scholarly journals NO Synthase but not NO, HNO or H2O2 Mediates Endothelium-Dependent Relaxation of Resistance Arteries from Patients with Resistant Cardiovascular Disease

2021 ◽  
Author(s):  
Maximilian Matthies ◽  
Kristoffer Rosenstand ◽  
Inger Nissen ◽  
Stan Muitjens ◽  
Lars Riber ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cardiovascular Disease ◽  
Superoxide Dismutase ◽  
Experimental Approach ◽  
Soluble Guanylyl Cyclase ◽  
No Synthase ◽  
Superoxide Dismutase 1 ◽  
Resistance Arteries ◽  
Parietal Pericardium ◽  
Endothelium Dependent Relaxation

Background and Purpose: Superoxide anions can reduce the bioavailability and actions of endothelium-derived NO. In human resistance-sized arteries, endothelium-dependent vasodilatation can be mediated by H2O2 instead of NO. We tested the hypotheses that in resistance arteries from patients with resistant cardiovascular disease (CVD), endothelium-dependent vasodilatation uses mechanisms that are either insensitive to oxidative stress or involve a reactive oxygen species. Experimental Approach: Small arteries were isolated from biopsies of the parietal pericardium of patients undergoing elective cardiothoracic surgery and were studied by immunohistochemical and organ chamber techniques. Key Results: NO-synthases 1, 2 and 3, superoxide dismutase 1 and catalase proteins were observed in the microvascular wall. Relaxing responses to bradykinin were endothelium dependent. During submaximal depolarization-induced contraction, these relaxations were inhibited by inhibitors of NO-synthases (NOS) and soluble guanylyl cyclase (sGC) but not by scavengers of NO or HNO, inhibitors of cyclooxygenases, neuronal NO-synthase, superoxide dismutase or catalase, or by exogenous catalase. During contraction stimulated by endothelin-1, these relaxations were not reduced by any of these interventions except DETCA which caused a small reduction. Conclusion and Implications: In resistance arteries from patients with resistant CVD, endothelium-dependent relaxations seem not to be mediated by NO, HNO or H2O2 although NOS and sGC can be involved. These vasodilator responses proceed during excessive oxidative stress.

Aging and oxidative stress alter DNA repair mechanisms in male germ cells of superoxide dismutase-1 null mice

2021 ◽  
Author(s):  
Paulina Nguyen-Powanda ◽  
Bernard Robaire
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Dna Repair ◽  
Superoxide Dismutase ◽  
Germ Cells ◽  
Superoxide Dismutase 1 ◽  
Male Germ Cells ◽  
Dna Repair Mechanisms ◽  
Repair Mechanisms ◽  
And Oxidative Stress

Abstract The efficiency of antioxidant defense system decreases with aging, thus resulting in high levels of reactive oxygen species (ROS) and DNA damage in spermatozoa. This damage can lead to genetic disorders in the offspring. There are limited studies investigating the effects of the total loss of antioxidants, such as superoxide dismutase-1 (SOD1), in male germ cells as they progress through spermatogenesis. In this study, we evaluated the effects of aging and removing SOD1 (in male germ cells of SOD1-null (Sod1−/−) mice) in order to determine the potential mechanism(s) of DNA damage in these cells. Immunohistochemical analysis showed an increase in lipid peroxidation and DNA damage in the germ cells of aged wild-type (WT) and Sod1−/− mice of all age. Immunostaining of OGG1, a marker of base excision repair (BER), increased in aged WT and young Sod1−/− mice. In contrast, immunostaining intensity of LIGIV and RAD51, markers of non-homologous end-joining (NHEJ) and homologous recombination (HR), respectively, decreased in aged and Sod1−/− mice. Gene expression analysis showed similar results with altered mRNA expression of these key DNA repair transcripts in pachytene spermatocytes and round spermatids of aged and Sod1−/− mice. Our study indicates that DNA repair pathway markers of BER, NHEJ, and HR are differentially regulated as a function of aging and oxidative stress in spermatocytes and spermatids, and aging enhances the repair response to increased oxidative DNA damage, whereas impairments in other DNA repair mechanisms may contribute to the increase in DNA damage caused by aging and the loss of SOD1.

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

scholarly journals Double Knockout of Peroxiredoxin 4 (Prdx4) and Superoxide Dismutase 1 (Sod1) in Mice Results in Severe Liver Failure

2018 ◽  
Vol 2018 ◽  
pp. 1-12 ◽  
Author(s):  
Takujiro Homma ◽  
Toshihiro Kurahashi ◽  
Jaeyong Lee ◽  
Atsunori Nabeshima ◽  
Sohsuke Yamada ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Superoxide Dismutase ◽  
Liver Failure ◽  
Liver Steatosis ◽  
Superoxide Dismutase 1 ◽  
Severe Liver ◽  
Double Knockout ◽  
Nonalcoholic Fatty Liver ◽  
Triglyceride Rich Lipoprotein ◽  
Young Stage

Mice that are deficient in superoxide dismutase 1 (Sod1), an antioxidative enzyme, are susceptible to developing liver steatosis. Peroxiredoxin 4 (Prdx4) catalyzes disulfide bond formation in proteins via the action of hydrogen peroxide and hence decreases oxidative stress and supports oxidative protein folding for the secretion of lipoproteins. Because elevated reactive oxygen species induce endoplasmic reticulum stress, this negative chain reaction is likely involved in the development of nonalcoholic fatty liver diseases and more advanced steatohepatitis (NASH). In the current study, we generated Prdx4 and Sod1 double knockout (DKO; Prdx4−/ySod1−/−) mice and examined whether the combined deletion of Prdx4 and Sod1 aggravated liver pathology compared to single knockout and wild-type mice. The secretion of triglyceride-rich lipoprotein was strikingly impaired in the DKO mice, leading to aggravated liver steatosis. Simultaneously, the activation of caspase-3 in the liver was observed. The hyperoxidation of Prdxs, a hallmark of oxidative stress, occurred in different isoforms that are uniquely associated with Sod1−/− and Prdx4−/y mice, and the effect was additive in DKO mouse livers. Because DKO mice spontaneously develop severe liver failure at a relatively young stage, they have the potential for use as a model for hepatic disorders and for testing other potential treatments.

Free-radical scavengers, thiol-containing reagents and endothelium-dependent relaxation in isolated rat and human resistance arteries

1993 ◽  
Vol 84 (3) ◽  
pp. 287-295 ◽  
Author(s):  
W. Sunman ◽  
A.D. Hughes ◽  
P.S. Sever
Keyword(s):  
Superoxide Dismutase ◽  
Free Radical ◽  
Methyl Ester ◽  
Enzyme Inhibitor ◽  
Subcutaneous Fat ◽  
Free Radical Scavengers ◽  
Radical Scavenger ◽  
Resistance Arteries ◽  
Rat Mesentery ◽  
Endothelium Dependent Relaxation

1. Small arteries were isolated from either rat mesentery or human subcutaneous fat, and mounted in a myograph for the measurement of isometric force. 2. Superoxide dismutase, either in the presence or absence of catalase, relaxed noradrenaline-induced tone. This effect was abolished by removal of the endothelium or incubation with an inhibitor of NO synthase, N-ω-nitro-L-arginine methyl ester. Catalase alone had a negligible effect on noradrenaline-induced tone. 3. Captopril, an angiotensin-converting enzyme inhibitor and putative free-radical scavenger, did not relax pre-contracted isolated vessels. N-Acetylcysteine caused an endothelium-independent relaxation of rat vessels. Similar effects were observed in human vessels. 4. Acetylcholine induced a concentration-dependent relaxation of isolated resistance arteries, which was inhibited by removal of the endothelium or N-ω-nitro-L-arginine methyl ester, but unaffected by indomethacin. Preincubation with captopril, N-acetylcysteine or catalase alone did not alter the acetylcholine concentration-response relationship, but superoxide dismutase in combination with catalase enhanced responses to acetylcholine, causing a six-fold increase in potency. 5. Superoxide dismutase causes endothelium-dependent relaxation of resistance arteries and potentiates responses to acetylcholine. This action is probably due to the ability of the enzyme to scavenge superoxide anions which inhibit endothelium-dependent relaxation. 6. N-Acetylcysteine causes an endothelium-independent relaxation of resistance arteries which is probably unrelated to the putative ability of this compound to scavenge superoxide radicals and may reflect a direct action on vascular smooth muscle.

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 Assessment of thyroid dysfunction, dyslipidemia and oxidative stress in hypertensive end stage chronic renal disease patients in a teaching hospital in Western Uttar Pradesh

2019 ◽  
Vol 10 (5) ◽  
pp. 13-18
Author(s):  
Poonam Kachhawa ◽  
Vivek Sinha
Keyword(s):  
Oxidative Stress ◽  
Cardiovascular Disease ◽  
Superoxide Dismutase ◽  
Renal Disease ◽  
Lipid Profile ◽  
Thyroid Dysfunction ◽  
Chronic Renal Disease ◽  
Economic Output ◽  
End Stage ◽  
And Oxidative Stress

Background: CKD is a serious health problem in worldwide. In developing nation, CKD has severe implication on health and economic output. The rapid increase of common risk factors such as hypertension (HTN), obesity and type 2 diabetes will result in greater and more burdens to developing country. There are many complications associated with CKD including thyroid dysfunction, dyslipidemia,hypertension and cardiovascular disease (CVD).It is generally seen that patients suffering from CKD are at high risk of cardiovascular disease. Aims and Objectives: The purpose of the study was to evaluate the diagnostic screening of thyroid dysfunction, dyslipidemia and oxidative stress in hypertensive end stage chronic renal disease patients. Materials and Methods: Thyroid status, Lipid profile, serum Urea, serum Creatinine, serum Uric acid, serum electrolyte, Catalase,Malondialdehyde (MDA) and Superoxide dismutase (SOD) were assayed in 160 subjects in which 80 patients of CKD were having hypertension and 80 healthy controls. Results: In our study, we found statistical significantly increased level of (p<0.001) of malondialdehyde (MDA) and significantly decreased level (p<0.001) of Catalase and Superoxide dismutase (SOD).There was found significantly increased level (p<0.001) of TSH in CKD associated with hypertension patients.We also found deranged lipid profile and renal functions in CKD associated with hypertension patients as compared to controls. Conclusion: In the present study, we arrived at conclusion that dyslipidemia and thyroid dysfunction is very common in CKD patients. Our study revealed that there was significant association between thyroid dysfunction and CKD progression and dyslipidemia. The antioxidant status is assessed through changes in antioxidant enzymatic activity in patients of CKD with hypertensive and data provide evidence of blood pressure modulation by measurable oxidative stress–related parameters.

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