Increased oxidative stress and apoptosis in peripheral blood mononuclear cells of fructose-fed rats

Porto, Marcella L.; Lírio, Layla Mendonça; Dias, Ananda T.; Batista, Alan T.; Campagnaro, Bianca Prandi; Mill, José Geraldo; Meyrelles, Silvana S.; Baldo, Marcelo Perim

doi:10.1016/j.tiv.2015.08.006

Cited by 42 publications

(37 citation statements)

References 28 publications

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“…As little as 10% fructose in the drinking water of rats leads to systemic oxidative stress and related pro-inflammatory conditions. 31 …”

Section: Discussionmentioning

confidence: 99%

Free radical scavenging reverses fructose-induced salt-sensitive hypertension

Zenner¹,

Gordish²,

Beierwaltes³

2017

IBPC

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We have previously reported that a moderate dietary supplementation of 20% fructose but not glucose leads to a salt-sensitive hypertension related to increased proximal sodium–hydrogen exchanger activity and increased renal sodium retention. We also found that while high salt increased renal nitric oxide formation, this was retarded in the presence of fructose intake. We hypothesized that at least part of the pathway leading to fructose-induced salt-sensitive hypertension could be due to fructose-induced formation of reactive oxygen species and inappropriate stimulation of renin secretion, all of which would contribute to an increase in blood pressure. We found that both 20% fructose intake and a high-salt diet stimulated 8-isoprostane excretion. The superoxide dismutase (SOD) mimetic tempol significantly reduced this elevated excretion. Next, we placed rats on a high-salt diet (4%) for 1 week in combination with normal rat chow or 20% fructose with or without chronic tempol administration. A fructose plus high-salt diet induced a rapid increase (15 mmHg) in systolic blood pressure and reversed high salt suppression of plasma renin activity. Tempol treatment reversed the pressor response and restored high salt suppression of renin. We conclude that fructose-induced salt-sensitive hypertension is driven by increased renal reactive oxygen species formation associated with salt retention and an enhanced renin–angiotensin system.

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“…As little as 10% fructose in the drinking water of rats leads to systemic oxidative stress and related pro-inflammatory conditions. 31 …”

Section: Discussionmentioning

confidence: 99%

Free radical scavenging reverses fructose-induced salt-sensitive hypertension

Zenner¹,

Gordish²,

Beierwaltes³

2017

IBPC

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“…As previously reported, emerging studies pointed the oxidative stress, especially the production of ROS, as key up-regulated TRPV1 mediators in a variety of pathologies [34] , including pain processes [7] , [8] . AOPPs can indirectly sensitize NADPH oxidase to cause ROS overproduction in many kinds of cells [17] , [45] , [46] , [47] , [48] . Herein, we stimulated DRG neurons with AOPPs-RSA at different concentrations and for different time durations.…”

Section: Discussionmentioning

confidence: 99%

Advanced oxidation protein products sensitized the transient receptor potential vanilloid 1 via NADPH oxidase 1 and 4 to cause mechanical hyperalgesia

et al. 2016

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Oxidative stress is a possible pathogenesis of hyperalgesia. Advanced oxidation protein products (AOPPs), a new family of oxidized protein compounds, have been considered as a novel marker of oxidative stress. However, the role of AOPPs in the mechanism of hyperalgesia remains unknown. Our study aims to investigate whether AOPPs have an effect on hyperalgesia and the possible underlying mechanisms. To identify the AOPPs involved, we induced hyperalgesia in rats by injecting complete Freund’s adjuvant (CFA) in hindpaw. The level of plasma AOPPs in CFA-induced rats was 1.6-fold in comparison with what in normal rats (P<0.05). After intravenous injection of AOPPs-modified rat serum albumin (AOPPs-RSA) in Sprague-Dawley rats, the paw mechanical thresholds, measured by the electronic von Frey system, significantly declined. Immunofluorescence staining indicated that AOPPs increased expressions of NADPH oxidase 1 (Nox1), NADPH oxidase 4 (Nox4), transient receptor potential vanilloid 1 (TRPV1) and calcitonin gene-related peptide (CGRP) in the dorsal root ganglia (DRG) tissues. In-vitro studies were performed on primary DRG neurons which were obtained from both thoracic and lumbar DRG of rats. Results indicated that AOPPs triggered reactive oxygen species (ROS) production in DRG neurons, which were significantly abolished by ROS scavenger N-acetyl-l-cysteine (NAC) and small-interfering RNA (siRNA) silencing of Nox1 or Nox4. The expressions of Nox1, Nox4, TRPV1 and CGRP were significantly increased in AOPPs-induced DRG neurons. And relevant siRNA or inhibitors notably suppressed the expressions of these proteins and the calcium influxes in AOPPs-induced DRG neurons. In conclusion, AOPPs increased significantly in CFA-induced hyperalgesia rats and they activated Nox1/Nox4-ROS to sensitize TRPV1-dependent Ca2+ influx and CGRP release which led to inducing mechanical hyperalgesia.

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“…Increasing evidences suggest that fructose-induced MetS is closely associated with chronic inflammation, characterized by elevated peripheral blood mononuclear cells, reduced bone marrow mononuclear cell viability [127], increased systemic inflammation cytokine concentration [127], as well as inflammation signaling activation in local tissues and organs, including liver, adipose, kidney, heart and brain [128]. …”

Section: Indirect Dangerous Factors In Tissue and Organ Dysfunctiomentioning

confidence: 99%

“…The acceleration of fructolysis in intestine may cause local inflammation and reduce tight junction protein (occludin and ZO-1) expression in intestine, documenting an increase in intestinal permeability [174]. Meanwhile, high levels of circulating inflammatory cytokines, which are often observed in fructose-fed animals or patients [127,128], may impair intestinal mucosal integrity and induce portal blood endotoxemia [175,176]. …”

Section: Indirect Dangerous Factors In Tissue and Organ Dysfunctiomentioning

confidence: 99%

High Dietary Fructose: Direct or Indirect Dangerous Factors Disturbing Tissue and Organ Functions

2017

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High dietary fructose is a major contributor to insulin resistance and metabolic syndrome, disturbing tissue and organ functions. Fructose is mainly absorbed into systemic circulation by glucose transporter 2 (GLUT2) and GLUT5, and metabolized in liver to produce glucose, lactate, triglyceride (TG), free fatty acid (FFA), uric acid (UA) and methylglyoxal (MG). Its extrahepatic absorption and metabolism also take place. High levels of these metabolites are the direct dangerous factors. During fructose metabolism, ATP depletion occurs and induces oxidative stress and inflammatory response, disturbing functions of local tissues and organs to overproduce inflammatory cytokine, adiponectin, leptin and endotoxin, which act as indirect dangerous factors. Fructose and its metabolites directly and/or indirectly cause oxidative stress, chronic inflammation, endothelial dysfunction, autophagy and increased intestinal permeability, and then further aggravate the metabolic syndrome with tissue and organ dysfunctions. Therefore, this review addresses fructose-induced metabolic syndrome, and the disturbance effects of direct and/or indirect dangerous factors on the functions of liver, adipose, pancreas islet, skeletal muscle, kidney, heart, brain and small intestine. It is important to find the potential correlations between direct and/or indirect risk factors and healthy problems under excess dietary fructose consumption.

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Increased oxidative stress and apoptosis in peripheral blood mononuclear cells of fructose-fed rats

Cited by 42 publications

References 28 publications

Free radical scavenging reverses fructose-induced salt-sensitive hypertension

Free radical scavenging reverses fructose-induced salt-sensitive hypertension

Advanced oxidation protein products sensitized the transient receptor potential vanilloid 1 via NADPH oxidase 1 and 4 to cause mechanical hyperalgesia

High Dietary Fructose: Direct or Indirect Dangerous Factors Disturbing Tissue and Organ Functions

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