scholarly journals Effect of Alkaloid Extract from African Jointfir (Gnetum africanum) Leaves on Manganese-Induced Toxicity in Drosophila melanogaster

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Ganiyu Oboh ◽  
Opeyemi Babatunde Ogunsuyi ◽  
Olatunde Isaac Awonyemi ◽  
Victor Ayomide Atoki
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Drosophila Melanogaster ◽  
Survival Rate ◽  
Ache Activity ◽  
Fruit Fly ◽  
Locomotor Performance ◽  
Oxygen Species ◽  
Novel Therapies ◽  
Wild Type

Metal-induced toxicity in fruit fly (Drosophila melanogaster) is one of the established models for studying neurotoxicity and neurodegenerative diseases. Phytochemicals, especially alkaloids, have been reported to exhibit neuroprotection. Here, we assessed the protective effect of alkaloid extract from African Jointfir (Gnetum africanum) leaf on manganese- (Mn-) induced toxicity in wild type fruit fly. Flies were exposed to 10 mM Mn, the alkaloid extract and cotreatment of Mn plus extract, respectively. The survival rate and locomotor performance of the flies were assessed 5 days posttreatment, at which point the flies were homogenized and assayed for acetylcholinesterase (AChE) activity, nitric oxide (NO), and reactive oxygen species (ROS) levels. Results showed that the extract significantly reverted Mn-induced reduction in the survival rate and locomotor performance of the flies. Furthermore, the extract counteracted the Mn-induced elevation in AChE activity, NO, and ROS levels. The alkaloid extract of the African Jointfir leaf may hence be a source of useful phytochemicals for the development of novel therapies for the management of neurodegeneration.

scholarly journals Production and scavenging of reactive oxygen species both affect reproductive success in male and female Drosophila melanogaster

2021 ◽  
Author(s):  
Biz R. Turnell ◽  
Luisa Kumpitsch ◽  
Klaus Reinhardt
Keyword(s):  
Reactive Oxygen Species ◽  
Drosophila Melanogaster ◽  
Reactive Oxygen ◽  
Cellular Aging ◽  
Ros Production ◽  
Oxygen Species ◽  
Wild Type ◽  
Ros Scavenging ◽  
Respiratory Pathway ◽  
Male And Female

AbstractSperm aging is accelerated by the buildup of reactive oxygen species (ROS), which cause oxidative damage to various cellular components. Aging can be slowed by limiting the production of mitochondrial ROS and by increasing the production of antioxidants, both of which can be generated in the sperm cell itself or in the surrounding somatic tissues of the male and female reproductive tracts. However, few studies have compared the separate contributions of ROS production and ROS scavenging to sperm aging, or to cellular aging in general. We measured reproductive fitness in two lines of Drosophila melanogaster genetically engineered to (1) produce fewer ROS via expression of alternative oxidase (AOX), an alternative respiratory pathway; or (2) scavenge fewer ROS due to a loss-of-function mutation in the antioxidant gene dj-1β. Wild-type females mated to AOX males had increased fecundity and longer fertility durations, consistent with slower aging in AOX sperm. Contrary to expectations, fitness was not reduced in wild-type females mated to dj-1β males. Fecundity and fertility duration were increased in AOX and decreased in dj-1β females, indicating that female ROS levels may affect aging rates in stored sperm and/or eggs. Finally, we found evidence that accelerated aging in dj-1β sperm may have selected for more frequent mating. Our results help to clarify the relative roles of ROS production and ROS scavenging in the male and female reproductive systems.

scholarly journals Somatic production of reactive oxygen species does not predict its production in sperm cells across Drosophila melanogaster lines

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Biz R. Turnell ◽  
Luisa Kumpitsch ◽  
Anne-Cécile Ribou ◽  
Klaus Reinhardt
Keyword(s):  
Reactive Oxygen Species ◽  
Drosophila Melanogaster ◽  
Reactive Oxygen ◽  
Future Research ◽  
Ros Production ◽  
Oxygen Species ◽  
Loss Of Function ◽  
Wild Type ◽  
Ros Scavenging ◽  
Transport Chain

Abstract Objective Sperm ageing has major evolutionary implications but has received comparatively little attention. Ageing in sperm and other cells is driven largely by oxidative damage from reactive oxygen species (ROS) generated by the mitochondria. Rates of organismal ageing differ across species and are theorized to be linked to somatic ROS levels. However, it is unknown whether sperm ageing rates are correlated with organismal ageing rates. Here, we investigate this question by comparing sperm ROS production in four lines of Drosophila melanogaster that have previously been shown to differ in somatic mitochondrial ROS production, including two commonly used wild-type lines and two lines with genetic modifications standardly used in ageing research. Results Somatic ROS production was previously shown to be lower in wild-type Oregon-R than in wild-type Dahomey flies; decreased by the expression of alternative oxidase (AOX), a protein that shortens the electron transport chain; and increased by a loss-of-function mutation in dj-1β, a gene involved in ROS scavenging. Contrary to predictions, we found no differences among these four lines in the rate of sperm ROS production. We discuss the implications of our results, the limitations of our study, and possible directions for future research.

scholarly journals Endotoxin Engages Mitochondrial Quality Control via an iNOS-Reactive Oxygen Species Signaling Pathway in Hepatocytes

2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Anthony Cyr ◽  
Lauran Chambers ◽  
Paul K. Waltz ◽  
Sean P. Whelan ◽  
Lauryn Kohut ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Quality Control ◽  
Mitochondrial Biogenesis ◽  
Organ Injury ◽  
Oxygen Species ◽  
Wild Type ◽  
Mitochondrial Quality Control

Background. Organ injury and dysfunction in sepsis accounts for significant morbidity and mortality. Adaptive cellular responses in the setting of sepsis prevent injury and allow for organ recovery. We and others have shown that part of the adaptive response includes regulation of cellular respiration and maintenance of a healthy mitochondrial population. Herein, we hypothesized that endotoxin-induced changes in hepatocyte mitochondrial respiration and homeostasis are regulated by an inducible nitric oxide synthase/nitric oxide (iNOS/NO)-mitochondrial reactive oxygen species (mtROS) signaling axis, involving activation of the NRF2 signaling pathway. Methods. Wild-type (C57Bl/6) or iNos-/- male mice were subjected to intraperitoneal lipopolysaccharide (LPS) injections to simulate endotoxemia. Individual mice were randomized to treatment with NO-releasing agent DPTA-NONOate, mtROS scavenger MitoTEMPO, or vehicle controls. Other mice were treated with scramble or Nrf2-specific siRNA via tail vein injection. Primary murine hepatocytes were utilized for in vitro studies with or without LPS stimulation. Oxygen consumption rates were measured to establish mitochondrial respiratory parameters. Western blotting, confocal microscopy with immunocytochemistry, and rtPCR were performed for analysis of iNOS as well as markers of both autophagy and mitochondrial biogenesis. Results. LPS treatment inhibited aerobic respiration in vitro in wild-type but not iNos-/- cells. Experimental endotoxemia in vivo or in vitro induced iNOS protein and mtROS production. However, induction of mtROS was dependent on iNOS expression. Furthermore, LPS-induced hepatic autophagy/mitophagy and mitochondrial biogenesis were significantly attenuated in iNos-/- mice or cells with NO or mtROS scavenging. These responses were rescued in iNos-/- mice via delivery of NO both in vivo and in vitro. Conclusions. These data suggest that regulation of mitochondrial quality control following hepatocyte LPS exposure is dependent at least in part on a NO-mtROS signaling network. Further investigation to identify specific agents that modulate this process may facilitate the prevention of organ injury in sepsis.

scholarly journals Loss of Autophagy Leads to Megakaryocytes Differentiation Failure and Defective Platelets Function

Blood ◽  
2014 ◽  
Vol 124 (21) ◽  
pp. 4148-4148 ◽  
Author(s):  
Yan Cao ◽  
Jinyang Cai ◽  
Xin Li ◽  
Yixuan Fang ◽  
Suping Zhang ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Flow Cytometry ◽  
Ache Activity ◽  
Bleeding Time ◽  
Biological Effects ◽  
Oxygen Species ◽  
Wild Type ◽  
Megakaryocytic Differentiation

Abstract Background Megakaryocytes (MKs), large progenitor cells residing in the bone marrow, are the source of platelets. In 2009, Colosetti P et al. reported that PMA and SB could induce megakaryocytic differentiation of the chronic myelogenous leukemia cell line K562 by triggering autophagy. It gives us the first insight of autophagy induction in in vitro megakaryocytic differentiation. Although Feng W et al. reported autophagy also exists in human platelets, the role of autophagy in megakaryocyte-platelet commitment axis remains poorly understood. In this study, we elucidated the biological effects of autophagy deficiency on megakaryopoiesis and thrombosis using hematopoietic system conditionally atg7 knockout mice. Methods and Materials To evaluate the biological effects of autophagy deficiency on platelets, the following experiments were performed: (1) complete blood count of wild type and atg7-/- mice, (2) the tail bleeding time assay of wild type and Atg7-/- mice, (3) the effect of atg7 knockout on platelet aggregation and activation of CD62P and JON/A (αIIbβ3) were analyzed by flow cytometry. To assess whether the observed changes in platelets of atg7-/- mice result in aberrations of megakaryopoiesis, the following experiments were performed: (1) the percentage of BM CD41+CD61+ cells was analyzed by flow cytometry, (2) the AchE activity assay of platelets and murine BM Lin- cells cultured with murine TPO and SCF, (3) Morphology of megakaryocytes derived from BM Lin- cells was evaluated by Wright-Giemsa staining, (4) megakaryocytic differentiation from BM Lin- cells was evaluated by CD41/forward-scatter (FSC) dot plot. To evaluate the role of reactive oxygen species in MK differentiation, the Lin- cells were stained with MitoTracker Green and MitoSox Red and then analyzed by flow cytometry. Results (1) The number of platelets in the peripheral blood of atg7-/- mice was significantly decreased (WT: 904.2±75.5, Atg7+/-: 942.8±136.3, Atg7-/-: 330.5±282.2, p<0.01), while the size of platelets (MPV) was increased compared with WT mice (WT: 5.6±0.1, Atg7+/-: 5.7±0.1, atg7-/-: 6.8±0.5, p<0.01). (2) The bleeding time was significantly longer (WT: 51.5±14.8s, Atg7-/-: 915.2±282.9s, p<0.01) and thrombin-induced platelet aggregation was decreased (WT: 97.5±2.5, Atg7+/-: 62.5±7.5, Atg7-/-: 7.75±7.25, p<0.05) in Atg7-/- mice than in wild-type mice. (3) The activation of CD62P (WT: 14.5±0.09, atg7+/-: 11.17±0.06, atg7-/-: 3.2±0.03, p<0.01) and JON/A (αIIbβ3) (WT: 48.1±0.1, atg7+/-: 13.5±0.1, atg7-/-: 5.9±0.2, p<0.01) was decreased in atg7-/- platelets. These results indicated that atg7-dependent autophagy is important for thrombosis and platelet function. (4) The percentage of CD41+CD61+ cells was decreased in bone marrow of atg7-/- mice (WT: 30.4±0.6, atg7+/-: 27.9±1.3, atg7-/-: 18.9±0.3, p<0.01). (5) In mice lacking autophagy, both the Lin- cells stimulated by TPO (WT: 0.35±0.03, atg7-/-: 0.22±0.05, p<0.01) and the platelets collected through the inferior vena cava (WT: 0.099±0.005, atg7-/-: 0.05±0.009, p<0.01) had significantly lower AChE activity compared with WT mice. (6) Low level of CD41+/FSChigh cells were seen in the in vitro culture of atg7-/- BM Lin- cells with TPO and SCF ( WT:5.6±2.2, Atg7-/-: 0.2±0.03, p<0.01). These results reflected a significant reduction in MK differentiation from autophagy defective hematopoietic progenitors. An accumulation of mitochondria (WT: 547.3±7.0, atg7-/-: 737.8±126.6, p<0.01) and mitochondrial superoxide (WT: 280.2±4.8, atg7-/-: 343.8±42.4, p<0.05) was found in atg7-/- BM Lin- cells, which may severely disturb the progress of MK differentiation. Conclusion Autophagy is essential for the megakaryopoiesis and thrombosis by maintaining mitochondrial homeostasis. Elevated reactive oxygen species might be the cause of megakaryocytic differentiation blockade. Disclosures No relevant conflicts of interest to declare.

Accelerated endothelial dysfunction in mild prediabetic insulin resistance: the early role of reactive oxygen species

2007 ◽  
Vol 293 (5) ◽  
pp. E1311-E1319 ◽  
Author(s):  
Edward R. Duncan ◽  
Simon J. Walker ◽  
Vivienne A. Ezzat ◽  
Stephen B. Wheatcroft ◽  
Jian-Mei Li ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Insulin Resistance ◽  
Reactive Oxygen Species ◽  
Type 2 Diabetes ◽  
Endothelial Dysfunction ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Wild Type

Insulin resistance is well established as an independent risk factor for the development of type 2 diabetes and cardiovascular atherosclerosis. Most studies have examined atherogenesis in models of severe insulin resistance or diabetes. However, by the time of diagnosis, individuals with type 2 diabetes already demonstrate a significant atheroma burden. Furthermore, recent studies suggest that, even in adolescence, insulin resistance is a progressive disorder that increases cardiovascular risk. In the present report, we studied early mechanisms of reduction in the bioavailability of the antiatheroscerotic molecule nitric oxide (NO) in very mild insulin resistance. Mice with haploinsufficiency for the insulin receptor (IRKO) are a model of mild insulin resistance with preserved glycemic control. We previously demonstrated that 2-mo-old (Young) IRKO mice have preserved vasorelaxation responses to ACh. This remained the case at 4 mo of age. However, by 6 mo, despite no significant deterioration in glucose homeostasis (Adult), IRKO mice had marked blunting of ACh-mediated vasorelaxation [IRKO maximum contraction response (Emax) 66 ± 5% vs. wild type 87 ± 4%, P < 0.01]. Despite the endothelial dysfunction demonstrated, aortic endothelial nitric oxide synthase (eNOS) mRNA levels were similar in Adult IRKO and wild-type mice, and, interestingly, aortic eNOS protein levels were increased, suggesting a compensatory upregulation in the IRKO. We then examined the potential role of reactive oxygen species in mediating early endothelial dysfunction. The superoxide dismutase mimetic Mn(III)tetrakis(1-methyl-4-pyridyl) porphyrin pentachloride (MnTMPyP) restored ACh relaxation responses in the Adult IRKO (Emax to ACh with MnTMPyP 85 ± 5%). Dihydroethidium fluorescence of aortas and isolated coronary microvascular endothelial cells confirmed a substantial increase in endothelium-derived reactive oxygen species in IRKO mice. These data demonstrate that mild insulin resistance is a potent substrate for accelerated endothelial dysfunction and support a role for endothelial cell superoxide production as a mechanism underlying the early reduction in NO bioavailability.

scholarly journals Neither Neutrophils nor Reactive Oxygen Species Contribute to Tissue Damage during Pneumocystis Pneumonia in Mice

2004 ◽  
Vol 72 (10) ◽  
pp. 5722-5732 ◽  
Author(s):  
Steve D. Swain ◽  
Terry W. Wright ◽  
Peter M. Degel ◽  
Francis Gigliotti ◽  
Allen G. Harmsen
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Knockout Mice ◽  
Tissue Damage ◽  
Reactive Oxygen ◽  
Lung Damage ◽  
Arterial Oxygen ◽  
Oxygen Species ◽  
Wild Type ◽  
Pulmonary Damage

ABSTRACT Neutrophils are implicated in the damage of lung tissue in many disease states, including infectious diseases and environmental insults. These effects may be due to oxidative or nonoxidative functions of the neutrophil or both. We examined the role of neutrophils in pulmonary damage during infection with the opportunistic fungal pathogen Pneumocystis sp. in four mouse models of neutrophil dysfunction. These were (i) a knockout of the gp91phox component of NADPH oxidase, in which reactive oxygen species (ROS) production is greatly reduced; (ii) a double knockout of gp91phox and inducible nitric oxide synthase, in which ROS and nitric oxide production is greatly decreased; (iii) a knockout of the chemokine receptor CXCR2, in which accumulation of intra-alveolar neutrophils is severely diminished; and (iv) antibody depletion of circulating neutrophils in wild-type mice with the monoclonal antibody RB6. Surprisingly, in each case, indicators of pulmonary damage (respiratory rates, arterial oxygen partial pressures, and intra-alveolar albumin concentrations) were the same in knockout mice and comparable wild-type mice. Therefore, whereas neutrophils are a valid correlative marker of lung damage during Pneumocystis infection, neither neutrophils nor ROS appear to be the causative agent of tissue damage. We also show that there is no difference in Pneumocystis burdens between wild-type and knockout mice, which supports the idea that neutrophils do not have a major role in the clearance of this organism.

The Role of Reactive Oxygen Species, Kinases, Hydrogen Sulfide, and Nitric Oxide in the Regulation of Autophagy and Their Impact on Ischemia and Reperfusion Injury in the Heart

2020 ◽  
Vol 16 ◽  
Author(s):  
Andrey Krylatov ◽  
Leonid Maslov ◽  
Sergey Y. Tsibulnikov ◽  
Nikita Voronkov ◽  
Alla Boshchenko ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Hydrogen Sulfide ◽  
Ischemia Reperfusion ◽  
Reactive Oxygen ◽  
Ischemia And Reperfusion ◽  
Oxygen Species ◽  
Ischemia And Reperfusion Injury ◽  
Adaptive Process

: There is considerable evidence in the heart that autophagy in cardiomyocytes is activated by hypoxia/reoxygenation (H/R) or in hearts by ischemia/reperfusion (I/R). Depending upon the experimental model and duration of ischemia, increases in autophagy in this setting maybe beneficial (cardioprotective) or deleterious (exacerbate I/R injury). Aside from the conundrum as to whether or not autophagy is an adaptive process, it is clearly regulated by a number of diverse molecules including reactive oxygen species (ROS), various kinases, hydrogen sulfide (H2S) and nitric oxide (NO). The purpose this review is to address briefly the controversy regarding the role of autophagy in this setting and to examine a variety of disparate molecules that are involved in its regulation.

Plasmonic Enhancement of Nitric Oxide Generation

Nanoscale ◽  
2021 ◽  
Author(s):  
Rachael Knoblauch ◽  
Chris Geddes
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Reactive Nitrogen Species ◽  
Reactive Oxygen ◽  
Reactive Nitrogen ◽  
Oxygen Species ◽  
Nitrogen Species ◽  
Plasmonic Enhancement ◽  
Cancer Treatments

While the utility of reactive oxygen species in photodynamic therapies for both cancer treatments and antimicrobial applications has received much attention, the inherent potential of reactive nitrogen species (RNS) including...

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