Human Gpx1 ELISA kit (4X96T)
- Known as:
- Human Gpx1 Enzyme-linked immunosorbent assay test reagent (4X96T)
- Catalog number:
- lf-ek0111
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Abfrontier
- Gene target:
- Human Gpx1 ELISA kit (4X96T)
Related genes to: Human Gpx1 ELISA kit (4X96T)
- Gene:
- GPX1 NIH gene
- Name:
- glutathione peroxidase 1
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 3p21.31
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2016-10-05
Related products to: Human Gpx1 ELISA kit (4X96T)
Related articles to: Human Gpx1 ELISA kit (4X96T)
- The progression from diabetes mellitus (DM) to diabetic retinopathy (DR) represents a dynamic pathological process in which vascular and metabolic alterations gradually lead to retinal damage. Understanding the molecular changes during this transition is critical for timely identification and intervention. - Source: PubMed
Publication date: 2026/06/10
Zhao JingCao YitaoChai ZhiXie HanghangGu DandanZhang YanchunNiu DonglingLiu HongliLei Ting - Migraine is a complex neurovascular disorder with a multifactorial pathophysiology involving genetic, metabolic, and environmental factors. Increasing evidence indicates that oxidative stress plays a key role in the development of migraine; however, it is unclear whether oxidative imbalance acts primarily as a causal factor or occurs as a consequence of migraine-related processes. Oxidative stress, defined as an imbalance between reactive oxygen species production and antioxidant defense mechanisms, contributes to neuronal hyperexcitability, mitochondrial dysfunction, and neuroinflammation-key mechanisms underlying migraine pathogenesis. Studies have shown elevated markers of oxidative damage and altered antioxidant enzyme activity in migraine patients. Simultaneously, metabolic and inflammatory changes associated with migraine may further exacerbate oxidative imbalance, suggesting a bidirectional relationship. Furthermore, genetic factors such as , , and significantly influence susceptibility to oxidative stress and migraine. The gene, encoding CGRP, links oxidative stress mechanisms with neurogenic inflammation and activation of the trigeminovascular system. This article reviews the current evidence regarding the role of oxidative stress in migraine and discusses its relationship to molecular and genetic mechanisms. Particular attention is given to genes involved in oxidative pathways, mitochondrial function, and inflammatory responses, which may help explain individual susceptibility and variability in clinical presentation. - Source: PubMed
Publication date: 2026/05/29
Szymanowicz OliwiaSłowikowski BartoszKonieczny MateuszLewandowski DominikOwecki WojciechJeżewska MariannaGoutor UlyanaJagodziński Paweł PKozubski WojciechDorszewska Jolanta - Dietary supplementation with probiotics is considered an effective strategy to enhance aquaculture production efficiency and disease resistance. Recent research has highlighted the value of using autochthonous probiotics in aquaculture. Herein, an autochthonous probiotic strain (Lactococcus lactis MA5) isolated from pond-raised hybrid catfish (Ictalurus punctatus × I. furcatus) in a previous study was investigated for its ability to improve host recovery from acute hypoxia and resistance to bacterial infection. Hybrid catfish were fed a control diet, or diets containing either 10 or 10CFU/g MA5 for 56 days. After the feeding trial, subsets of fish were subjected to either acute hypoxia stress challenge or Edwardsiella ictaluri challenge. Fish fed MA5 exhibited enhanced growth performance without changes to body condition indices. Following acute hypoxia challenge, MA5-supplemented fish showed increased blood hemoglobin, red blood cell counts, and total protein concentration compared to the control. In addition, MA5 led to upregulated expression of gpx1, a gene encoding an antioxidant enzyme, in the intestine. Lastly, fish fed 10CFU/g of MA5 displayed significantly higher survival when exposed to E. ictaluri. These data suggest dietary supplementation with the autogenous probiotic L. lactis MA5 can promote growth, support acute hypoxia recovery, and improve resistance to E. ictaluri in hybrid catfish. - Source: PubMed
Publication date: 2026/06/25
Huang JingOlder Caitlin EHeckman Taylor IJordan Heather RGriffin Matt JAllen Peter JGrant Reifers JGoodman Penelope MYamamoto Fernando Y - Cyclopiazonic acid (CPA), a neurotoxin produced by Penicillium and Aspergillus genera, induces oxidative stress and neuronal damage, mechanisms implicated in neurodegenerative diseases. This study investigates the oxidative stress induced by CPA in SH-SY5Y human neuroblastoma cells, focusing on mitochondrial membrane potential, mitochondrial superoxide levels, ROS production, lipid peroxidation and gene expression. Additionally, the cytoprotective effects of extra virgin olive oil (EVOO) extract, along with its major polyphenols oleuropein (OLE) and tyrosol (TYR), were evaluated. CPA exposure increased mitochondrial superoxide levels and lipid peroxidation, reducing mitochondrial membrane potential, although no intracellular ROS generation was observed. Gene expression analysis revealed downregulation of antioxidant defense genes (nrf2, nos2, ho1, cat, keap1, nqo1, gpx1 and gsr), with the strongest repression observed for nos2 (93%), nqo1 (83%) and ho1 (79%) at the highest CPA concentration, consistent with oxidative stress markers. EVOO extract demonstrated protective effects, enhancing cell viability across all CPA assayed concentrations (400-600 nM). Conversely, TYR and OLE exhibited variable and concentration-dependent effects, also showing protection to a lesser extent, while EVOO extract proved to be more effective due to synergistic interactions among its phenolic components. Overall, CPA induces mitochondrial oxidative damage as a key mechanism of neurotoxicity, while EVOO phenolics mitigate this toxicity. - Source: PubMed
Publication date: 2026/06/02
Martínez-Alonso CarmenRodríguez-Carrasco YelkoRuiz María-José - Chronically elevated circulating free fatty acids (FFAs) are key drivers of lipotoxic injury by triggering a self-amplifying oxidative stress-inflammation cascade, thereby contributing to metabolic and cardiovascular diseases. Vascular endothelial dysfunction represents an early and causal event in this process. Although black tea-derived theaflavins (TFs) possess antioxidant and anti-inflammatory properties, the subtype-specific and tissue-parallel effects of TFs against FFA-induced oxidative-inflammatory injury remain incompletely understood. - Source: PubMed
Publication date: 2026/06/09
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