Nitric oxide : biology and chemistry最新文献

{"title":"Application of hydrogen sulfide donor conjugates in different diseases","authors":"Rui Zhang,&nbsp;Wumei Shi,&nbsp;Xiaoyan Wu,&nbsp;Qingfeng Yu,&nbsp;Ying Xiao","doi":"10.1016/j.niox.2024.11.008","DOIUrl":"10.1016/j.niox.2024.11.008","url":null,"abstract":"<div><div>As an endogenous gas signaling molecule, hydrogen sulfide (H₂S) has been proved to have a variety of biological activities. Studies have shown that in some disease state H₂S concentration in the body is lower than normal state. Based on these findings, exogenous H₂S supplementation is expected to be an effective treatment for many diseases. In recent years, a lot of H₂S-releasing substances, namely H₂S donors, have emerged as H₂S sources. Specifically, various H₂S donors also could be connected to drugs or compounds to form H₂S donor conjugates. Many studies have found that H₂S donor conjugates can not only retain the activity of the parent drug, but also reduce the adverse effects of the parent drug, this makes H₂S donor conjugates to be a new kind of drug candidates. In this article, H₂S donor conjugates will be reviewed and classified according to different diseases, such as inflammation, cardiovascular and cerebrovascular diseases, diseases of central nervous system and cancer. This review aims to provide an idea for researchers for further study of H₂S and H₂S donor conjugates.</div></div>","PeriodicalId":19357,"journal":{"name":"Nitric oxide : biology and chemistry","volume":"154 ","pages":"Pages 128-139"},"PeriodicalIF":3.2,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142813841","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Critical role of hydrogen sulfide in the management of neurodegenerative disease","authors":"Rajashree Pawar ,&nbsp;Dheeraj Pandey ,&nbsp;Saba Naqvi ,&nbsp;Abha Sharma","doi":"10.1016/j.niox.2024.11.006","DOIUrl":"10.1016/j.niox.2024.11.006","url":null,"abstract":"<div><div>Hydrogen sulfide has been known to humans for about 300 years and the previous studies emphasize only on its toxic side effects. In the last two decennium, researchers have varied their perspectives and insights towards H₂S biology based on experimental findings. It has been found that H₂S is an endogenic gaseous signaling molecule in many organisms and plays a crucial role in many systems and diseases. Early reports suggest that H₂S as a neuromodulator influences calcium levels within the brain cells which ultimately control memory, learning, and cognition. It has also been observed that some complications in the pathogenesis of neurodegenerative diseases are due to anomalies in the biosynthesis and metabolism of H₂S. This review focuses on the role of H₂S in the pathophysiology of major neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, Huntington's disease and Vascular dementia. H₂S was observed to have a protective role in the above-mentioned neurological conditions and the H₂S donor therapy may help in disease management. The H₂S gas displays a neuroprotective role and protects against cellular damage thereby declining the neurological conditions. Some studies have revealed that treatment with H₂S donors has improved neuronal damage, restored memory and cognition in animal models. In this review, we have discussed the role of H₂S donors as neuroprotective agents with examples of some of the natural and synthetic H₂S donors, and also briefly enumerated the molecules used to detect H₂S in neurodegenerative diseases.</div></div>","PeriodicalId":19357,"journal":{"name":"Nitric oxide : biology and chemistry","volume":"154 ","pages":"Pages 77-85"},"PeriodicalIF":3.2,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142693321","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Enhancing S-nitrosoglutathione reductase decreases S-nitrosylation of ERO1α and reduces neuronal death in secondary traumatic brain injury","authors":"Guangjie Liu ,&nbsp;Dengfeng Lu ,&nbsp;Jie Wu ,&nbsp;Shixin Wang ,&nbsp;Aojie Duan ,&nbsp;Yubo Ren ,&nbsp;Yu Zhang ,&nbsp;Lei Meng ,&nbsp;Renjie Shou ,&nbsp;Haiying Li ,&nbsp;Zhong Wang ,&nbsp;Zongqi Wang ,&nbsp;Xiaoou Sun","doi":"10.1016/j.niox.2024.11.005","DOIUrl":"10.1016/j.niox.2024.11.005","url":null,"abstract":"<div><div>Traumatic brain injury (TBI) has the highest incidence of all common neurological disorders, along with high mortality and disability rates. Pathological conversion of excess nitric oxide (NO) to S-nitrosoglutathion (GSNO) after TBI leads to high S-nitrosylation of intracellular proteins, causing nitrative stress. GSNO reductase (GSNOR) plays an important role by regulating GSNO and SNO-proteins (PSNOs) and as a redox regulator of the nervous system. However, the effect of GSNOR on protein S-nitrosylation in secondary brain injury after TBI is not clear. <em>In vivo</em> TBI model was established in male C57BL/6 mice via controlled cortical impact (CCI). Neuron-targeted GSNOR-overexpression adeno-associated virus (AAV) was constructed and administered to mice by stereotactic cortical injection. The results showed that NO, GSNO, neuronal protein S-nitrosylation and neuronal death increased after TBI, while the level and activity of GSNOR decreased. Overexpression of GSNOR by AAV decreased GSNO and NO and improved short-term neurobehavioral outcomes in mice. GSNOR overexpression can reduce endoplasmic reticulum stress and neuronal death by reducing the S-nitrosylation of ERO1α via H₂O₂ generation and plays a neuroprotective role. In conclusion, our results suggest that GSNOR regulating S-nitrosylation of ERO1α may participate in neuronal death, and overexpression of GSNOR in neurons after experimental brain injury alleviates secondary brain injury. Our research provides a potential therapeutic approach for the treatment of TBI.</div></div>","PeriodicalId":19357,"journal":{"name":"Nitric oxide : biology and chemistry","volume":"154 ","pages":"Pages 29-41"},"PeriodicalIF":3.2,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142681587","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Downregulation of neuronal nitric oxide synthase (nNOS) within the paraventricular nucleus in Ins2Akita-type-1 diabetic mice contributes to sympatho-excitation","authors":"Tapan A. Patel ,&nbsp;Lie Gao ,&nbsp;Shane H. Boomer ,&nbsp;Xuefei Liu ,&nbsp;Kaushik P. Patel ,&nbsp;Hong Zheng","doi":"10.1016/j.niox.2024.11.001","DOIUrl":"10.1016/j.niox.2024.11.001","url":null,"abstract":"<div><div>Activation of both renin-angiotensin system (RAS) and the sympathetic system is the primary etiologic event in developing cardiovascular complications in diabetes mellitus (DM). However, the precise mechanisms for sympathetic activation in DM have not been elucidated. Here we attempted to investigate diabetes-linked cardiovascular dysregulation due to angiotensin II (Ang II)-mediated reduction in neuronal nitric oxide (NO) synthase (nNOS) within the paraventricular neuleus (PVN). In the present study, we used Ins2^+/−Akita (a spontaneous, insulin-dependent genetic diabetic non-obese murine model) and wild-type (WT) littermates mice as controls. At 14 weeks of age, we found the Akita mice had increased renal sympathetic nerve activity and elevated levels of plasma norepinephrine. There was decreased expression of nNOS protein (Akita 0.43 ± 0.11 vs. WT 0.75 ± 0.05, P &lt; 0.05) in the PVN of Akita mice. Akita mice had increased expression of angiotensin-converting enzyme (ACE) (Akita 0.58 ± 0.05 vs. WT 0.34 ± 0.04, P &lt; 0.05) and Ang II type 1 receptor (Akita 0.49 ± 0.03 vs. WT 0.29 ± 0.09, P &lt; 0.05), decreased expressions of ACE2 (Akita 0.17 ± 0.05 vs. WT 0.27 ± 0.03, P &lt; 0.05) and angiotensin (1–7) Mas receptor (Akita 0.46 ± 0.02 vs. WT 0.77 ± 0.07, P &lt; 0.05). Futher, there were increased protein levels of protein inhibitor of nNOS (PIN) (Akita 1.75 ± 0.08 vs. WT 0.71 ± 0.09, P &lt; 0.05) with concomitantly decreased catalytically active dimers of nNOS (Akita 0.11 ± 0.04 vs. WT 0.19 ± 0.02, P &lt; 0.05) in the PVN in Akita mice. Our studies suggest that activation of the excitatory arm of RAS, leads to a decrease NO, causing an over-activation of the sympathetic drive in DM.</div></div>","PeriodicalId":19357,"journal":{"name":"Nitric oxide : biology and chemistry","volume":"154 ","pages":"Pages 1-7"},"PeriodicalIF":3.2,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142624990","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exogenous sodium nitroprusside exhibits multiple positive roles in alleviating cadmium toxicity in tobacco (Nicotiana tabacum L.)","authors":"Kejin Song ,&nbsp;Hongwei Li ,&nbsp;Kunjian Yang ,&nbsp;Tengfei Ma ,&nbsp;Yingying Hu ,&nbsp;Ji Chen ,&nbsp;Shunqin Zhu ,&nbsp;Wanhong Liu","doi":"10.1016/j.niox.2024.11.002","DOIUrl":"10.1016/j.niox.2024.11.002","url":null,"abstract":"<div><div>As a donor of the gaseous signaling molecule nitric oxide (NO), sodium nitroprusside (SNP) has been shown to play a positive role in enhancing plant resistance to abiotic stress. However, its role in alleviating cadmium (Cd) toxicity in tobacco (<em>Nicotiana tabacum</em> L.) is not fully understood. This study found that Cd stress significantly inhibited tobacco growth. At the same time, 150 μM SNP was the most effective concentration in alleviating Cd toxicity in seedlings, restoring three stress tolerance indicators—MDA, H₂O₂, and proline—to control levels. Exogenous SNP mitigated Cd-induced oxidative stress by promoting the accumulation of non-enzymatic antioxidants (total phenolics and flavonoids) and activating key antioxidant enzymes (SOD, CAT, POD, APX, and GR) along with their gene expression. SNP also facilitated Cd accumulation in the root cell wall and prevented Cd translocation from roots to shoots. Additionally, SNP altered Cd's subcellular distribution, promoting its sequestration in vacuoles and cell walls, which may be related to the NO-mediated upregulation of the metallothionein gene <em>NtMT2F</em> and the phytochelatin gene <em>NtPCS2</em>. The addition of SNP significantly increased the proportion of Cd in less toxic chemical forms, with the residual Cd fraction in the Cd + SNP group reaching 7.30 %, higher than the 4.86 % in the Cd-only group. Furthermore, exogenous SNP counteracted Cd's inhibition of nitrate reductase (NR) activity, promoting endogenous NO production. This study systematically reveals the positive roles of exogenous SNP in mitigating Cd toxicity in tobacco, offering valuable insights for producing low-Cd tobacco.</div></div>","PeriodicalId":19357,"journal":{"name":"Nitric oxide : biology and chemistry","volume":"154 ","pages":"Pages 8-18"},"PeriodicalIF":3.2,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142639332","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"S-Denitrosylation counteracts local inflammation and improves survival in mice infected with K. pneumoniae","authors":"Filipe Rodolfo Moreira Borges Oliveira ,&nbsp;Thiele Osvaldt Rosales ,&nbsp;Daiane Mara Bobermin,&nbsp;Marina Delgobo,&nbsp;Alfeu Zanotto-Filho,&nbsp;Regina Sordi,&nbsp;Jamil Assreuy","doi":"10.1016/j.niox.2024.12.001","DOIUrl":"10.1016/j.niox.2024.12.001","url":null,"abstract":"<div><h3>Aim</h3><div>Sepsis and septic shock remain are significant causes of mortality in the world. The inflammatory response should be at the basis of all organ dysfunction such as cardiovascular dysfunction, characterized by severe hypotension refractory to volume replacement and vasoconstrictor therapy. Nitric oxide (NO) has been implicated as a key element in both inflammatory and cardiovascular components of sepsis. In addition to activating soluble guanylate cyclase and potassium channels, NO also modifies proteins post-translationally by reacting with protein thiol groups, yielding S-nitrosothiols (RS-NO), which can act as endogenous NO reservoirs. Besides its use in quantifying free sulfhydryl groups of proteins and non-protein thiols, DTNB [5,5′-dithiobis-(2-nitrobenzoic acid)] has also been used as a pharmacological tool due to its specificity for oxidizing reactive sulfhydryl groups. Here we aimed to investigate the effects of DTNB in the inflammatory aspects of a sepsis model and to verify whether its effects can be attributed to S-denitrosylation.</div></div><div><h3>Methods</h3><div>Anesthetized female Swiss mice were intratracheally injected with 1 × 10⁸ CFU of <em>K. pneumoniae</em>. Twelve hours after pneumonia-induced sepsis, the animals were injected with vehicle (sodium bicarbonate 5 %, s.c.) or DTNB (31.5, 63 and 126 μmol/kg, s.c.). Twenty-four hours post-sepsis induction, plasma, bronchoalveolar lavage (BAL), and lung tissues were collected for assays (protein, cell count, nitrite + nitrate levels (NOx), cytokine levels, and sulfhydryl groups). In addition, lung S-nitrosylated proteins were visualized by a modified tissue assay for S-nitrosothiols.</div></div><div><h3>Results</h3><div>Sepsis induced a significant vascular leakage in the lungs and elevated NOx levels in BAL, both reduced by DTNB. BAL leukocytosis and elevated IL-1β induced by sepsis were also reduced by DTNB, whereas it did not affect bacterial dissemination to liver, heart and BAL. Sepsis reduced free sulfhydryl groups in BAL and lung and DTNB did not change it. On the other hand, DTNB substantially reduced protein S-nitrosylation levels in the lung parenchyma and halved sepsis-induced mortality in septic mice.</div></div><div><h3>Conclusion</h3><div>Our results show that the administration of DTNB 12 h after bacterial instillation reduced most of the local inflammatory parameters and, more importantly, decreased mortality. These beneficial effects may be due to S-denitrosylation of RS-NO pools carried out by DTNB. Since DTNB was effective in reducing the inflammatory process after its onset, this mechanism of action could serve as a valuable proof of concept for compounds that can be useful to interfere with sepsis outcome.</div></div>","PeriodicalId":19357,"journal":{"name":"Nitric oxide : biology and chemistry","volume":"154 ","pages":"Pages 105-114"},"PeriodicalIF":3.2,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142795063","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The relationship of nitric oxide synthase 3(NOS3) gene polymorphism in the risk of pulmonary arterial hypertension: A systematic review and meta-analysis","authors":"Kang Yi ,&nbsp;Tao Guo ,&nbsp;Wen-Xin Wang ,&nbsp;Shao-E He ,&nbsp;Xin Zhang ,&nbsp;Jian-Guo Xu ,&nbsp;Zi-Qiang Wang ,&nbsp;Fan-Ning Wang ,&nbsp;Tao You","doi":"10.1016/j.niox.2024.11.009","DOIUrl":"10.1016/j.niox.2024.11.009","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Background&lt;/h3&gt;&lt;div&gt;We performed the present study to better elucidate the correlation of nitric oxide synthase 3 (NOS3) gene polymorphism with the risk of pulmonary arterial hypertension (PAH).&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Material/methods&lt;/h3&gt;&lt;div&gt;According to the designed search strategy, a systematic literature search was performed through the PubMed, Embase, Web of Science, Cochrane Library, CNKI, VIP and Wan Fang databases to collect published case-control studies on the correlation between NOS3 gene polymorphism and PAH. The search deadline was December 26, 2023. Two reviewers independently screened the literature, extracted data and evaluated the quality according to the inclusion and exclusion criteria. Meta-analysis was performed using RevMan 5.4 software. The odds ratio (OR) and 95 % confidence interval (CI) of the genotype distribution were used as the effect indicators.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Results&lt;/h3&gt;&lt;div&gt;A total of 11 eligible studies were included, involving three single nucleotide polymorphism (SNP) sites of the NOS3 gene: G894T (rs1799983), 4b/4a (rs61722009), and T-786C (rs2070744). The meta-analysis revealed that for PAH analysis, 4 genetic models of NOS3 G894T polymorphism increased the risk of PAH: the allele model (T vs G, OR = 1.9, 95%CI [1.16, 3.11],P = 0.01), the homozygote model (GG vs TT, OR = 1.91, 95%CI [1.04, 3.51], P = 0.04), the heterozygote model (GG vs GT, OR = 3.19, 95%CI [1.65, 6.19], P = 0.0006) and the dominant model (GT + TT vs GG, OR = 3.06, 95%CI [1.54, 6.09], P = 0.001). In the subgroups analysis, the NOS3 G894T polymorphism was found to be associated with the risk of PAH subgroups, including CHD combined with PAH and COPD combined with PAH, Particularly, there is a highly significant correlation with CHD combined with PAH. 2 genetic models of NOS3 4b/4a polymorphism increased the risk of PAH: the homozygote model (BB vs AA, OR = 2.1, 95%CI [1.02, 4.35], P = 0.04) and the recessive model (BB + BA vs AA, OR = 2.55, 95%CI [1.27, 5.11], P = 0.009). In the subgroups analysis, the NOS3 4b/4a polymorphism was found to be associated with the susceptibility of CHD combined with PAH. The results of the combined analysis of each gene model of NOS3 T-786C gene polymorphism sites were not statistically significant, and their P values were all&gt;0.05. The NOS3 G894T and NOS3 4b/4a gene polymorphism had been found to be associated with the risk of PAH in different regional and racial subgroups. In contrast to the NOS3 G894T gene polymorphism, which increased the risk of PAH development in the yellow race subgroup, the NOS3 4b/4a gene polymorphism reduced the risk of PAH development in the white race subgroup and was a protective factor.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Conclusions&lt;/h3&gt;&lt;div&gt;The NOS3 G894T (rs1799983) and NOS3 4b/4a (rs61722009) gene polymorphism have a strong correlation with the risk of PAH, with this association varying among different regions and ethnicities. However, it is still necessary to expand the sample ","PeriodicalId":19357,"journal":{"name":"Nitric oxide : biology and chemistry","volume":"154 ","pages":"Pages 51-76"},"PeriodicalIF":3.2,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142695740","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hydrogen sulfide alleviates endothelial glycocalyx damage and promotes placental angiogenesis in rats exposed to cigarette smoke","authors":"Kexin Zhang ,&nbsp;Geng Wu ,&nbsp;Yonglan Chen ,&nbsp;Qunying Hu ,&nbsp;Yuanyuan Li ,&nbsp;Xinyue Jiang ,&nbsp;Chunfu Gu ,&nbsp;Na Zhang ,&nbsp;Fusheng Zhao","doi":"10.1016/j.niox.2024.12.002","DOIUrl":"10.1016/j.niox.2024.12.002","url":null,"abstract":"<div><div>Our previous study has shown that hydrogen sulfide (H₂S) can attenuate cigarette smoke exposure (CSE)-induced placental injury in rats. This study investigated whether H₂S alleviates CSE-induced endothelial glycocalyx (eGC) impairment and promotes placental angiogenesis in rats. Twenty-four pregnant rats were randomly divided into four groups: control, NaHS (a donor of H₂S), CSE, and CSE + NaHS. On gestational day 21, rat placentas were collected to detect H₂S levels and protein expression of the H₂S-synthesizing enzymes, cystathionine beta synthase (CBS), cystathionine gamma-lyase (CGL), and 3-mercaptopyruvate sulfurtransferase (3-MST), using a C-7Az fluorescent probe, H₂S testing kit, and western blotting, respectively. Transmission electron microscopy and double immunofluorescence staining were performed to observe the placental eGC alterations. Placental angiogenesis, vascular endothelial proliferation and apoptosis, and protein expression levels of the PI3K/AKT/mTOR signaling pathway were assessed in rat placentas. The results showed that the administration of NaHS markedly attenuated the reduction in H₂S levels and the decrease in CBS, CGL, and 3-MST expression caused by CSE in rat placentas. Notably, NaHS treatment distinctly alleviated eGC damage and facilitated placental angiogenesis in CSE-treated rats. NaHS administration effectively promoted placental vascular endothelial proliferation and suppressed endothelial apoptosis in CSE-treated rats. Furthermore, NaHS treatment markedly elevated the phosphorylation of PI3K, AKT, and mTOR in the placenta of CSE-treated rats. Taken together, these results indicate that exogenous administration of H₂S can alleviate CSE-induced eGC damage and promote placental angiogenesis in CSE-treated rats, suggesting that H₂S may be a novel therapeutic agent for the treatment of CSE-associated vascular disease.</div></div>","PeriodicalId":19357,"journal":{"name":"Nitric oxide : biology and chemistry","volume":"154 ","pages":"Pages 115-127"},"PeriodicalIF":3.2,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142791849","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Investigation of the susceptibility of clinical infection loads to nitric oxide antibacterial treatment","authors":"Lori M. Estes Bright ,&nbsp;Arnab Mondal ,&nbsp;Vicente Pinon ,&nbsp;Anil Kumar ,&nbsp;Stephen Thompson ,&nbsp;Elizabeth J. Brisbois ,&nbsp;Hitesh Handa","doi":"10.1016/j.niox.2024.11.003","DOIUrl":"10.1016/j.niox.2024.11.003","url":null,"abstract":"<div><div>The persistent infection of medical devices by opportunistic pathogens has led to the development of antimicrobial medical device polymers. Nitric oxide (NO) is an endogenous antimicrobial molecule that is released through the degradation of synthetic donor molecules such as <em>S</em>-nitroso-<em>N</em>-acetylpenicillamine (SNAP) embedded into polymer membranes. It is hypothesized that the clinical success of these polymers is enhanced by the physiological release of NO and the consequent prevention of infection. However, such NO-releasing materials have never been evaluated against microbial loads that are commensurate with clinical infection levels. This study aimed to develop a standardized polymer film impregnated with SNAP that consistently releases NO and evaluates its efficacy against bacterial loads that represent clinical infection parameters. Microbial loads of 10³, 10⁵, and 10⁸ (colony-forming units) CFU mL⁻¹ were exposed to the NO-releasing polymer, corresponding to bloodstream infections, catheter-associated urinary tract infections, and standard laboratory exposure levels that have been reported in the scientific literature. By 24 h, SNAP films led to &gt;1 log reduction of adhered and viable <em>E. coli</em> at all tested microbial loads compared to control polydimethylsiloxane (PDMS). Further, SNAP films displayed no viable adhered <em>S. aureus</em> at the 10³ microbial level for the entire study and showed total planktonic killing by 8 h. NO localization within bacterial cells adhering to the films was evaluated, revealing higher NO uptake and consequent bacterial killing by SNAP samples. This unique study shows that NO-releasing polymers not only kill bacteria adhered to the polymer surface, but localized delivery leads to environmental planktonic bacterial killing that prevents adhesion from occurring. Furthermore, the promising findings of NO-releasing polymers in scientific research indicate their potential for successful application in clinical settings to prevent infections.</div></div>","PeriodicalId":19357,"journal":{"name":"Nitric oxide : biology and chemistry","volume":"154 ","pages":"Pages 19-28"},"PeriodicalIF":3.2,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142676257","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nitric oxide and mitochondrial function in cardiovascular diseases","authors":"Haoqi Li ,&nbsp;Zijie Cheng ,&nbsp;Dan Wu ,&nbsp;Qingxun Hu","doi":"10.1016/j.niox.2024.11.007","DOIUrl":"10.1016/j.niox.2024.11.007","url":null,"abstract":"<div><div>Nitric oxide (NO) has been highlighted as an important factor in cardiovascular system. As a signaling molecule in the cardiovascular system, NO can relax blood vessels, lower blood pressure, and prevent platelet aggregation. Mitochondria serve as a central hub for cellular metabolism and intracellular signaling, and their dysfunction can lead to a variety of diseases. Accumulating evidence suggests that NO can act as a regulator of mitochondria, affecting mitochondrial function and cellular activity, which in turn mediates the onset and progression of disease. However, there is a lack of comprehensive understanding of how NO regulates mitochondrial function in the cardiovascular system. This review aims to summarize the regulation of mitochondrial function by nitric oxide in cardiovascular related diseases, as well as the multifaceted and complex roles of NO in the cardiovascular system. Understanding the mechanism of NO mediated mitochondrial function can provide new insights for the prevention and treatment of cardiovascular diseases.</div></div>","PeriodicalId":19357,"journal":{"name":"Nitric oxide : biology and chemistry","volume":"154 ","pages":"Pages 42-50"},"PeriodicalIF":3.2,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142693322","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}