High-salt diet enhances hippocampal oxidative stress and cognitive impairment in mice

D 3 dopamine receptor (D 3 R) deficient mice have renin-dependent hypertension but the hypertension is mild and is not associated with oxidative stress. In order to determine if any compensatory mechanism in the kidney is involved in the regulation of blood pressure with disruption of D 3 R, we measured the renal protein expression of dopamine receptors in D 3 R homozygous (D 3 -/-) and heterozygous (D 3 +/-) knockout mice and their wild type (D 3 +/+) littermates. D 5 dopamine receptor (D 5 R) (169±23%, reported as % of D 3 +/+, n=5/group) expression was increased but D 4 dopamine receptors protein expression (59±8%) was decreased, while no significant changes were found with D 1 and D 2 dopamine receptors. Immunocytochemistry showed a stronger renal staining of D 5 R but without a change in renal tubule cell distribution in D 3 -/- relative to D 3 +/+ mice. D 5 R abundance was also increased in D 3 +/- (205±30%, n=5/group) relative to D 3 +/+ mice, while D 1 R abundance was similar between D 3 +/- and D 3 +/+ mice. The increase in D 5 R expression was abolished while blood pressure was increased further in D 3 -/- mice fed a high salt diet. Treatment of the D 1 -like (including D 1 and D 5 receptors) antagonist, SCH23390 , increased the blood pressure to a greater extent in anesthetized D 3 -/- mice than in D 3 +/+ mice (n=4/group), suggesting that the upregulation of D 5 R may modulate the hypertension in mice caused by the disruption of D 3 R. Since dopamine inhibits the NADPH oxidase-induced production of reactive oxygen species (ROS) via the D 5 R, we also measured the protein expression of NOXs in the kidney and isoprostane in the urine. No NADPH oxidase subunit was increased in D 3 -/- and D 3 +/- mice relative to D 3 +/+ mice fed a normal or salt high salt diet, and urinary isoprostane excretion was also similar in D 3 -/- and D 3 +/+ mice. Our findings suggest that the upregulation of D 5 R may minimize the hypertension and prevent oxidative stress in D 3 -/- mice.

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Cyperus esculentus L. (tigernut) mitigates high salt diet‐associated testicular toxicity in Wistar rats by targeting testicular steroidogenesis, oxidative stress and inflammation

Andrologia ◽

10.1111/and.13780 ◽

2020 ◽

Vol 52 (11) ◽

Author(s):

Justina Nwandimma Nwangwa ◽

Augustine Lishilinimye Udefa ◽

Ernest Atelhe Amama ◽

Inah Onete Inah ◽

Hamza Joseph Ibrahim ◽

...

Keyword(s):

Oxidative Stress ◽

Wistar Rats ◽

High Salt ◽

Testicular Toxicity ◽

Cyperus Esculentus ◽

High Salt Diet ◽

Salt Diet ◽

Testicular Steroidogenesis

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Helicobacter pylori AdaptationIn Vivoin Response to a High-Salt Diet

Infection and Immunity ◽

10.1128/iai.00918-15 ◽

2015 ◽

Vol 83 (12) ◽

pp. 4871-4883 ◽

Cited By ~ 11

Author(s):

John T. Loh ◽

Jennifer A. Gaddy ◽

Holly M. Scott Algood ◽

Silvana Gaudieri ◽

Simon Mallal ◽

...

Keyword(s):

Oxidative Stress ◽

Helicobacter Pylori ◽

High Salt ◽

Mongolian Gerbils ◽

High Salt Diet ◽

Salt Diet ◽

Content Type ◽

Regular Diet ◽

H Pylori ◽

And Oxidative Stress

Helicobacter pyloriexhibits a high level of intraspecies genetic diversity. In this study, we investigated whether the diversification ofH. pyloriis influenced by the composition of the diet. Specifically, we investigated the effect of a high-salt diet (a known risk factor for gastric adenocarcinoma) onH. pyloridiversification within a host. We analyzedH. pyloristrains isolated from Mongolian gerbils fed either a high-salt diet or a regular diet for 4 months by proteomic and whole-genome sequencing methods. Compared to the input strain and output strains from animals fed a regular diet, the output strains from animals fed a high-salt diet produced higher levels of proteins involved in iron acquisition and oxidative-stress resistance. Several of these changes were attributable to a nonsynonymous mutation infur(fur-R88H). Further experiments indicated that this mutation conferred increased resistance to high-salt conditions and oxidative stress. We propose a model in which a high-salt diet leads to high levels of gastric inflammation and associated oxidative stress inH. pylori-infected animals and that these conditions, along with the high intraluminal concentrations of sodium chloride, lead to selection ofH. pyloristrains that are most fit for growth in this environment.

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High-salt diet increases glomerular ACE/ACE2 ratio leading to oxidative stress and kidney damage

Nephrology Dialysis Transplantation ◽

10.1093/ndt/gfr600 ◽

2011 ◽

Vol 27 (5) ◽

pp. 1793-1800 ◽

Cited By ~ 33

Author(s):

Stella Bernardi ◽

Barbara Toffoli ◽

Cristina Zennaro ◽

Christos Tikellis ◽

Silvia Monticone ◽

...

Keyword(s):

Oxidative Stress ◽

Kidney Damage ◽

High Salt ◽

High Salt Diet ◽

Salt Diet

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Melatonin prevents kidney injury in a high salt diet-induced hypertension model by decreasing oxidative stress

Journal of Pineal Research ◽

10.1111/jpi.12287 ◽

2015 ◽

Vol 60 (1) ◽

pp. 48-54 ◽

Cited By ~ 28

Author(s):

Avshalom Leibowitz ◽

Alexander Volkov ◽

Konstantin Voloshin ◽

Chen Shemesh ◽

Iris Barshack ◽

...

Keyword(s):

Oxidative Stress ◽

Kidney Injury ◽

High Salt ◽

High Salt Diet ◽

Salt Diet ◽

Induced Hypertension

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Alamandine alleviates hypertension and renal damage via oxidative-stress attenuation in Dahl rats

Cell Death Discovery ◽

10.1038/s41420-022-00822-y ◽

2022 ◽

Vol 8 (1) ◽

Author(s):

Juexiao Gong ◽

Man Luo ◽

Yonghong Yong ◽

Shan Zhong ◽

Peng Li

Keyword(s):

Oxidative Stress ◽

Renal Dysfunction ◽

Renal Damage ◽

High Salt ◽

High Salt Diet ◽

Salt Diet ◽

Renal Tubular Cells ◽

Induced Hypertension

AbstractAlamandine (Ala) is a novel member of the renin–angiotensin-system (RAS) family. The present study aimed to explore the effects of Ala on hypertension and renal damage of Dahl salt-sensitive (SS) rats high-salt diet-induced, and the mechanisms of Ala on renal-damage alleviation. Dahl rats were fed with high-salt diets to induce hypertension and renal damage in vivo, and HK-2 cells were treated with sodium chloride (NaCl) to induce renal injury in vitro. Ala administration alleviated the high-salt diet-induced hypertension, renal dysfunction, and renal fibrosis and apoptosis in Dahl SS rats. The HK-2 cells’ damage, and the increases in the levels of cleaved (c)-caspase3, c-caspase8, and c-poly(ADP-ribose) polymerase (PARP) induced by NaCl were inhibited by Ala. Ala attenuated the NaCl-induced oxidative stress in the kidney and HK-2 cells. DETC, an inhibitor of SOD, reversed the inhibitory effect of Ala on the apoptosis of HK-2 cells induced by NaCl. The NaCl-induced increase in the PKC level was suppressed by Ala in HK-2 cells. Notably, PKC overexpression reversed the moderating effects of Ala on the NaCl-induced apoptosis of HK-2 cells. These results show that Ala alleviates high-salt diet-induced hypertension and renal dysfunction. Ala attenuates the renal damage via inhibiting the PKC/reactive oxygen species (ROS) signaling pathway, thereby suppressing the apoptosis in renal tubular cells.

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High-Salt Diet in the Pre- and Postweaning Periods Leads to Amygdala Oxidative Stress and Changes in Locomotion and Anxiety-Like Behaviors of Male Wistar Rats

Frontiers in Behavioral Neuroscience ◽

10.3389/fnbeh.2021.779080 ◽

2022 ◽

Vol 15 ◽

Author(s):

Pedro Ernesto de Pinho Tavares Leal ◽

Alexandre Alves da Silva ◽

Arthur Rocha-Gomes ◽

Tania Regina Riul ◽

Rennan Augusto Cunha ◽

...

Keyword(s):

Oxidative Stress ◽

Wistar Rats ◽

Redox State ◽

Redox Status ◽

High Salt ◽

Standard Diet ◽

High Salt Diet ◽

Salt Diet ◽

Plus Maze ◽

Male Wistar Rats

High-salt (HS) diets have recently been linked to oxidative stress in the brain, a fact that may be a precursor to behavioral changes, such as those involving anxiety-like behavior. However, to the best of our knowledge, no study has evaluated the amygdala redox status after consuming a HS diet in the pre- or postweaning periods. This study aimed to evaluate the amygdala redox status and anxiety-like behaviors in adulthood, after inclusion of HS diet in two periods: preconception, gestation, and lactation (preweaning); and only after weaning (postweaning). Initially, 18 females and 9 male Wistar rats received a standard (n = 9 females and 4 males) or a HS diet (n = 9 females and 5 males) for 120 days. After mating, females continued to receive the aforementioned diets during gestation and lactation. Weaning occurred at 21-day-old Wistar rats and the male offspring were subdivided: control-control (C-C)—offspring of standard diet fed dams who received a standard diet after weaning (n = 9–11), control-HS (C-HS)—offspring of standard diet fed dams who received a HS diet after weaning (n = 9–11), HS-C—offspring of HS diet fed dams who received a standard diet after weaning (n = 9–11), and HS-HS—offspring of HS diet fed dams who received a HS diet after weaning (n = 9–11). At adulthood, the male offspring performed the elevated plus maze and open field tests. At 152-day-old Wistar rats, the offspring were euthanized and the amygdala was removed for redox state analysis. The HS-HS group showed higher locomotion and rearing frequency in the open field test. These results indicate that this group developed hyperactivity. The C-HS group had a higher ratio of entries and time spent in the open arms of the elevated plus maze test in addition to a higher head-dipping frequency. These results suggest less anxiety-like behaviors. In the analysis of the redox state, less activity of antioxidant enzymes and higher levels of the thiobarbituric acid reactive substances (TBARS) in the amygdala were shown in the amygdala of animals that received a high-salt diet regardless of the period (pre- or postweaning). In conclusion, the high-salt diet promoted hyperactivity when administered in the pre- and postweaning periods. In animals that received only in the postweaning period, the addition of salt induced a reduction in anxiety-like behaviors. Also, regardless of the period, salt provided amygdala oxidative stress, which may be linked to the observed behaviors.

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Involvement of NLRP3 inflammasome in the impacts of sodium and potassium on insulin resistance in normotensive Asians

British Journal Of Nutrition ◽

10.1017/s0007114517002926 ◽

2018 ◽

Vol 119 (2) ◽

pp. 228-237 ◽

Cited By ~ 11

Author(s):

Zhaofei Wan ◽

Wen Wen ◽

Keyu Ren ◽

Dong Zhou ◽

Junhui Liu ◽

...

Keyword(s):

Oxidative Stress ◽

Insulin Resistance ◽

Nlrp3 Inflammasome ◽

Fasting Blood Glucose ◽

High Salt ◽

Inflammasome Activation ◽

High Salt Diet ◽

Salt Loading ◽

Salt Diet ◽

Active Effects

AbstractSalt, promoting oxidative stress, contributes to insulin resistance, whereas K, inhibiting oxidative stress, improves insulin sensitivity. Oxidative stress activation of NLRP3 inflammasome is a central player in the induction of insulin resistance. Therefore, we hypothesised that NLRP3 inflammasome may mediate the effects of salt and K on insulin resistance. In all, fifty normotensive subjects were recruited from a rural community of Northern China. The protocol included a low-salt diet for 7 d, then a high-salt diet for 7 d and a high-salt diet with K supplementation for another 7 d. In addition, THP-1 cells were cultured in different levels of Na with and without K. The results showed that salt loading elevated fasting blood glucose, insulin and C-peptide levels, as well as insulin resistance, whereas K supplementation reversed them. Meanwhile, additional K reversed the active effects of high salt on NLRP3 inflammasome in both the subjects and THP-1 cells, and the change of insulin resistance index notably related with the alteration of plasma IL-1β, the index of NLRP3 inflammasome activation, during intervention in the subjects. Additional K ameliorated oxidative stress induced by high salt in both the subjects and cultured THP-1 cells, and the change of oxidative stress related with the alteration of plasma IL-1β during intervention in the subjects. In vitro, antioxidant N-acetyl-l-cysteine significantly prevented the active effects of high Na or oxidant Rosup on NLRP3 inflammasome, so did K. Our study indicates that oxidative stress modulation of NLRP3 inflammasome may be involved in the impacts of Na and K on insulin resistance.

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Impact of high fat/high salt diet on myocardial oxidative stress

Clinical and Experimental Hypertension ◽

10.1080/10641963.2016.1226894 ◽

2017 ◽

Vol 39 (2) ◽

pp. 126-132 ◽

Cited By ~ 9

Author(s):

Fadia Mayyas ◽

Karem H. Alzoubi ◽

Zahraa Al-Taleb

Keyword(s):

Oxidative Stress ◽

High Salt ◽

High Fat ◽

High Salt Diet ◽

Salt Diet ◽

Myocardial Oxidative Stress

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Renal Overexpression of Atrial Natriuretic Peptide and Hypoxia Inducible Factor-1αas Adaptive Response to a High Salt Diet

BioMed Research International ◽

10.1155/2014/936978 ◽

2014 ◽

Vol 2014 ◽

pp. 1-10 ◽

Cited By ~ 1

Author(s):

Silvana Lorena Della Penna ◽

Gabriel Cao ◽

Andrea Carranza ◽

Elsa Zotta ◽

Susana Gorzalczany ◽

...

Keyword(s):

Oxidative Stress ◽

Atrial Natriuretic Peptide ◽

Natriuretic Peptide ◽

Adaptive Response ◽

Hypoxia Inducible Factor ◽

High Salt ◽

High Salt Diet ◽

Salt Diet ◽

Sodium Overload ◽

Atrial Natriuretic

In the kidney, a high salt intake favors oxidative stress and hypoxia and causes the development of fibrosis. Both atrial natriuretic peptide (ANP) and hypoxia inducible factor (HIF-1α) exert cytoprotective effects. We tested the hypothesis that renal expression of ANP and HIF-1αis involved in a mechanism responding to the oxidative stress produced in the kidneys of rats chronically fed a high sodium diet. Sprague-Dawley rats were fed with a normal salt (0.4% NaCl) (NS) or a high salt (8% NaCl) (HS) diet for 3 weeks, with or without the administration of tempol (T), an inhibitor of oxidative stress, in the drinking water. We measured the mean arterial pressure (MAP), glomerular filtration rate (GFR), and urinary sodium excretion (UVNa). We evaluated the expression of ANP, HIF-1α, and transforming growth factor (TGF-β1) in renal tissues by western blot and immunohistochemistry. The animals fed a high salt diet showed increased MAP andUVNalevels and enhanced renal immunostaining of ANP, HIF-1α, and TGF-β1. The administration of tempol together with the sodium overload increased the natriuresis further and prevented the elevation of blood pressure and the increased expression of ANP, TGF-β1, and HIF-1αcompared to their control. These findings suggest that HIF-1αand ANP, synthesized by the kidney, are involved in an adaptive mechanism in response to a sodium overload to prevent or attenuate the deleterious effects of the oxidative stress and the hypoxia on the development of fibrosis.Erratum to “Renal Overexpression of Atrial Natriuretic Peptide and Hypoxia Inducible Factor-1α as Adaptive Response to a High Salt Diet”

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