Human SOD1 / Cu-Zn SOD Protein
- Known as:
- Human SOD1 / Cu-Zn antioxidant enzyme Protein
- Catalog number:
- SO1-H5148
- Product Quantity:
- 1mg
- Category:
- -
- Supplier:
- acrobyosystems
- Gene target:
- Human SOD1 / Cu- SOD Protein
Related genes to: Human SOD1 / Cu-Zn SOD Protein
- Gene:
- SOD1 NIH gene
- Name:
- superoxide dismutase 1
- Previous symbol:
- ALS, ALS1
- Synonyms:
- IPOA
- Chromosome:
- 21q22.11
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2019-04-23
Related products to: Human SOD1 / Cu-Zn SOD Protein
Related articles to: Human SOD1 / Cu-Zn SOD Protein
- The aberrant aggregation of human superoxide dismutase 1 (hSOD1) into β-sheet-rich amyloid fibrils is a crucial process in the pathogenesis of amyotrophic lateral sclerosis (ALS), enhancing motor neuron degeneration and disease progression. The P66R mutation in SOD1 destabilizes local structure and promotes β-sheet-driven fibrillation, which makes it a suitable model for exploring approaches for reducing pathogenic aggregation. Here, we evaluate silymarin, a polyphenolic compound with known antioxidant and neuroprotective properties, for its potential to inhibit P66R-hSOD1 aggregation. ThT fluorescence and transmission electron microscopy analyses demonstrate a significant decrease in amyloid fibril formation in the presence of silymarin; in addition, FTIR spectroscopy confirms the suppression of β-sheet formation. Fluorescence quenching and ANS binding assays indicate a moderate-affinity binding between silymarin and the mutant protein, along with a reduction in surface hydrophobicity. Hemolysis assays confirm its protective effect against membrane damage induced by aggregates, while molecular docking and dynamic simulations indicate that silymarin stabilizes aggregation-prone areas with hydrogen bonding and hydrophobic interactions, thereby promoting compact conformations and reducing solvent-exposed surfaces. The findings identified silymarin as an effective anti-amyloidogenic agent that reduces β-sheet accumulation and fibril formation while also decreasing cytotoxicity, highlighting its potential as a therapeutic candidate for ALS. - Source: PubMed
Publication date: 2026/06/05
Hosseinpoor ZahraSeyedalipour BagherBehjou Nasrin KeivanHosseinkhani SamanBaziyar Payam - Gunshot residue (GSR) is an airborne mixture of chemicals and particles released after firearm discharge. There is limited information on cardiopulmonary effects of GSR specifically in a health relevant size fraction. This study evaluates the acute cardiopulmonary effects of GSR (particles ≤2.5 µm; GSR PM) and investigates the role of the receptor for advanced glycation end-products (RAGE) signaling cascade in the mediation of inflammation and oxidative stress using wild-type (WT) and RAGE knockout (RKO) mice. GSR PM collected during a law enforcement pistol training contained characteristic GSR markers (lead, copper, and 2,4- dinitrotoluene). Right ventricle measurements were lower in the GSR PM treated animals compared to the control indicating potential pulmonary vasodilation regardless of genotype. Lead content in the heart was significantly higher in the GSR PM exposed mice, indicating systemic circulation. Inflammatory markers (NF-κB, TNF-α, SOD-1 and 2) in the lungs of RKO animals were significantly lower compared to the WT groups. The cardiovascular effects, differential inflammatory expression, and influence of RAGE signaling pathway on the cardiorespiratory response to GSR PM highlight the need for further investigation of longer exposure durations, mechanistic influences, and a more extensive chemical characterization of GSR PM in toxicological assessments. - Source: PubMed
Publication date: 2026/06/04
Smith Samuel CQuiñones Gabriela OrtizSayam Abu S MRobinson Samuel LSpecht Aaron JStewart James ARoper Courtney - We compared the salivary proteome and metaproteome of individuals with real-world dietary patterns differing in fiber intake (i.e., high- versus low-fiber intake) to examine whether their diet was associated with distinct molecular signatures in saliva. - Source: PubMed
Publication date: 2026/06/06
Vargas Cesia JRivera CésarMarín Lina MDuran-Aguero SamuelFernández Constanza E - The present study evaluated variations in growth performance, intestine morphometry, cardio-pulmonary function, hepatic lipogenesis, and telomere dynamic of broiler chickens as influenced by dietary supplementation of gunnera, thyme, and liquorice. The experiment was conducted in a high-altitude region (2,100 m) with a total of 500 one-day-old chicks (Ross 308). Five dietary treatments included a control diet, the control + gunnera powder (GP), the control + thyme powder (TP), and the control + liquorice powder (LP). TP and GP were supplemented at 7.5 g/kg and LP was supplemented at 3.75 and 7.5 g/kg. Results showed that weight gain, feed conversion ratio (FCR), and villus dimensions (height, width, and absorptive surface area) in the duodenum, jejunum, and ileum were improved by all herb supplements when compared to the control (P < 0.05). Herbal supplements elevated circulatory levels of nitric oxide (NO), and ferric-reducing antioxidant power (FRAP) whereas they lowered circulatory levels of malondialdehyde (MDA), triacylglycerol (TAG), total cholesterol (TC), and low-density lipoproteins cholesterol (LDL). Phytobiotic supplementations were associated with a decline in the T, R, and S wave amplitudes of the Lead II electrocardiogram (ECG) (P < 0.05). Dietary supplements caused an up-regulation of inducible nitric oxide synthase (iNOS), superoxide dismutase 1 (SOD1), and glutathione peroxidase (GPX) but decreased the expression of key hepatic lipogenic enzymes (fatty acid synthase (FAS) and hydroxy-methylglutaryl-CoA reductase (HMGCR) (P < 0.05). Chickens consumed herbs had higher telomeric DNA quantity in the liver relative to the control counterparts (P < 0.05). In conclusion, while the phytobiotics suppressed lipogenesis, they improved antioxidant defense, intestinal and cardio-pulmonary functions, and hepatic telomere length in broiler chicks subjected to hypobaric hypoxia. - Source: PubMed
Publication date: 2026/06/04
Abaszadeh SamiraAhmadipour BehnamGhasemi RanaHassanpour HosseinKhajali Fariborz - Somatosensory cortex hyperexcitability is present in the pre-symptomatic stage of amyotrophic lateral sclerosis (ALS) as evidenced by brain recordings, but its synaptic basis remains unclear. We examined synaptic plasticity, the density of asymmetric (putative excitatory) and symmetric (putative inhibitory) synapses, dendritic spine morphology, and the putative excitatory/inhibitory (E/I) ratio in the B2 barrel of the somatosensory cortex in female mice of an ALS mouse model. Transgenic mice, B6SJL-Tg (SOD1*G93A)1Gur/J, were used as the ALS model, and wild-type (WT) B6SJL/F1 mice served as controls. ALS mice were allocated to experimental groups based on disease stage (pre-symptomatic, onset, or terminal) and training condition (swim-trained or untrained). Swim training was applied after the first onset of symptoms (clinical score 1). We analyzed and quantified the density of asymmetric (putative excitatory) and symmetric (putative inhibitory) synapses and E/I ratios using serial electron micrographs to understand how these parameters change during disease progression and whether swim training influences this process. Our results showed stage-dependent alterations in asymmetric (putative excitatory) and symmetric (putative inhibitory) synaptic architecture in ALS. The obtained data showed an increase in the excitatory synaptic density in the presymptomatic ALS mice. This finding is consistent with previous reports of early cortical hyperexcitability and may reflect structural alterations associated with an initial increase in excitatory synapses before disease onset. Importantly, we report here an increase in inhibitory synapses at disease onset. TEM-based synaptic density quantification revealed reduced excitatory synapse density in the B2 barrel of the somatosensory cortex of trained ALS mice compared to WT controls, alongside a trend toward a reduced putative excitatory/inhibitory synaptic ratio. However, as no significant differences were detected between trained and untrained ALS mice, the contribution of swim training to these alterations remains unclear. Notably, swim training was not associated with detectable adverse effects on somatosensory cortex ultrastructure, excitatory synapse density, or the putative excitatory/inhibitory ratio, supporting previous observations that swim training is well tolerated under these experimental conditions. To our knowledge, these results provide the first TEM-based ultrastructural characterization of synaptic architecture in swim-trained SOD1-G93A mice, although further studies are needed to establish the underlying mechanisms and therapeutic relevance in ALS. - Source: PubMed
Publication date: 2026/06/04
Saadat AnbariehJasińska MałgorzataCedro BartoszPiekarska AlicjaFlis Damian JZiółkowski WiesławPyza Elżbieta