scholarly journals Biochemical Hallmarks of Oxidative Stress-Induced Overactivation of Xenopus Eggs

2019 ◽  
Vol 2019 ◽  
pp. 1-7 ◽  
Author(s):  
Alexander A. Tokmakov ◽  
Misaki Awamura ◽  
Ken-Ichi Sato
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Protein Content ◽  
Molecular Mechanisms ◽  
Low Frequency ◽  
Cytoplasmic Protein ◽  
Lipofuscin Accumulation ◽  
Progressive Development ◽  
Biochemical Analyses ◽  
Dose Dependent

Egg overactivation occurs with a low frequency in the populations of naturally ovulated frog eggs. At present, its natural inducers, molecular mechanisms, and intracellular events remain unknown. Using microscopic and biochemical analyses, we demonstrate here that high levels of hydrogen peroxide-induced oxidative stress can cause time- and dose-dependent overactivation of Xenopus eggs. Lipofuscin accumulation, decrease of soluble cytoplasmic protein content, and depletion of intracellular ATP were found to take place in the overactivated eggs. Progressive development of these processes suggests that egg overactivation unfolds in a sequential and ordered fashion.

scholarly journals Expression of a Heterologous Manganese Superoxide Dismutase Gene in Intestinal Lactobacilli Provides Protection against Hydrogen Peroxide Toxicity

2004 ◽  
Vol 70 (8) ◽  
pp. 4702-4710 ◽  
Author(s):  
Jose M. Bruno-Bárcena ◽  
Jason M. Andrus ◽  
Stephen L. Libby ◽  
Todd R. Klaenhammer ◽  
Hosni M. Hassan
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Manganese Superoxide Dismutase ◽  
Lactobacillus Reuteri ◽  
Shuttle Vector ◽  
Streptococcus Thermophilus ◽  
Gene Encoding ◽  
Superoxide Dismutase Gene ◽  
Living Organisms ◽  
Biochemical Analyses

ABSTRACT In living organisms, exposure to oxygen provokes oxidative stress. A widespread mechanism for protection against oxidative stress is provided by the antioxidant enzymes: superoxide dismutases (SODs) and hydroperoxidases. Generally, these enzymes are not present in Lactobacillus spp. In this study, we examined the potential advantages of providing a heterologous SOD to some of the intestinal lactobacilli. Thus, the gene encoding the manganese-containing SOD (sodA) was cloned from Streptococcus thermophilus AO54 and expressed in four intestinal lactobacilli. A 1.2-kb PCR product containing the sodA gene was cloned into the shuttle vector pTRK563, to yield pSodA, which was functionally expressed and complemented an Escherichia coli strain deficient in Mn and FeSODs. The plasmid, pSodA, was subsequently introduced and expressed in Lactobacillus gasseri NCK334, Lactobacillus johnsonii NCK89, Lactobacillus acidophilus NCK56, and Lactobacillus reuteri NCK932. Molecular and biochemical analyses confirmed the presence of the gene (sodA) and the expression of an active gene product (MnSOD) in these strains of lactobacilli. The specific activities of MnSOD were 6.7, 3.8, 5.8, and 60.7 U/mg of protein for L. gasseri, L. johnsonii, L. acidophilus, and L. reuteri, respectively. The expression of S. thermophilus MnSOD in L. gasseri and L. acidophilus provided protection against hydrogen peroxide stress. The data show that MnSOD protects cells against hydrogen peroxide by removing O2 ·− and preventing the redox cycling of iron. To our best knowledge, this is the first report of a sodA from S. thermophilus being expressed in other lactic acid bacteria.

scholarly journals Amaranth Leaf Extract Protects Against Hydrogen Peroxide Induced Oxidative Stress in Drosophila Melanogaster

2021 ◽  
Author(s):  
Johnmark Ndinawe ◽  
Hellen W. Kinyi
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Antioxidant Activity ◽  
Ascorbic Acid ◽  
Drosophila Melanogaster ◽  
Leaf Extract ◽  
Dependent Manner ◽  
Polyphenol Compounds ◽  
Dose Dependent

Abstract ObjectiveAmaranths leaves are rich in ascorbic acid and polyphenol compounds which have antioxidant activity. The aim of this study was to evaluate their in vivo antioxidant activity. The effect of consumption of Amaranth leaf extract on in vivo antioxidant activity, catalase enzyme activity and H2O2 induced oxidative stress in Drosophila melanogaster flies was assessed.ResultsConsumption of Amaranth leaf extract was associated with increased survival on exposure to H202 in a dose dependent manner in Drosophila melanogaster flies.

scholarly journals Low Doses of Imidacloprid Induce Oxidative Stress and Neural Cell Disruption in Earthworm Eisenia fetida

2021 ◽  
Vol 84 ◽  
pp. 1-11
Author(s):  
Artem Huslystyi ◽  
Victor Nedzvetsky ◽  
Serhii Yermolenko ◽  
Viktor Gasso ◽  
Vladyslav Petrushevskyi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nervous System ◽  
Molecular Mechanisms ◽  
Neuron Specific Enolase ◽  
Stress Generation ◽  
Low Doses ◽  
Neuronal Marker ◽  
Dose Dependent Decrease ◽  
Species Production ◽  
Dose Dependent

Imidacloprid is a widely used pesticide that belongs to the class of neonicotinoids. There is a piece of rising evidence that neonicotinoids exert cytotoxic effects in non-target organisms including vertebrate species such as mammals. Nevertheless, dose-limiting toxicity and molecular mechanisms of neonicotinoids' deleterious effects are still poorly understood. In accord to imidacloprid fate in the environment, the most of used pesticide is absorbed in the soil. Therefore, earthworms, which are prevailing soil organisms, could be considered as a target of neonicotinoids toxicity. The earthworm’s simple nervous system is a prospective model for neurotoxicological studies. We exposed earthworms to imidacloprid in a paper contact test with a doses range of 0.1‑0.4 µg/cm2 for 14 days. In the present work, we studied the imidacloprid effect on oxidative stress generation and neuronal marker neuron-specific enolase (NSE) expression. The exposure to imidacloprid induced a dose-dependent decrease in NSE. Both reactive oxygen species production and lipid peroxidation level were upregulated as well. Observed NSE decline suggests imidacloprid-caused disturbance in earthworm neuron cells. Obtained data have shown that relatively low doses of imidacloprid are potent to induce cytotoxicity in neurons. Furthermore, neurotoxicity could be recognized as one of an individual scenario of the general imidacloprid toxicity. Thus, presented results suggest the cytotoxicity of imidacloprid low doses in non-target organisms and hypothesize that NSE downregulation could be estimated as a biomarker of neonicotinoid cytotoxicity in a nervous system of non-insect species.

scholarly journals Effects of Low-Dose versus High-Doseγ-Tocotrienol on the Bone Cells Exposed to the Hydrogen Peroxide-Induced Oxidative Stress and Apoptosis

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Nizar Abd Manan ◽  
Norazlina Mohamed ◽  
Ahmad Nazrun Shuid
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Antioxidant Enzymes ◽  
Low Dose ◽  
Bone Cells ◽  
Dependent Manner ◽  
Low Doses ◽  
Antioxidant Enzymes Activities ◽  
High Doses ◽  
Dose Dependent

Oxidative stress and apoptosis can disrupt the bone formation activity of osteoblasts which can lead to osteoporosis. This study was conducted to investigate the effects ofγ-tocotrienol on lipid peroxidation, antioxidant enzymes activities, and apoptosis of osteoblast exposed to hydrogen peroxide (H2O2). Osteoblasts were treated with 1, 10, and 100 μM ofγ-tocotrienol for 24 hours before being exposed to 490 μM (IC50) H2O2for 2 hours. Results showed thatγ-tocotrienol prevented the malondialdehyde (MDA) elevation induced by H2O2in a dose-dependent manner. As for the antioxidant enzymes assays, all doses ofγ-tocotrienol were able to prevent the reduction in SOD and CAT activities, but only the dose of 1 μM of GTT was able to prevent the reduction in GPx. As for the apoptosis assays,γ-tocotrienol was able to reduce apoptosis at the dose of 1 and 10 μM. However, the dose of 100 μM ofγ-tocotrienol induced an even higher apoptosis than H2O2. In conclusion, low doses ofγ-tocotrienol offered protection for osteoblasts against H2O2toxicity, but itself caused toxicity at the high doses.

scholarly journals Manmade Electromagnetic Fields and Oxidative Stress—Biological Effects and Consequences for Health

2021 ◽  
Vol 22 (7) ◽  
pp. 3772
Author(s):  
David Schuermann ◽  
Meike Mevissen
Keyword(s):  
Oxidative Stress ◽  
Electromagnetic Fields ◽  
Communication Systems ◽  
Genome Stability ◽  
Molecular Mechanisms ◽  
Biological Effects ◽  
Experimental Studies ◽  
Low Frequency ◽  
International Agency ◽  
Extremely Low Frequency

Concomitant with the ever-expanding use of electrical appliances and mobile communication systems, public and occupational exposure to electromagnetic fields (EMF) in the extremely-low-frequency and radiofrequency range has become a widely debated environmental risk factor for health. Radiofrequency (RF) EMF and extremely-low-frequency (ELF) MF have been classified as possibly carcinogenic to humans (Group 2B) by the International Agency for Research on Cancer (IARC). The production of reactive oxygen species (ROS), potentially leading to cellular or systemic oxidative stress, was frequently found to be influenced by EMF exposure in animals and cells. In this review, we summarize key experimental findings on oxidative stress related to EMF exposure from animal and cell studies of the last decade. The observations are discussed in the context of molecular mechanisms and functionalities relevant to health such as neurological function, genome stability, immune response, and reproduction. Most animal and many cell studies showed increased oxidative stress caused by RF-EMF and ELF-MF. In order to estimate the risk for human health by manmade exposure, experimental studies in humans and epidemiological studies need to be considered as well.

scholarly journals The Antioxidant Enzymes Activity From the Poly-extromophilic Yarrowia lipolytica Yeast Under Oxidative Stress During Long-lasting Cultivation

2020 ◽  
Vol 6 (12) ◽  
pp. 23-35
Author(s):  
V. Sekova ◽  
E. Bobrova ◽  
E. Isakova ◽  
Yu. Deryabina
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Yarrowia Lipolytica ◽  
Growth Stage ◽  
Redox Status ◽  
Stationary Growth ◽  
Signaling Mechanisms ◽  
The Impact ◽  
Dose Dependent ◽  
Logarithmic Growth

Hydrogen peroxide is one of the most widespread reactive oxygen species, which can diffuse through cell membranes, causing changes in the redox status of cells and the development of oxidative stress. The results show that the effects caused by hydrogen peroxide are dose-dependent and can lead to both damage to cells and an increase in their resistance to oxidative stress. In this study, we assayed the effect of various concentrations of H2O2 on the redox status of the Yarrowia lipolytica yeast during long-lasting cultivation. The oxidant application to the cells in the logarithmic growth stage was shown to delay the impact on the ROS level in the late stationary growth stage. In this case, the dependence of the injected concentration on the redox status is not linear, which suggests triggering different signaling mechanisms by various concentrations of the oxidant.

Induction of Oxidative Stress and Glutathione Depletion by ABT-737, a Novel Small Molecule Inhibitor of Bcl-2, Contributes to Cytotoxicity in Leukemia Cells.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 4336-4336
Author(s):  
Joya Chandra ◽  
Adrienne Howard ◽  
Kathleen Jensen ◽  
Ray Meyn
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Cell Death ◽  
Small Molecule ◽  
Buthionine Sulfoximine ◽  
Redox Status ◽  
Lymphocytic Leukemia ◽  
Glutathione Depletion ◽  
Dose Dependent Increase ◽  
Dose Dependent

Abstract The Bcl-2 family of proteins regulate the process of cell death. Bcl-2 and Bcl-xL are potent anti-apoptotic members that are overexpressed in a number of malignancies, providing a means to evade cell death, which has been described as a characteristic hallmark of cancer. Several lines of evidence suggest that Bcl-2 and Bcl-xL possess anti-oxidant properties. Overexpression of Bcl-2 is protective against menadione and hydrogen peroxide induced cell death and causes an increase in intracellular levels of glutathione (GSH), the most abundant antioxidant defense. In the present study, we utilized a novel small molecule to test effects of Bcl-2 inhibition on intracellular redox status. ABT-737 is a first generation inhibitor of Bcl-2, Bcl-xL and Bcl-w and and acts as a mimic of the BH3-only antagonists of these family members. Exposure of acute lymphocytic leukemia (ALL) cells to ABT-737 caused a dose dependent increase in intracellular levels reactive oxygen species (ROS), namely superoxide and hydrogen peroxide. This dose dependent increase in intracellular oxidants was significantly less pronounced in cells treated with the less active enantiomer of ABT-737. A greater than 50% decrease in intracellular GSH levels was seen with similar doses of ABT-737 and the combination of buthionine sulfoximine, an agent that depletes GSH levels further, with ABT-737, caused synergistic cell death. These data were verified using cells transfected with a tetracycline repressable Bcl-2 expression plasmid. Taken together, our data identifies a novel sequelae for Bcl-2 inhibition: the induction of oxidative stress. Combination therapies utilizing ABT-737 or its analogs may be devised based on the observed effects on the redox environment.

scholarly journals Amaranth leaf extract protects against hydrogen peroxide induced oxidative stress in Drosophila melanogaster

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Ndinawe Johnmark ◽  
Hellen W. Kinyi
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Antioxidant Activity ◽  
Drosophila Melanogaster ◽  
Leaf Extract ◽  
Ethanolic Extract ◽  
Dependent Manner ◽  
Polyphenol Compounds ◽  
Dose Dependent

Abstract Objective Amaranths leaves are rich in ascorbic acid and polyphenol compounds which have antioxidant activity. The aim of this study was to evaluate their in vivo antioxidant activity. The effect of consumption of Amaranth leaf extract on in vivo antioxidant activity, catalase enzyme activity and H2O2 induced oxidative stress in Drosophila melanogaster flies was assessed. Results Consumption of Amaranth leaf extract was associated with increased survival on exposure to H2o2 in a dose dependent manner in Drosophila melanogaster flies. The study concludes that the ethanolic extract of Amaranth leaves offer protection against hydrogen peroxide-induced oxidative stress.

scholarly journals The Peroxisome-Autophagy Redox Connection: A Double-Edged Sword?

2021 ◽  
Vol 9 ◽  
Author(s):  
Hongli Li ◽  
Celien Lismont ◽  
Iulia Revenco ◽  
Mohamed A. F. Hussein ◽  
Cláudio F. Costa ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Molecular Mechanisms ◽  
Protective Role ◽  
Local Concentration ◽  
Comprehensive Overview ◽  
Selective Autophagy ◽  
Bidirectional Relationship ◽  
Health And Disease ◽  
To Receive

Peroxisomes harbor numerous enzymes that can produce or degrade hydrogen peroxide (H2O2). Depending on its local concentration and environment, this oxidant can function as a redox signaling molecule or cause stochastic oxidative damage. Currently, it is well-accepted that dysfunctional peroxisomes are selectively removed by the autophagy-lysosome pathway. This process, known as “pexophagy,” may serve a protective role in curbing peroxisome-derived oxidative stress. Peroxisomes also have the intrinsic ability to mediate and modulate H2O2-driven processes, including (selective) autophagy. However, the molecular mechanisms underlying these phenomena are multifaceted and have only recently begun to receive the attention they deserve. This review provides a comprehensive overview of what is known about the bidirectional relationship between peroxisomal H2O2 metabolism and (selective) autophagy. After introducing the general concepts of (selective) autophagy, we critically examine the emerging roles of H2O2 as one of the key modulators of the lysosome-dependent catabolic program. In addition, we explore possible relationships among peroxisome functioning, cellular H2O2 levels, and autophagic signaling in health and disease. Finally, we highlight the most important challenges that need to be tackled to understand how alterations in peroxisomal H2O2 metabolism contribute to autophagy-related disorders.

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