Adaptations to oxidative stress in Zea mays roots under short-term Pb2+ exposure

Biologia ◽  
2015 ◽  
Vol 70 (2) ◽  
Author(s):  
Gurpreet Kaur ◽  
Harminder Pal Singh ◽  
Daizy Rani Batish ◽  
Ravinder Kumar Kohli
Keyword(s):  
Oxidative Stress ◽  
Zea Mays ◽  
Toxic Effect ◽  
Contaminated Soils ◽  
Sharp Decrease ◽  
Crop Productivity ◽  
Animal Life ◽  
Short Term

AbstractLead (Pb), a widespread contaminant in terrestrial landscape, is highly detrimental to plant and animal life. Specifically, Pb-contaminated soils cause a sharp decrease in crop productivity, thereby posing a serious risk to agriculture. A study was planned to investigate the toxic effect of Pb

scholarly journals Oxidative Stress, Glutathione Metabolism, and Liver Regeneration Pathways Are Activated in Hereditary Tyrosinemia Type 1 Mice upon Short-Term Nitisinone Discontinuation

Genes ◽  
2020 ◽  
Vol 12 (1) ◽  
pp. 3
Author(s):  
Haaike Colemonts-Vroninks ◽  
Jessie Neuckermans ◽  
Lionel Marcelis ◽  
Paul Claes ◽  
Steven Branson ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stress Response ◽  
Liver Regeneration ◽  
The Body ◽  
Glutathione Metabolism ◽  
Short Term ◽  
Therapeutic Regime ◽  
Tyrosinemia Type 1 ◽  
Hereditary Tyrosinemia

Hereditary tyrosinemia type 1 (HT1) is an inherited condition in which the body is unable to break down the amino acid tyrosine due to mutations in the fumarylacetoacetate hydrolase (FAH) gene, coding for the final enzyme of the tyrosine degradation pathway. As a consequence, HT1 patients accumulate toxic tyrosine derivatives causing severe liver damage. Since its introduction, the drug nitisinone (NTBC) has offered a life-saving treatment that inhibits the upstream enzyme 4-hydroxyphenylpyruvate dioxygenase (HPD), thereby preventing production of downstream toxic metabolites. However, HT1 patients under NTBC therapy remain unable to degrade tyrosine. To control the disease and side-effects of the drug, HT1 patients need to take NTBC as an adjunct to a lifelong tyrosine and phenylalanine restricted diet. As a consequence of this strict therapeutic regime, drug compliance issues can arise with significant influence on patient health. In this study, we investigated the molecular impact of short-term NTBC therapy discontinuation on liver tissue of Fah-deficient mice. We found that after seven days of NTBC withdrawal, molecular pathways related to oxidative stress, glutathione metabolism, and liver regeneration were mostly affected. More specifically, NRF2-mediated oxidative stress response and several toxicological gene classes related to reactive oxygen species metabolism were significantly modulated. We observed that the expression of several key glutathione metabolism related genes including Slc7a11 and Ggt1 was highly increased after short-term NTBC therapy deprivation. This stress response was associated with the transcriptional activation of several markers of liver progenitor cells including Atf3, Cyr61, Ddr1, Epcam, Elovl7, and Glis3, indicating a concreted activation of liver regeneration early after NTBC withdrawal.

Effect of Short-Term Temperature Increase on the Performance of a Mesophilic UASB Reactor

1990 ◽  
Vol 22 (9) ◽  
pp. 183-190 ◽  
Author(s):  
J. B. van Lier ◽  
J. Rintala ◽  
J. L. Sanz Martin ◽  
G. Lettinga
Keyword(s):  
Sharp Decrease ◽  
Methanogenic Bacteria ◽  
Decay Rates ◽  
Uasb Reactor ◽  
Short Term ◽  
Retention Capacity ◽  
Temperature Shock ◽  
Biomass Retention ◽  
Propionate Oxidation ◽  
Ph Decrease

A study was carried out to assess the effects of short-term temperature increments on the treatment efficiency and methane production of UASB reactors at a working temperature of 37-39°C. Two different substrates were used to determine the effects on the several bacterial groups involved in the digestion process. One reactor was fed with defined synthetic acidified wastewater the other with unacidified wastewaler from a distillery process. Shocks of 5-24 hrs were applied at temperatures in the range of 45 to 61°C. Up to 45°C no detrimental effects were noticeable. Higher temperatures led to a sharp decrease of the activity of the different microbial populations as a result of elevated decay rates. Propionate oxidation turned out to be the most sensitive for temperature increments, whereas the acidogenic bacteria were least affected. Temperature shocks of 55 and 61°C led to a decrease of 50% of the overall efficiency after 10 and 3 hrs, respectively. By means of batch experiments decay rates of 0.44 and > 10 hr −1 of the methanogenic bacteria were estimated at 55 and 65°C respectively. As temporary inactivation of the mesophilic bacteria during a temperature shock was found to be unlikely, reactor recovery is dependent on the bacterial growth and the biomass retention capacity of the reactor. When unacidified wastewater is treated, a pH decrease has to be considered during a temperature shock.

Alfalfa plant-derived biostimulant stimulate short-term growth of salt stressed Zea mays L. plants

2012 ◽  
Vol 364 (1-2) ◽  
pp. 145-158 ◽  
Author(s):  
Andrea Ertani ◽  
Michela Schiavon ◽  
Adele Muscolo ◽  
Serenella Nardi
Keyword(s):  
Zea Mays ◽  
Zea Mays L ◽  
Short Term ◽  
Alfalfa Plant

Short-term high-fat feeding exacerbates degeneration in retinitis pigmentosa by promoting retinal oxidative stress and inflammation

2021 ◽  
Vol 118 (43) ◽  
pp. e2100566118
Author(s):  
Oksana Kutsyr ◽  
Agustina Noailles ◽  
Natalia Martínez-Gil ◽  
Lucía Maestre-Carballa ◽  
Manuel Martinez-Garcia ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Retinitis Pigmentosa ◽  
Retinal Degeneration ◽  
Gut Microbiome ◽  
Cell Activation ◽  
High Fat ◽  
Short Term ◽  
Oxidative Markers ◽  
Degenerative Disorders ◽  
Inflammatory State

A high-fat diet (HFD) can induce hyperglycemia and metabolic syndromes that, in turn, can trigger visual impairment. To evaluate the acute effects of HFD feeding on retinal degeneration, we assessed retinal function and morphology, inflammatory state, oxidative stress, and gut microbiome in dystrophic retinal degeneration 10 (rd10) mice, a model of retinitis pigmentosa, fed an HFD for 2 to 3 wk. Short-term HFD feeding impaired retinal responsiveness and visual acuity and enhanced photoreceptor degeneration, microglial cell activation, and Müller cell gliosis. HFD consumption also triggered the expression of inflammatory and oxidative markers in rd10 retinas. Finally, an HFD caused gut microbiome dysbiosis, increasing the abundance of potentially proinflammatory bacteria. Thus, HFD feeding drives the pathological processes of retinal degeneration by promoting oxidative stress and activating inflammatory-related pathways. Our findings suggest that consumption of an HFD could accelerate the progression of the disease in patients with retinal degenerative disorders.

SHORT-TERM RESPONSES TO CADMIUM EXPOSURE IN THE ESTUARINE POLYCHAETE LAEONEREIS ACUTA (POLYCHAETA, NEREIDIDAE): SUBCELLULAR DISTRIBUTION AND OXIDATIVE STRESS GENERATION

2006 ◽  
Vol 25 (5) ◽  
pp. 1337 ◽  
Author(s):  
Juliana Zomer Sandrini ◽  
Francesco Regoli ◽  
Daniele Fattorini ◽  
Alessandra Notti ◽  
Alan Ferreira Inácio ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Subcellular Distribution ◽  
Cadmium Exposure ◽  
Stress Generation ◽  
Short Term ◽  
And Oxidative Stress
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