Nitric oxide : biology and chemistry最新文献

{"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":"2024-11-20","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}

{"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":"2024-11-19","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":"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":"2024-11-17","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":"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":"2024-11-14","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":"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":"2024-11-07","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":"Neurogenic-derived 6-nitrodopamine is the most potent endogenous modulator of the mouse urinary bladder relaxation","authors":"Mariana Gonçalves de Oliveira ,&nbsp;José Britto-Junior ,&nbsp;Douglas Rafael Martins Dias ,&nbsp;Luise Gabriela Santos Pereira ,&nbsp;Silvana Chiavegatto ,&nbsp;Idam Hermawan ,&nbsp;Hiroaki Shimokawa ,&nbsp;Masato Tsutsui ,&nbsp;Edson Antunes ,&nbsp;Gilberto De Nucci","doi":"10.1016/j.niox.2024.10.010","DOIUrl":"10.1016/j.niox.2024.10.010","url":null,"abstract":"<div><div>6-Nitrodopamine (6-ND) modulates vas deferens, seminal vesicles, and corpus cavernosum contractility; however, its role on the lower urinary tract organs has not been evaluated. Investigations of isolated urinary bladders from wild-type (WT) mice revealed 6-ND release was comparable to that of dopamine and adrenaline, whereas noradrenaline was hardly detected, as assessed by liquid chromatography coupled to tandem mass spectrometry. <em>In vitro</em>, 6-ND induced concentration-dependent relaxations in carbachol pre-contracted bladders with high potency (pEC₅₀: 8.04 ± 0.86), independently of eNOS/sGC activity. Co-incubation of 6-ND (1–10 μM) antagonizes the contractile effects of acetylcholine (p &lt; 0.05). Experiments using nitric oxide synthase (NOS) knockout mice demonstrated that 6-ND release from isolated urinary bladder was significantly reduced by neuronal NOS (nNOS^−/−) deletion and abolished by triple NOSs deletion (n/i/eNOS^−/−), while no significant changes were observed in endothelial (eNOS^−/−) or inducible (iNOS^−/−) knockout mice. Incubation with tetrodotoxin resulted in a significant decrease in 6-ND release in bladders obtained from WT, but not in nNOS^−/− mice. The bladders from nNOS^−/− and n/i/eNOS^−/− mice exhibited significantly higher contractile responses to electric field stimulation (EFS), compared to eNOS^−/−, iNOS^−/−, or WT bladders. The hyperreactivity observed in triple NOS knockouts was reversed by the incubation with bladder mucosal layer obtained from a donor WT mice, but not with the muscular layer. These findings clearly demonstrate 6-ND is the most potent endogenous relaxing agent of urinary bladder, and inhibition of its release is associated with bladder hyperreactivity.</div></div>","PeriodicalId":19357,"journal":{"name":"Nitric oxide : biology and chemistry","volume":"153 ","pages":"Pages 98-105"},"PeriodicalIF":3.2,"publicationDate":"2024-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142471019","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":"Generation and characterization of a conditional eNOS knock out mouse model for cell-specific reactivation of eNOS in gain-of-function studies","authors":"Anthea LoBue ,&nbsp;Zhixin Li ,&nbsp;Sophia K. Heuser ,&nbsp;Junjie Li ,&nbsp;Francesca Leo ,&nbsp;Lukas Vornholz ,&nbsp;Luke S. Dunaway ,&nbsp;Tatsiana Suvorava ,&nbsp;Brant E. Isakson ,&nbsp;Miriam M. Cortese-Krott","doi":"10.1016/j.niox.2024.10.009","DOIUrl":"10.1016/j.niox.2024.10.009","url":null,"abstract":"<div><div>Nitric oxide (NO) produced by endothelial nitric oxide synthase (eNOS) in the vessel wall regulates blood pressure and cardiovascular hemodynamics. In this study, we generated conditional eNOS knock out (KO) mice characterized by a duplicated/inverted exon 2 flanked with two pairs of loxP regions (eNOS^inv/inv); a Cre-recombinase activity induces cell-specific reactivation of eNOS, as a result of a flipping of the inverted exon 2 (eNOS^fl). This work aimed to test the efficiency of the Cre-mediated cell-specific recombination and the resulting eNOS expression/function. As proof of concept, we crossed eNOS^inv/inv mice with DeleterCre^pos (DelCre^pos) mice, expressing Cre recombinase in all cells. We generated heterozygous eNOS^fl/inv or homozygous eNOS^fl/fl mice, and eNOS^inv/inv littermate mice. We found that both eNOS^fl/fl and eNOS^fl/inv mice express eNOS and the overall expression level depends on the number of mutated alleles, while eNOS^inv/inv mice did not show any eNOS expression. Vascular endothelial function was restored in eNOS^fl/fl and eNOS^fl/inv mice, as determined by ACh-dependent vasodilation of aortic rings. Cre-dependent reactivation of eNOS in eNOS^fl/fl and eNOS^fl/inv mice rescued eNOS^inv/inv (phenotypically global eNOS KO) mice from hypertension. These findings demonstrate that eNOS expression is restored in eNOS^fl/fl mice at comparable physiological levels of WT mice, and its functional activity is independent on the number of the reactivated alleles. Therefore, eNOS^inv/inv mice are a useful model for studying the effects of conditional reactivation of eNOS and gene dosage effects in specific cells for gain-of-function studies.</div></div>","PeriodicalId":19357,"journal":{"name":"Nitric oxide : biology and chemistry","volume":"153 ","pages":"Pages 106-113"},"PeriodicalIF":3.2,"publicationDate":"2024-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142471018","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":"A systematic review and dose‒response meta-analysis of the association between nitrate & nitrite intake and gastroesophageal cancer risk","authors":"Mohammadreza Ghasemi ,&nbsp;Mohammad Bahrami koutenaei ,&nbsp;Alireza Ghasemi ,&nbsp;Reza Alizadeh-navaei ,&nbsp;Mahmood Moosazadeh","doi":"10.1016/j.niox.2024.10.007","DOIUrl":"10.1016/j.niox.2024.10.007","url":null,"abstract":"<div><h3>Objective</h3><div>The objective of this systematic review and dose‒response meta-analysis was to assess the associations between the dietary consumption of nitrate and nitrite and the risk of gastric and esophageal cancer.</div></div><div><h3>Methods</h3><div>MEDLINE, Scopus, Embase, Web of Science, Proquest, and Google Scholar were searched until April 1, 2024. Articles were selected by two independent researchers on the basis of the inclusion and exclusion criteria. Data regarding the study design, type of exposure and outcomes, intervals of intake of nitrate or nitrite in each layer, OR/RR/HR of the relationship for each layer of intake, total sample size, and number of cases of gastric or esophageal cancer were extracted. The certainty of the evidence was rated via the GRADE method. The pooled odds ratios, risk ratios, and dose‒response analyses were calculated via Stata version 17.0. The best-fit dose‒response model was assessed by the P value for linearity and nonlinearity. Study heterogeneity was assessed via the I² and Q tests.</div></div><div><h3>Results</h3><div>We found 2124 nonredundant studies, 234 of which were potentially relevant. Eighteen articles met the inclusion criteria and were included in the review. The results of the meta-analysis revealed a significant positive association between nitrite intake and gastric cancer in both case‒control studies (OR = 1.29, 95 % CI = 1.09–1.52, P value = 0.001, I² = 1.91 %) and cohort studies (RR = 1.17, 95 % CI = 1.00–1.37, P value = 0.04, I² = 0.00 %). In addition, case‒control studies revealed a nonsignificant inverse association between nitrate intake and gastric cancer incidence (OR = 0.71, 95 % CI = 0.50–1.01, P value = 0.06, I² = 74.89 %), and cohort studies (RR = 0.89, 95 % CI = 0.73–1.09, P value = 0.27, I² = 0.00 %). Case‒control studies also revealed no significant correlation between nitrite intake and esophageal cancer incidence (OR = 1.48, 95 % CI = 0.91 to 2.42, P value = 0.12, I² = 0.001 %). Nitrites correlated linearly with gastric cancer (linearity P value = 0.001). The most appropriate fit models for the relationship between nitrate and gastric cancer were both piecewise linear and natural polynomial regression (quadratic) models (P values = 0.003 and 0.005, respectively). There was no significant publication bias.</div></div><div><h3>Conclusion</h3><div>According to this meta-analysis, high consumption of nitrites was associated with an increased risk of gastric cancer in case‒control and cohort studies with a linear regression model, and dietary nitrate intake was not associated with the risk of gastric cancer in either case‒control or cohort studies. These findings are inconclusive and require confirmation in future prospective studies with robust methodologies and adjustments for potential confounders.</div></div>","PeriodicalId":19357,"journal":{"name":"Nitric oxide : biology and chemistry","volume":"153 ","pages":"Pages 61-71"},"PeriodicalIF":3.2,"publicationDate":"2024-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142471020","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 ameliorated endothelial dysfunction in hyperhomocysteinemia rats: Mechanism of IRE1α/JNK pathway-mediated autophagy","authors":"Yuan Gao ,&nbsp;Jiao Xu ,&nbsp;Kaichuan He ,&nbsp;Qi Guo ,&nbsp;Lin Xiao ,&nbsp;Sheng Jin ,&nbsp;Danyang Tian ,&nbsp;Xu Teng ,&nbsp;Cuixia An ,&nbsp;Hongmei Xue ,&nbsp;Yuming Wu","doi":"10.1016/j.niox.2024.10.008","DOIUrl":"10.1016/j.niox.2024.10.008","url":null,"abstract":"<div><div>Previous studies showed that hyperhomocysteinemia (HHcy) induced endothelial dysfunction by endoplasmic reticulum (ER) stress induction and autophagy stimulation. This study aimed to determine the effect of hydrogen sulfide (H₂S) in homocysteine (Hcy)-induced endothelial dysfunction and observe the possible mechanism involved. Male Wistar rats (160–180g) were used and randomly divided into four groups: Control group, HHcy group, HHcy+Sodium hydrosulfide (NaHS) group and NaHS group. Rats were fed with 2% high methionine diet for 8 weeks to set up HHcy model. Plasma concentration of Hcy was measured by ELISA. Endothelium-dependent and non-endothelium-dependent vasodilation of rat renal arteries were determined by myograph. The protein expression of cystathionine-γ-lyase (CSE), ER stress- and autophagy-related proteins in renal arteries or human umbilical vein endothelial cells (HUVECs) were analyzed by western blotting. The endothelial function was impaired in HHcy rats and HUVECs. NaHS supplementation could improve the ACh-induced vasodilation, however it was eliminated by ER stress inducer Tunicamycin (TM) or autophagy inducer Rapamycin. Western blotting in renal arteries showed that Glucose-regulated protein 78 (GRP78) and three branches of ER stress (p-IRE1α, p-PERK, ATF6) , p-JNK1+p-JNK2 were downregulated, simultaneously the autophagy marker Beclin1, LC3BII/LC3BI ratio were decreased and p62 was increased with NaHS treatment in HHcy rats. In HUVECs, IRE1α-JNK induced autophagy was involved in HHcy-induced endothelial dysfunction, while NaHS stimulation reversed the protein expression in IRE1α/JNK-autophagy pathway with Hcy incubation. This study might suggest that endothelial dysfunction induced by HHcy might be correlated with IRE1α-JNK-autophagy axis pathway, which was suppressed by exogenous supplementation of H₂S donor, NaHS.</div></div>","PeriodicalId":19357,"journal":{"name":"Nitric oxide : biology and chemistry","volume":"153 ","pages":"Pages 72-81"},"PeriodicalIF":3.2,"publicationDate":"2024-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142471021","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":"An updated mechanistic overview of nitric oxide in drought tolerance of plants","authors":"Sakshi Saini ,&nbsp;Priyanka Sharma ,&nbsp;Pooja Pooja ,&nbsp;Asha Sharma","doi":"10.1016/j.niox.2024.10.006","DOIUrl":"10.1016/j.niox.2024.10.006","url":null,"abstract":"<div><div>Drought stress, an inevitable global issue due to climate change, hinders plant growth and yield. Nitric oxide (NO), a tiny gaseous signaling compound is now gaining massive attention from the plant science community due to its unparalleled array of mechanisms for ameliorating various abiotic stresses, including drought. Supplementation of NO has shown its astounding effect in improving drought tolerance by prominently influencing its tendency to modulate stomatal movement and reduce oxidative stress; it can enormously affect the various other physio-biochemical processes such as root structure, photosynthesis, osmolyte cumulation, and seed establishment of plants due to its amalgamation with a wide range of molecules during drought conditions. The production and inhibition of root development majorly depend on NO concentration and/or experimental conditions. As a lipophilic free gasotransmitter, NO readily reacts with free metals and oxygen species and has been shown to enhance or reduce the redox homeostasis of plants, depending on whether acting in a chronic or acute mode. NO can easily alter the enzymes, protein activities, and genomic transcriptional and post-translational modifications that assist functional retrieval from water stress. Although progress is ongoing, much work remains to be done to describe the proper target site and mechanistic approach of this vibrant molecule in plant drought tolerance. This detailed review navigates through the comprehensive and clear picture of the mechanistic potential of NO in drought stress following molecular approaches and suggests effective physiological and biochemical strategies to overcome the negative impacts of drought. We explore its potential to increase crop production, thereby ensuring global food security in drought-prone areas. In an era marked by unrelenting climatic conditions, the implications of NO show a promising approach to sustainable farming, providing a beacon of hope for future crop productivity.</div></div>","PeriodicalId":19357,"journal":{"name":"Nitric oxide : biology and chemistry","volume":"153 ","pages":"Pages 82-97"},"PeriodicalIF":3.2,"publicationDate":"2024-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142471017","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}