287 EFFECT OF FOLLICULAR AGING ON THE ATP CONTENT AND DISTRIBUTION OF MITOCHONDRIA IN BOVINE OOCYTES

2015 ◽  
Vol 27 (1) ◽  
pp. 232
Author(s):  
D. Dadarwal ◽  
F. Dias ◽  
G. Adams ◽  
J. Singh
Keyword(s):  
Oxidative Stress ◽  
Atp Content ◽  
Exact Test ◽  
Atp Assay ◽  
Follicular Waves ◽  
Mitochondrial Data ◽  
Mitochondrial Population ◽  
Mitochondrial Distribution ◽  
Bovine Oocytes

Our objective was to determine how follicular aging affects the distribution and content of mitochondrial population and ATP in in vivo-matured bovine oocytes. We hypothesised that in vivo-matured bovine oocytes obtained from aged follicles (84 h of gonadotropin starvation) have altered mitochondrial distribution and decreased cytoplasmic ATP content compared to those obtained immediately at the end of a superstimulatory protocol (no starvation). Follicular waves were synchronized by ablation 5 to 8 d after ovulation and a CIDR device was given. Starting on the day of wave emergence (Day 0), short FSH and FSH starvation groups (n = 5 heifers each) were given 8 doses of FSH im over 4 d and the long FSH group (n = 4) was given 14 doses over 7 d. Two doses of PGF were given on Day 4 (short FSH) or Day 7 (FSH starvation and long FSH groups), the CIDR was removed, and LH was given 24 h after second PGF treatment. The ovaries were removed 24 h later by colpotomy and cumulus-oocyte-complexes (COC) were collected from follicles ≥8 mm. Denuded oocytes were either stained with Mitotracker Deep Red FM and imaged by confocal microscopy or processed for ATP assay. Mitochondria numbers were assessed by segmentation of 3D datasets. Proportions of COC within each grade were compared using Fischer's exact test, and ATP and mitochondrial data were compared by analysis of variance. Short and long FSH groups had a greater proportion of Grade 1 expanded COC than the FSH starvation group (P = 0.02). The ATP content of oocytes (from expanded COC) tended to be higher in the long FSH group than short FSH (P = 0.09), and the FSH starvation group was intermediate. The ATP content of oocytes from compact COC did not differ among groups (P = 0.49). The proportion of mitochondrial clusters was highest (P = 0.01) and the proportion of individual mitochondria was lowest (P = 0.01) in the FSH starvation group compared to short and long FSH groups. Mitochondria from the long FSH and FSH starvation groups had twice the relative intensity compared to the short FSH group (P < 0.01). In conclusion, follicular aging (FSH starvation) was associated with a decrease in oocyte morphologic grade and marked clustering of mitochondria, which may be a reflection of oxidative stress and atresia.

scholarly journals Aging-related Changes in In Vitro-matured Bovine Oocytes: Oxidative Stress, Mitochondrial Activity and ATP Content After Nuclear Maturation

2014 ◽  
Vol 60 (2) ◽  
pp. 136-142 ◽  
Author(s):  
Keisuke KOYAMA ◽  
Sung-Sik KANG ◽  
Weiping HUANG ◽  
Yojiro YANAGAWA ◽  
Yoshiyuki TAKAHASHI ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Activity ◽  
Atp Content ◽  
Nuclear Maturation ◽  
Bovine Oocytes

scholarly journals XinJiaCongRongTuSiZiWan Protects TP-Induced Rats from Oxidative Stress Injury via Mitophagy Mediated PINK1/ Parkin Signaling Pathway

2021 ◽  
Author(s):  
Jin Yan ◽  
Disi Deng ◽  
Min Liu ◽  
Yeke Wu ◽  
Keming Wu
Keyword(s):  
Oxidative Stress ◽  
Cell Viability ◽  
Signaling Pathway ◽  
Atp Content ◽  
Stress Injury ◽  
Primordial Follicles ◽  
Apoptosis Rate ◽  
Oxidative Stress Injury

Abstract Background: Oxidative stress is one of main molecular mechanisms involved in toxicity of triptolide (TP). Although our group has discovered the effectiveness of XinJiaCongRongTuSiZiWan (XJCRTSZW) on premature ovarian failure (POF) and polycystic ovary syndrome (PCOS), whether the protective role of XJCRTSZW being associated with oxidative stress is still totally understood. Methods: Adult female Sprague-Dawley rats and human ovarian granulosa cell lines were treated with TP, and then treated with XinJiaCongRongTuSiZiWan (XJCRTSZW). Histological analysis and follicle count were executed using H&E staining. Hormone (E2, AMH, P, FSH and LH) concentrations, oxidative stress indicators (SOD and MDA), apoptosis rate, ATP content, mitochondrial membrane potential (MMP), cell viability, mitophagy and relative mRNA and protein levels (LC3-Ⅱ/LC3-Ⅰ, p62, Hsp60, PINK1 and Parkin) were detected by ELISA, commercial biochemical detection kits, flow cytometry, JC-1 staining, CCK-8, transmission electron microscope and western blotting respectively. Results: XJCRTSZW treatment observably ameliorated the TP-induced the pathological symptoms, including the decreased primordial follicles, primary follicles and secondary follicles numbers in the cortical area, the increased numbers of atretic follicles, necrotic and shedding, and nuclear constriction and collapse with cystic dilatation in vivo. Furthermore, XJCRTSZW treatment observably enhanced the TP-induced reduction of E2, AMH and P concentrations, SOD concentrations, ATP content, MMP, p62 and Hsp60 mRNA and protein level, but, diminished the TP-induced elevation of FSH and LH concentrations, MDA level, ROS level, apoptosis rate, mitophagy, and the mRNA and protein expression of LC3-Ⅱ/LC3-Ⅰ, PINK1 and Parkin both in vivo and in vitro. In addition, XJCRTSZW treatment markedly increased the TP-induced reduction of cell viability in vitro.Conclusion: XinJiaCongRongTuSiZiWan protects TP-induced rats from oxidative stress injury via mitophagy mediated PINK1/ Parkin signaling pathway.

scholarly journals Glutathione Ethyl Ester Protects In Vitro-Maturing Bovine Oocytes against Oxidative Stress Induced by Subsequent Vitrification/Warming

2020 ◽  
Vol 21 (20) ◽  
pp. 7547
Author(s):  
Tania García-Martínez ◽  
Meritxell Vendrell-Flotats ◽  
Iris Martínez-Rodero ◽  
Erika Alina Ordóñez-León ◽  
Manuel Álvarez-Rodríguez ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Ethyl Ester ◽  
Mitochondrial Activity ◽  
Cell Stage ◽  
Developmental Potential ◽  
Expression Of Genes ◽  
Mitochondrial Distribution ◽  
Targeted Gene Expression ◽  
Bovine Oocytes

This study aimed to examine whether the addition of glutathione ethyl ester (GSH-OEt) to the in vitro maturation (IVM) medium would improve the resilience of bovine oocytes to withstand vitrification. The effects of GSH-OEt on spindle morphology, levels of reactive oxygen species (ROS), mitochondrial activity and distribution, and embryo developmental potential were assessed together with the expression of genes with a role in apoptosis (BAX, BCL2), oxidative-stress pathways (GPX1, SOD1), water channels (AQP3), implantation (IFN-τ) and gap junctions (CX43) in oocytes and their derived blastocysts. Vitrification gave rise to abnormal spindle microtubule configurations and elevated ROS levels. Supplementation of IVM medium with GSH-OEt before vitrification preserved mitochondrial distribution pattern and diminished both cytoplasmic and mitochondrial ROS contents and percentages of embryos developing beyond the 8-cell stage were similar to those recorded in fresh non-vitrified oocytes. Although not significantly different from control vitrified oocytes, vitrified oocytes after GSH-OEt treatment gave rise to similar day 8-blastocyst and hatching rates to fresh non-vitrified oocytes. No effects of GSH-OEt supplementation were noted on the targeted gene expression of oocytes and derived blastocysts, with the exception of GPX1, AQP3 and CX43 in derived blastocysts. The addition of GSH-OEt to the IVM medium before vitrification may be beneficial for embryo development presumably as the consequence of additional anti-oxidant protection during IVM.

Glial cytotoxicity of low doses of cadmium as a model of heavy metal pollution influence on vertebrates

2020 ◽  
Vol 31 (1) ◽  
pp. 3-10
Author(s):  
V. S. Nedzvetsky ◽  
V. Ya. Gasso ◽  
A. M. Hahut ◽  
I. A. Hasso
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Oxidative Damage ◽  
Cadmium Chloride ◽  
Glioma Cells ◽  
Low Doses ◽  
Genotoxic Effects ◽  
Cadmium Ions

Cadmium is a common transition metal that entails an extremely wide range of toxic effects in humans and animals. The cytotoxicity of cadmium ions and its compounds is due to various genotoxic effects, including both DNA damage and chromosomal aberrations. Some bone diseases, kidney and digestive system diseases are determined as pathologies that are closely associated with cadmium intoxication. In addition, cadmium is included in the list of carcinogens because of its ability to initiate the development of tumors of several forms of cancer under conditions of chronic or acute intoxication. Despite many studies of the effects of cadmium in animal models and cohorts of patients, in which cadmium effects has occurred, its molecular mechanisms of action are not fully understood. The genotoxic effects of cadmium and the induction of programmed cell death have attracted the attention of researchers in the last decade. In recent years, the results obtained for in vivo and in vitro experimental models have shown extremely high cytotoxicity of sublethal concentrations of cadmium and its compounds in various tissues. One of the most studied causes of cadmium cytotoxicity is the development of oxidative stress and associated oxidative damage to macromolecules of lipids, proteins and nucleic acids. Brain cells are most sensitive to oxidative damage and can be a critical target of cadmium cytotoxicity. Thus, oxidative damage caused by cadmium can initiate genotoxicity, programmed cell death and inhibit their viability in the human and animal brains. To test our hypothesis, cadmium cytotoxicity was assessed in vivo in U251 glioma cells through viability determinants and markers of oxidative stress and apoptosis. The result of the cell viability analysis showed the dose-dependent action of cadmium chloride in glioma cells, as well as the generation of oxidative stress (p <0.05). Calculated for 48 hours of exposure, the LD50 was 3.1 μg×ml-1. The rates of apoptotic death of glioma cells also progressively increased depending on the dose of cadmium ions. A high correlation between cadmium concentration and apoptotic response (p <0.01) was found for cells exposed to 3–4 μg×ml-1 cadmium chloride. Moreover, a significant correlation was found between oxidative stress (lipid peroxidation) and induction of apoptosis. The results indicate a strong relationship between the generation of oxidative damage by macromolecules and the initiation of programmed cell death in glial cells under conditions of low doses of cadmium chloride. The presented results show that cadmium ions can induce oxidative damage in brain cells and inhibit their viability through the induction of programmed death. Such effects of cadmium intoxication can be considered as a model of the impact of heavy metal pollution on vertebrates.

The Pattern of Ventricular Remodeling Influences the Level of Oxidative Stress in Heart Failure Patients

2017 ◽  
Vol 68 (7) ◽  
pp. 1506-1511
Author(s):  
Cerasela Mihaela Goidescu ◽  
Anca Daniela Farcas ◽  
Florin Petru Anton ◽  
Luminita Animarie Vida Simiti
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Ventricular Remodeling ◽  
Clinical Laboratory ◽  
Left Ventricular ◽  
Control Group ◽  
Reactive Protein ◽  
Lv Mass ◽  
Few Data

Oxidative stress (OS) is increased in chronic diseases, including cardiovascular (CV), but there are few data on its effects on the heart and vessels. The isoprostanes (IsoP) are bioactive compounds, with 8-iso-PGF25a being the most representative in vivo marker of OS. They correlate with the severity of heart failure (HF), but because data regarding OS levels in different types of HF are scarce, our study was aimed to evaluate it by assessing the urinary levels of 8-iso-PGF2aand its correlations with various biomarkers and parameters. Our prospective study included 53 consecutive patients with HF secondary to ischemic heart disease or dilative cardiomyopathy, divided according to the type of HF (acute, chronic decompensated or chronic compensated HF). The control group included 13 hypertensive patients, effectively treated. They underwent clinical, laboratory - serum NT-proBNP, creatinine, uric acid, lipids, C reactive protein (CRP) and urinary 8-iso-PGF2a and echocardiographic assessment. HF patients, regardless the type of HF, had higher 8-iso-PGF2a than controls (267.32pg/�mol vs. 19.82pg/�mol, p[0.001). The IsoP level was directly correlated with ejection fraction (EF) (r=-0.31, p=0.01) and NT-proBNP level (r=0.29, p=0.019). The relative wall thickness (RWT) was negatively correlated with IsoP (r=-0.55, p[0.001). Also 8-iso-PGF25a was higher by 213.59pg/�mol in the eccentric left ventricular (LV) hypertrophy subgroup comparing with the concentric subgroup (p=0.014), and the subgroups with severe mitral regurgitation (MR) and moderate/severe pulmonary hypertension (PAH) had the highest 8-iso-PGF2a levels. Male sex, severe MR, moderate/severe PAH, high LV mass and low RWT values were predictive for high OS level in HF patients.Eccentric cardiac remodeling, MR severity and PAH severity are independent predictors of OS in HF patients.

Exploiting Anti-Inflammation Effects of Flavonoids in Chronic Inflammatory Diseases

2020 ◽  
Vol 26 (22) ◽  
pp. 2610-2619 ◽  
Author(s):  
Tarique Hussain ◽  
Ghulam Murtaza ◽  
Huansheng Yang ◽  
Muhammad S. Kalhoro ◽  
Dildar H. Kalhoro
Keyword(s):  
Oxidative Stress ◽  
Chronic Diseases ◽  
Inflammatory Diseases ◽  
Therapeutic Option ◽  
Cellular Level ◽  
Antiinflammatory Drugs ◽  
Suitable Alternative ◽  
Chronic Inflammatory Diseases

Background: Inflammation is a complex response of the host defense system to different internal and external stimuli. It is believed that persistent inflammation may lead to chronic inflammatory diseases such as, inflammatory bowel disease, neurological and cardiovascular diseases. Oxidative stress is the main factor responsible for the augmentation of inflammation via various molecular pathways. Therefore, alleviating oxidative stress is effective a therapeutic option against chronic inflammatory diseases. Methods: This review article extends the knowledge of the regulatory mechanisms of flavonoids targeting inflammatory pathways in chronic diseases, which would be the best approach for the development of suitable therapeutic agents against chronic diseases. Results: Since the inflammatory response is initiated by numerous signaling molecules like NF-κB, MAPK, and Arachidonic acid pathways, their encountering function can be evaluated with the activation of Nrf2 pathway, a promising approach to inhibit/prevent chronic inflammatory diseases by flavonoids. Over the last few decades, flavonoids drew much attention as a potent alternative therapeutic agent. Recent clinical evidence has shown significant impacts of flavonoids on chronic diseases in different in-vivo and in-vitro models. Conclusion: Flavonoid compounds can interact with chronic inflammatory diseases at the cellular level and modulate the response of protein pathways. A promising approach is needed to overlook suitable alternative compounds providing more therapeutic efficacy and exerting fewer side effects than commercially available antiinflammatory drugs.

Phytosomal Curcumin Elicits Anti-tumor Properties Through Suppression of Angiogenesis, Cell Proliferation and Induction of Oxidative Stress in Colorectal Cancer

2019 ◽  
Vol 24 (39) ◽  
pp. 4626-4638 ◽  
Author(s):  
Reyhaneh Moradi-Marjaneh ◽  
Seyed M. Hassanian ◽  
Farzad Rahmani ◽  
Seyed H. Aghaee-Bakhtiari ◽  
Amir Avan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Colorectal Cancer ◽  
Therapeutic Potential ◽  
Vegf Signaling ◽  
Anticancer Effects ◽  
Inhibition Of Angiogenesis ◽  
Underlying Mechanisms ◽  
Apoptotic Activity

Background: Colorectal cancer (CRC) is one of the most common causes of cancer-associated mortality in the world. Anti-tumor effect of curcumin has been shown in different cancers; however, the therapeutic potential of novel phytosomal curcumin, as well as the underlying molecular mechanism in CRC, has not yet been explored. Methods: The anti-proliferative, anti-migratory and apoptotic activity of phytosomal curcumin in CT26 cells was assessed by MTT assay, wound healing assay and Flow cytometry, respectively. Phytosomal curcumin was also tested for its in-vivo activity in a xenograft mouse model of CRC. In addition, oxidant/antioxidant activity was examined by DCFH-DA assay in vitro, measurement of malondialdehyde (MDA), Thiol and superoxidedismutase (SOD) and catalase (CAT) activity and also evaluation of expression levels of Nrf2 and GCLM by qRT-PCR in tumor tissues. In addition, the effect of phytosomal curcumin on angiogenesis was assessed by the measurement of VEGF-A and VEGFR-1 and VEGF signaling regulatory microRNAs (miRNAs) in tumor tissue. Results: Phytosomal curcumin exerts anti-proliferative, anti-migratory and apoptotic activity in-vitro. It also decreases tumor growth and augmented 5-fluorouracil (5-FU) anti-tumor effect in-vivo. In addition, our data showed that induction of oxidative stress and inhibition of angiogenesis through modulation of VEGF signaling regulatory miRNAs might be underlying mechanisms by which phytosomal curcumin exerted its antitumor effect. Conclusion: Our data confirmed this notion that phytosomal curcumin administrates anticancer effects and can be used as a complementary treatment in clinical settings.

Targeting PPARalpha in Alzheimer's Disease

2018 ◽  
Vol 15 (4) ◽  
pp. 345-354 ◽  
Author(s):  
Barbara D'Orio ◽  
Anna Fracassi ◽  
Maria Paola Cerù ◽  
Sandra Moreno
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Molecular Mechanisms ◽  
Redox Homeostasis ◽  
Antioxidant Response ◽  
Peroxisome Proliferator ◽  
Prevailing Paradigm

Background: The molecular mechanisms underlying Alzheimer's disease (AD) are yet to be fully elucidated. The so-called “amyloid cascade hypothesis” has long been the prevailing paradigm for causation of disease, and is today being revisited in relation to other pathogenic pathways, such as oxidative stress, neuroinflammation and energy dysmetabolism. The peroxisome proliferator-activated receptors (PPARs) are expressed in the central nervous system (CNS) and regulate many physiological processes, such as energy metabolism, neurotransmission, redox homeostasis, autophagy and cell cycle. Among the three isotypes (α, β/δ, γ), PPARγ role is the most extensively studied, while information on α and β/δ are still scanty. However, recent in vitro and in vivo evidence point to PPARα as a promising therapeutic target in AD. Conclusion: This review provides an update on this topic, focussing on the effects of natural or synthetic agonists in modulating pathogenetic mechanisms at AD onset and during its progression. Ligandactivated PPARα inihibits amyloidogenic pathway, Tau hyperphosphorylation and neuroinflammation. Concomitantly, the receptor elicits an enzymatic antioxidant response to oxidative stress, ameliorates glucose and lipid dysmetabolism, and stimulates autophagy.

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