Oxis Oxidative Stress, Mark, Trevi, Gen, Research, Bio, Markers, Antibody list.

Bioxys Oxidative Stress

 Oxidative Assays kits for Health Research

Bioxys Antioxidant Bio-markers
Superoxide Dismutase Detection test SOD-525
Total Glutathione test
GSH 420
Glutathione test GSH-400
Glutathione Peroxidase intra-cellular test cGPx-340
Glutathione Peroxidase in plasma test kit pl-GPx-EIA
Glutathione Reductase test GR-340
GSH/GSSG Ratio measurement GSH/GSSG-412
Catalase test Catalase-520
Antioxidant Potential measurement kit AOP-490
Bioxys Oxidative Stress Bio-markers
MDA/ 4-Hydroxyalkenals Elisa LPO-586
8-Isoprostane Elisa 8-ISO-EIA
Hydrogen Peroxide test H2O2-560
8-Hydroxydeoxyguanosine Elisa 8-OHdG-EIA
Hydroxyalkenals HAE-586
Malondialdehyde MDA-586
Urinary 8-Epi-Prostaglandin-F2α Urinary 8-EPI-PGF
Aconitase Aconitase-340
α1-Antiproteinase α1AP-410
Nitrotyrosine Elisa NT-EIA
Bioxys Inflammatory Bio-markers
Myeloperoxidase or MPO Elisa MPO-EIA
Lactoferrin Elisa Lactof-EIA
Bioxys Nitric Oxide Bio-markers
Nitric Oxide (Enzymatic) NO-22110
Nitric Oxide (Non-Enzymatic) NO-22111
Nitric Oxide Synthase (Radioactive) NOS-22112
Nitric Oxide Synthase (Colorimetric) Elisa 96 well test kit NOS-22113
International Research council Oregon product family Applied Bio Taq Systems

Mitochiondrial 8OHdG

  • Oxidative Stress Kits
  • Antibodies for Research
  • Antioxidant Research
  • biomarkers
  • Catalases
  • Elisa readers
  • TAQ Enzymes
  • Free radicals
  • Glutathione test
  • Lipid Peroxidation tests
  • MPO and Cardi MPO research
  • Nitric Oxide International standard
  • Nitrosative
  • Nitrotyrosine
  • Research assay development
  • Roentgen
  • Superoxide
  • Superoxide Dismutase Test
  • X-ray damage

Published by:

Portland Health Research Inc., OR, USA

References:

  1. Endothelin A Receptor Blockade Reduces Diabetic Renal Injury via an Anti-Inflammatory Mechanism   [PubMed
  2. Mihm MJ, Seifert JL, Coyle CM, Bauer JA. Diabetes related cardiomyopathy Time dependent echocardiographic evaluation in an experimental rat model. Life Sciences. 2001;69:527–542. [PubMed[Google Scholar]
  3. Estey C, Seifert EL, Aguer C, Moffat C, Harper M-E. Calorie restriction in mice overexpressing UCP3: evidence that prior mitochondrial uncoupling alters response. Exp Gerontol. 2012;47:361–371. [PMC free article] [PubMed[Google Scholar]
  4. VERVAECKE, LAUREN SUZANNE, Ph.D. Acute and Chronic Exercise Effects on
    NrF2 and Antioxidants in the Muscle and Brain Tissue of Sprague Dawley Rats. (2017) [UNCG]
  5. TY – CHAP
    AU – Seifert, Roland
    PY – 2019/07/20
    SP – 181
    EP – 193
    SN – 978-3-030-18898-6
    T1 – Drugs for Treatment of Respiratory Tract Diseases
    DO – 10.1007/978-3-030-18899-3_14
    Asthma is characterized by inflammation of the bronchi and hyper-reactivity of the respiratory tract smooth muscle cells. Both factors lead to increased respiratory tract resistance. The goal is to normalize these physiological changes. In intermittent asthma, SABAs are administered on demand. In mild asthma, IGCR agonists are added as long-term medication. In moderate asthma, IGCR agonists + LABAs are used. In severe asthma, LTRAs can be applied; status asthmatic’s may be treated with theophylline. In very severe asthma, systemic GCR agonists, IgE inhibitors, and IL-5 inhibitors are additional therapy options. COPD is mostly due to chronic tobacco consumption, resulting in irreversible respiratory tract obstruction, emphysema, and inflammation. Initially, LABAs and/or LAMAs are administered. If these drug classes are not sufficient, the nonselective PDE inhibitor theophylline or selective PDE4 inhibitors are added. IGCR agonists should only be given cautiously because these drugs increase the risk of pneumonia. CF is an autosomal-recessive disease in which genetically heterogeneous CFTR defects result in the formation of viscous secretions, ultimately leading to chronic pneumonia with problem pathogens and dysfunction of multiple organs. CFTR potentiators and CFTR correctors constitute the first specific drugs to normalize CFTR function.