? production in the cells. 相似文献
60.
The present study was undertaken to test the hypothesis that activation of cell membrane associated protein kinase C (PKC) plays a role in stimulating cell membrane associated phospholipase A2 (PLA2) activity, and subsequent liberation of arachidonic acid (AA) under exposure of rabbit pulmonary arterial smooth muscle cells to the oxidant hydrogen peroxide (H2O2). Exposure of the smooth muscle cells to H2O2 dose-dependently stimulates [14C] AA release, and enhances the cell membrane associated PLA2 activity. Pretreatment of the cells with protein kinase C (PKC) inhibitors H7 and sphingosine prevent the cell membrane associated PLA2 activity, and AA release caused by H2O2. Treatment of the smooth muscle cells with H2O2 stimulates the cell membrane associated PKC activity. Pretreatment of the cells with an antioxidant vitamin E prevents H2O2 caused stimulation of the cell membrane associated PKC activity. The cell membrane associated PLA2 and PKC activities correlate linearly. These results suggest that H2O2 caused stimulation of the smooth muscle cell membrane associated PLA2 activity, and subsequent liberation of AA can occur through an increase in the activity of the cell membrane associated PKC. (Mol Cell Biochem122: 9–15, 1993)Abbreviations AA
Arachidonic Acid
- PLA2
Phospholipase A2
- PKC
Protein Kinase C
- PBS
Phosphate Buffered Saline
- HBPS
Hank's Buffered Physiological Saline
- HEPES
4-(2-Hydroxyethyl)-1-Piperazine N-2-Ethanesulfonate
- FCS
Fetal Calf Serum
- ATP
Adenosine Triphosphate
- H7
1-(5-isoquinolinesulfonyl)-2-methyl-piperazine
- DMEM
Dulbecco's Modified Eagles Medium
- TCA
Trichloroacetic Acid 相似文献