scholarly journals The Role of 2% Rebamipide Eye Drops Related to Conjunctival Differentiation in Superoxide Dismutase-1 (Sod1) Knockout Mice

2018 ◽  
Vol 59 (3) ◽  
pp. 1675 ◽  
Author(s):  
Takashi Kojima ◽  
Cem Simsek ◽  
Ayako Igarashi ◽  
Kazue Aoki ◽  
Kazunari Higa ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
Knockout Mice ◽  
Eye Drops ◽  
Superoxide Dismutase 1

Ascorbic acid and CoQ10 ameliorate the reproductive ability of superoxide dismutase 1-deficient female mice†

2019 ◽  
Author(s):  
Naoki Ishii ◽  
Takujiro Homma ◽  
Jaeyong Lee ◽  
Hikaru Mitsuhashi ◽  
Ken-ichi Yamada ◽  
...  
Keyword(s):  
Ascorbic Acid ◽  
Superoxide Dismutase ◽  
Coenzyme Q10 ◽  
Knockout Mice ◽  
Knockout Mouse ◽  
Superoxide Dismutase 1 ◽  
Wild Type ◽  
Positive Effects ◽  
Reproductive Ability ◽  
Ascorbic Acid Supplementation

Abstract Superoxide dismutase 1 suppresses oxidative stress within cells by decreasing the levels of superoxide anions. A dysfunction of the ovary and/or an aberrant production of sex hormones are suspected causes for infertility in superoxide dismutase 1-knockout mice. We report on attempts to rescue the infertility in female knockout mice by providing two antioxidants, ascorbic acid and/or coenzyme Q10, as supplements in the drinking water of the knockout mice after weaning and on an investigation of their reproductive ability. On the first parturition, 80% of the untreated knockout mice produced smaller litter sizes compared with wild-type mice (average 2.8 vs 7.3 pups/mouse), and supplementing with these antioxidants failed to improve these litter sizes. However, in the second parturition of the knockout mice, the parturition rate was increased from 18% to 44–75% as the result of the administration of antioxidants. While plasma levels of progesterone at 7.5 days of pregnancy were essentially the same between the wild-type and knockout mice and were not changed by the supplementation of these antioxidants, sizes of corpus luteum cells, which were smaller in the knockout mouse ovaries after the first parturition, were significantly ameliorated in the knockout mouse with the administration of the antioxidants. Moreover, the impaired vasculogenesis in uterus/placenta was also improved by ascorbic acid supplementation. We thus conclude that ascorbic acid and/or coenzyme Q10 are involved in maintaining ovarian and uterus/placenta homeostasis against insults that are augmented during pregnancy and that their use might have positive effects in terms of improving female fertility.

Potential Role of the Porcine Superoxide Dismutase 1 (SOD1) Gene in Pig Reproduction

2013 ◽  
Vol 24 (1) ◽  
pp. 1-9 ◽  
Author(s):  
D. Bjerre ◽  
L. B. Madsen ◽  
T. Mark ◽  
S. Cirera ◽  
K. Larsen ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
Potential Role ◽  
Superoxide Dismutase 1 ◽  
Sod1 Gene

Survival role of superoxide dismutase 1 on human granulosa luteinized cells in vitroSurvival role of superoxide dismutase 1 on human granulosa luteinized cells in vitro

2011 ◽  
Vol 45 (04) ◽  
pp. 175-181
Author(s):  
J. Dineva ◽  
I. Vangelov ◽  
R. Abrashev ◽  
K. Todorova ◽  
D. Gulenova ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
Superoxide Dismutase 1

scholarly journals Oxidation of the Tryptophan 32 Residue of Human Superoxide Dismutase 1 Caused by Its Bicarbonate-dependent Peroxidase Activity Triggers the Non-amyloid Aggregation of the Enzyme

2014 ◽  
Vol 289 (44) ◽  
pp. 30690-30701 ◽  
Author(s):  
Fernando R. Coelho ◽  
Asif Iqbal ◽  
Edlaine Linares ◽  
Daniel F. Silva ◽  
Filipe S. Lima ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
Peroxidase Activity ◽  
Oxidation Products ◽  
Superoxide Dismutase 1 ◽  
Amyloid Aggregation ◽  
Post Translational Modifications ◽  
Covalent Dimer ◽  
Als Patients ◽  
Lateral Sclerosis

The role of oxidative post-translational modifications of human superoxide dismutase 1 (hSOD1) in the amyotrophic lateral sclerosis (ALS) pathology is an attractive hypothesis to explore based on several lines of evidence. Among them, the remarkable stability of hSOD1WT and several of its ALS-associated mutants suggests that hSOD1 oxidation may precede its conversion to the unfolded and aggregated forms found in ALS patients. The bicarbonate-dependent peroxidase activity of hSOD1 causes oxidation of its own solvent-exposed Trp32 residue. The resulting products are apparently different from those produced in the absence of bicarbonate and are most likely specific for simian SOD1s, which contain the Trp32 residue. The aims of this work were to examine whether the bicarbonate-dependent peroxidase activity of hSOD1 (hSOD1WT and hSOD1G93A mutant) triggers aggregation of the enzyme and to comprehend the role of the Trp32 residue in the process. The results showed that Trp32 residues of both enzymes are oxidized to a similar extent to hSOD1-derived tryptophanyl radicals. These radicals decayed to hSOD1-N-formylkynurenine and hSOD1-kynurenine or to a hSOD1 covalent dimer cross-linked by a ditryptophan bond, causing hSOD1 unfolding, oligomerization, and non-amyloid aggregation. The latter process was inhibited by tempol, which recombines with the hSOD1-derived tryptophanyl radical, and did not occur in the absence of bicarbonate or with enzymes that lack the Trp32 residue (bovine SOD1 and hSOD1W32F mutant). The results support a role for the oxidation products of the hSOD1-Trp32 residue, particularly the covalent dimer, in triggering the non-amyloid aggregation of hSOD1.

scholarly journals Senescence marker protein-30/superoxide dismutase 1 double knockout mice exhibit increased oxidative stress and hepatic steatosis

FEBS Open Bio ◽  
2014 ◽  
Vol 4 (1) ◽  
pp. 522-532 ◽  
Author(s):  
Yoshitaka Kondo ◽  
Hirofumi Masutomi ◽  
Yoshihiro Noda ◽  
Yusuke Ozawa ◽  
Keita Takahashi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Superoxide Dismutase ◽  
Hepatic Steatosis ◽  
Knockout Mice ◽  
Superoxide Dismutase 1 ◽  
Marker Protein ◽  
Double Knockout

Effects of Oxidative Stress on the Conjunctiva in Cu, Zn-Superoxide Dismutase-1 (Sod1)–Knockout Mice

2015 ◽  
Vol 56 (13) ◽  
pp. 8382 ◽  
Author(s):  
Takashi Kojima ◽  
Murat Dogru ◽  
Osama M. A. Ibrahim ◽  
Tais Hitomi Wakamatsu ◽  
Masataka Ito ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Superoxide Dismutase ◽  
Knockout Mice ◽  
Superoxide Dismutase 1

scholarly journals Ovarian Function in Superoxide Dismutase 1 and 2 Knockout Mice

Endocrinology ◽  
1998 ◽  
Vol 139 (9) ◽  
pp. 4008-4011 ◽  
Author(s):  
Martin M. Matzuk ◽  
Lianna Dionne ◽  
Qiuxia Guo ◽  
T. Rajendra Kumar ◽  
Russell M. Lebovitz
Keyword(s):  
Superoxide Dismutase ◽  
Knockout Mice ◽  
Ovarian Function ◽  
Superoxide Dismutase 1

The Effects of 2% Rebamipide Ophthalmic Solution on the Tear Functions and Ocular Surface of the Superoxide Dismutase-1 (Sod1) Knockout Mice

2013 ◽  
Vol 54 (12) ◽  
pp. 7793 ◽  
Author(s):  
Takeshi Ohguchi ◽  
Takashi Kojima ◽  
Osama M. Ibrahim ◽  
Taeko Nagata ◽  
Takahiko Shimizu ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
Knockout Mice ◽  
Ocular Surface ◽  
Ophthalmic Solution ◽  
Superoxide Dismutase 1

scholarly journals Arabidopsis iron superoxide dismutase 1 protects against methyl viologen-induced oxidative stress in a copper-dependent manner

2021 ◽  
Author(s):  
Pavol Melicher ◽  
Petr Dvořák ◽  
Yuliya Krasylenko ◽  
Alexey Shapiguzov ◽  
Jaakko Kangasjärvi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Superoxide Dismutase ◽  
Methyl Viologen ◽  
Accumulation Rate ◽  
Growth Media ◽  
Dependent Manner ◽  
Superoxide Dismutase 1 ◽  
Iron Superoxide Dismutase ◽  
Antioxidative Function

AbstractIron superoxide dismutase 1 (FSD1) was recently characterized as a plastidial, cytoplasmic, and nuclear superoxide dismutase with osmoprotective and antioxidative functions. However, its role in oxidative stress tolerance is not well understood. Here, we characterized the role of FSD1 in response to methyl viologen (MV)-induced oxidative stress in Arabidopsis thaliana. The findings demonstrated that the antioxidative function of FSD1 depends on the availability of Cu2+ in growth media. Prolonged MV exposure led to a decreased accumulation rate of superoxide, higher levels of hydrogen peroxide production, and higher protein carbonylation in the fsd1 mutants and transgenic plants lacking a plastidial pool of FSD1, compared to the wild type. MV led to a rapid increase in FSD1 activity, followed by a decrease. Chloroplastic localization of FSD1 is necessary for these changes. Proteomic analysis showed that the sensitivity of the fsd1 mutants coincided with decreased abundance of ferredoxin and light PSII harvesting complex proteins, with altered levels of signaling proteins. Collectively, the study provides evidence for the conditional antioxidative function of FSD1 and its possible role in signaling.

scholarly journals Deletion of Superoxide Dismutase 1 Blunted Inflammatory Aortic Remodeling in Hypertensive Mice under Angiotensin II Infusion

Antioxidants ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 471
Author(s):  
Yasunaga Shiraishi ◽  
Norio Ishigami ◽  
Takehiko Kujiraoka ◽  
Atsushi Sato ◽  
Masanori Fujita ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
Angiotensin Ii ◽  
Superoxide Dismutase 1 ◽  
Superoxide Anions ◽  
Vascular Hypertrophy ◽  
Blood Pressures ◽  
Aortic Remodeling ◽  
Deficient Mice ◽  
Cytosolic Sod

Superoxide dismutase (SOD) is an enzyme that catalyzes the dismutation of two superoxide anions (O2·−) into hydrogen peroxide (H2O2) and oxygen (O2) and is generally known to protect against oxidative stress. Angiotensin II (AngII) causes vascular hypertrophic remodeling which is associated with H2O2 generation. The aim of this study is to investigate the role of cytosolic SOD (SOD1) in AngII-induced vascular hypertrophy. We employed C57/BL6 mice (WT) and SOD1 deficient mice (SOD1−/−) with the same background. They received a continuous infusion of saline or AngII (3.2 mg/kg/day) for seven days. The blood pressures were equally elevated at 1.5 times with AngII, however, vascular hypertrophy was blunted in SOD1−/− mice compared to WT mice (WT mice 91.9 ± 1.13 µm versus SOD1−/− mice 68.4 ± 1.41 µm p < 0.001). The elevation of aortic interleukin 6 (IL-6) and phosphorylation of pro-inflammatory STAT3 due to AngII were also blunted in SOD1−/− mice’s aortas. In cultured rat vascular smooth muscle cells (VSMCs), reducing expression of SOD1 with siRNA decreased AngII induced IL-6 release as well as phosphorylation of STAT3. Pre-incubation with polyethylene glycol (PEG)-catalase also attenuated phosphorylation of STAT3 due to AngII. These results indicate that SOD1 in VSMCs plays a role in vascular hypertrophy due to increased inflammation caused by AngII, probably via the production of cytosolic H2O2.

Sign in / Sign up

Export Citation Format

Share Document