These findings suggest that identification of pre-symptomatic behavioral changes in murine models of ALS may point to early neural abnormalities selectively associated with mutations in the Cu/Zn superoxide dismutase (SOD1) gene.
In fact, motor neurons in neonatal mutant SOD mice display important alterations in their intrinsic electrical properties, synaptic inputs and morphology that are accompanied by subtle behavioral abnormalities.
Extra-motor manifestations including executive functions, social cognition, and behavioral changes are now well recognized as important features of ALS, and are associated with frontotemporal and frontostriatal network disruption.
Our findings indicate that the oral administration of AAs prevents rotenone-induced behavioral changes and oxidative stress, in part due to a modulatory action on the mitochondria and SOD gene expression.
No signs of apoptosis or abnormal cell morphology were observed in the brain following FAC-LIP administration, and there were no significant changes in the levels of SOD and MDA, except in the cerebellum and hippocampus.
Various molecular mechanisms were involved in effects of phytochemicals including antioxidant (through down-regulation of H<sub>2</sub>O<sub>2</sub>, MDA, ROS and upregulation of SOD), anti-inflammatory (through reduction of proinflammatory cytokines, i.e., IL-1ß, IL-6, IL-8, TGF-β, TNF-α, NF-κB), immunomodulatory, antibacterial (against Propionibacterium acnes and Propionibacterium granulosum), antiandrogenic, reducing sebum production, and lipogenesis inhibitory activities.
To investigate the genetic polymorphisms of mitochondrial large ribosomal subunit (mtLSU)-rRNA, dihydrofolate reductase (DHFR), dihydropteroate synthase (DHPS), cytochrome b (CYB), and superoxide dismutase (SOD) genes and its correlation with clinical outcomes of Pneumocystis jirovecii pneumonia in acquired immune deficiency(AIDS) patients.
Differing effects of copper,zinc superoxide dismutase overexpression on neurotoxicity elicited by nitric oxide, reactive oxygen species, and excitotoxins.
Compared with AMI uncomplicated with arrhythmia group, the patients had unusual ambulatory electrocardiography had increased (P <0.05), peripheral blood SOD and Na+-K+-ATP enzymes had decreased, peripheral blood MDA had increased in AMI complicated with arrhythmia group (P <0.05).
Phikud Navakot Modulates the Level of Pro-Inflammatory Mediators and the Protein Expression of SOD1 and 2 and the Nrf2/HO-1 Signaling Pathway in Rats with Acute Myocardial Infarction.
Biochemical tests, PON-1 and oxidative stress parameters (malonyl dialdehyde, MDA; superoxide dismutase, SOD; total antioxidant capacity, TAC) were evaluated in the sera of patients with acute pancreatitis at admission (day 0), day 3 and day 10 of follow-up, between June and September 2017.
Furthermore, using an astroglial cell line, primary culture of astrocytes, and tissue samples from G93A-SOD1 mice, we show that CTE-SUMO-1 is targeted to promyelocytic leukemia nuclear bodies.
However, patients with adenocarcinoma and non-adenocarcinoma showed differences in SOD and catalase activity among different genotypes in comparison with controls.
Flavokawain C inhibited the growth of HT-29 human colon adenocarcinoma cellsFlavokawain C induced apoptosis in HT-29 cells, associated with an increase in reactive oxygen species and a decrease in SOD activityFlavokawain C induced cell cycle arrest at the G<sub>1</sub> and G<sub>2</sub>/M phases via upregulation of p21 and p27 in HT-29 cellsHT-29 cells treated with flavokawain C caused downregulation of XIAP, c-IAP1, and c-IAP2, and upregulation of GADD153.
The genetic abnormalities include mutations within: (1) Hesx1 (IGHD, SOD or CPHD); (2) Lhx3 (CPHD with preservation of cortisol secretion and a short stiff neck); (3) Lhx4 (GH, TSH and ACTH deficiency with cerebellar hypoplasia); (4) Prop1 (variable CPHD often associated with pituitary masses); (5) POU1F1 (GH, prolactin and TSH deficiency); (6) GHRHR (IGHD) and (7) GH1 (IGHD).
This article gives an outline of molecular biological approaches to analysis of neurological disorders such as giant cell glioblastoma (GGBM) and amyotrophic lateral sclerosis (ALS), and their respective animal models: p53 knockout mice for GGBM and mutant superoxide dismutase-1 transgenic mice for ALS.
In the present study non-cytotoxic dose of oxidants, H<sub>2</sub>O<sub>2</sub> (100 μM) and GO (10 μU/ml) was used to induce moderate oxidative stress via generating ROS in human glioblastoma cell line U-87 MG cells, which showed a marked increase in the antioxidant capacity as studied by measuring the modulation in expression levels and activities of superoxide dismutase (SOD1 and SOD2) and catalase (CAT) enzymes, and the GSH content.