Side-Stream Cigarette Smoke Induces Dose–Response in Systemic Inflammatory Cytokine Production and Oxidative Stress

2002 ◽  
Vol 227 (9) ◽  
pp. 823-829 ◽  
Author(s):  
Jin Zhang ◽  
Yingying Liu ◽  
Jiaqi Shi ◽  
Douglas F. Larson ◽  
Ronald Ross Watson

Side-stream cigarette smoke (SSCS), a major component of secondhand smoke, induces reactive oxygen species, which promote oxidative damage in tissues and organs. Inflammatory cytokines play an important role in the pathogenesis of atherosclerosis and heart failure. The present 4-month study examined the effect of various chronic SSCS exposure levels on splenic inflammatory cytokine secretion, heart contractile function, and pathology at 60- and 120-min per day, 5 days per week, for a total of 16 weeks. Tissue vitamin E level and lipid peroxide production also were tested to estimate the oxidative stress. The study found that the pro-inflammatory cytokines, interleukin (IL)-6, tumor necrosis factor (TNF)-α, and IL-1β, significantly increased in 120-min SSCS-exposed mice. Decreased stroke volume and increased peripheral arterial resistance were observed in mice exposed to 120-min SSCS per day. Heart pathology was only found in 120-min SSCS-exposed mice. Cardiac and hepatic antioxidant vitamin E levels were decreased as a result of oxidative stress. Hepatic lipid peroxides were Increased upon 60-min SSCS exposure. The data also demonstrated that the cardiac α-tocopherol level has a strong correlation with stroke volume; splenic IL-1β has a strong negative correlation with stroke volume; splenic TNF-α has a very strong negative correlation with stroke volume. In conclusion, SSCS exposure induced systemic inflammatory responses. SSCS exposure also accentuated systemic lipid peroxidation with depletion of cardiac and hepatic antioxidant vitamin E level. Finally, SSCS exposure at 120 min per day decreased stroke volume and increased vascular resistance. Systemic IL-1 β and TNF-α production are responsible for heart contractile dysfunction. Free radicals may be responsible for the progression to heart contractile dysfunction induced, in part, by SSCS. Oxidized lipoprotein could contribute to the vascular functional changes. Exploring the mechanism of vascular dysfunction in mice is warranted. A more precise quantification of the smoking exposure dose in mice needs to be determined as well.

2019 ◽  
Vol 1 (7) ◽  
pp. 34-38
Author(s):  
E. V. Dontsova ◽  
O. Yu. Olisova ◽  
L. S. Kruglova

Objectives: to study communications of separate components of the metabolic syndrome (MS) and immune and oxidative characteristics of patients with psoriasis in combination with MS. Methods. The research included 312 patients with psoriasis having diagnostic signs of a metabolic syndrome. Biochemical and immunological researches were conducted by means of immunofermental and immunokhemilyuminestsentny analyses. Results. At patients with psoriasis at a combination to MS abdominal obesity, a giperleptinemiya, insulin resistance, high oxidizing potential and hyperactivity of interleukins (ILS) -1β,-6,-8, a factor of a necrosis of tumors an alpha (FNO-α), interferon scale (INF-γ) are noted. the waist circle’ is characteristic direct weak correlation with the pro-inflammatory tsitokina oxidized by lipoproteins of blood (LDL-ok) and with the general oxidizing ability of blood (OOS), weak negative correlation of an indicator - with the general antioxidant ability of blood (OAS) and superoxide dismutase (SOD). The HOMA-IR index has direct correlation link of moderate force with levels of a leptin of blood, LDL-ok, OOS, pro-inflammatory tsitokin, negative correlation of moderate force - with OAS, SOD. At patients with psoriasis with MS direct strong correlation link of level of a leptin of blood with activity of the studied pro-inflammatory cytokine, LDL-ok, OOS moderated is established with the level of insulin in the blood., the HOMA-IR index, strong negative correlation with OAS, SOD. Conclusion. Presence at patients with psoriasis of signs of a metabolic syndrome is followed by increase in activity of immune and inflammatory mechanisms, development of oxidative stress.


2014 ◽  
Vol 280 (1) ◽  
pp. 97-106 ◽  
Author(s):  
Irene Riezzo ◽  
Emanuela Turillazzi ◽  
Stefania Bello ◽  
Santina Cantatore ◽  
Daniela Cerretani ◽  
...  

2021 ◽  
Vol 15 (9) ◽  
pp. 2952-2954
Author(s):  
Roomisa Anis ◽  
Misbah-ul- Qamar ◽  
Ayesha Shafqat ◽  
Ayesha Aftab ◽  
Zarafshan Bader ◽  
...  

Lead (Pb) is an abundant and one of the most lethal metals found in the earth’s crust. Its use by humans dates back to thousands of year. Even the low doses of lead are responsible for the production of reactive oxygen species which leads to oxidative load. This oxidative stress mitigates production of malondialdehyde (MDA) and down regulates antioxidant enzyme superoxide dismutase (SOD). Study Design: Quasi experimental Study. Place and duration of study: Department of Biochemistry, ANMCH, Islamabad, Pakistan in collaboration with NIH, Islamabad from November, 2018 to April, 2019. Methodology: A total of 40 BALB/c mice were divided into two groups of 20 mice each. Group  was given normal standard diet. Group  was given lead acetate in drinking water with normal diet without any supplementation. Levels of malondialdehyde were measured by using Thiobarbituric acid reactive substances (TBARS) and Superoxide Dismutase (SOD) was estimated by xanthine oxidase method at the end of study. Results: The results of our study showed increase in MDA and decrease in SOD in lead treated group when compared with the control group. Pearson correlation was applied to assess the degree of association between two parameters, it showed significant negative correlation with value of r = -0.96 and p-value of 0.001 Conclusion: It was concluded from our study that increase in MDA leads to decrease in SOD indicating strong negative correlation in lead poisoned mice. Key words: Lead poisoning, Malondialdehyde, Oxidative Stress, Superoxide Dismutase


2007 ◽  
Vol 292 (5) ◽  
pp. F1404-F1410 ◽  
Author(s):  
You-Lin Tain ◽  
Gary Freshour ◽  
Anna Dikalova ◽  
Kathy Griendling ◽  
Chris Baylis

Chronic kidney disease is accompanied by nitric oxide (NO) deficiency and oxidative stress, which contribute to progression. We investigated whether the antioxidant vitamin E could preserve renal function and NO bioavailability and reduce oxidative stress in the 5/6th nephrectomy (NX) rat model. We studied the following three groups of male Sprague-Dawley rats: sham ( n = 6), 5/6 NX control ( n = 6), and 5/6 NX treated with vitamin E (5,000 IU/kg chow; n = 5). The 5/6 NX group showed increased severity of glomerulosclerosis vs. sham, and this was ameliorated by vitamin E therapy. Both 5/6 NX groups showed similar elevations in plasma creatinine and proteinuria and decreased 24-h creatinine clearance compared with sham. There was increased NADPH-dependent superoxide production in 5/6 NX rats vs. sham that was prevented by vitamin E. Total NO production was similarly reduced in both 5/6 NX groups. There was unchanged abundance of endothelial nitric oxide synthesis (NOS) in renal cortex and medulla and neuronal (n) NOS in medulla. However, in kidney cortex, 5/6 NX rats had lower nNOS abundance than sham, which was restored by vitamin E. An increased plasma asymmetric dimethylarginine occurred with 5/6 NX associated with decreased renal dimethylarginine dimethylaminohydrolase activity and increased type 1 protein arginine methyltransferase expression.


Author(s):  
Manouchehr Iranparvar Alamdari ◽  
Shahram Habibzadeh ◽  
Bita Shahbazzadegan ◽  
Mohammad Mazani ◽  
Amir Bigdeli ◽  
...  

Background: Diabetes type 2 associates with increased oxidative stress and reduced antioxidant. Vitamin E supplementation reduces oxidative stress in diabetic patients. We intended to measure the level of this vitamin in these patients to assess its relationship in control of patients' diabetes by designing present study.Methods: This is a descriptive and cross-sectional study and carried out on 186 patients with diabetes type 2 diagnosis. The levels of HbA1C (measured by HPLC method), TG, cholesterol, HDL, LDL and Cr were measured, and given to that the level of HbA1C lower than 7 (controlled group) and or more than 7 (uncontrolled group), patients were divided in two groups. Were designed a check list involved questions such as age and information of each patient associated with measured vitamin E level were entered into the check list and after that were analyzed data.Results: In the existing study 186 diabetic patients were examined. From within examined patients, 129 (69.3%) were women and the rest were men and average patients age were 53.33±11.2. In this study was observed there was no direct correlation between the level of cholesterol (p=0.284), LDL (p=0.538( and HDL (p=0.362) with controlled DM II in patients while in uncontrolled diabetic the triglyceride levels was more than those with controlled blood sugar significantly (p=0.046(. The average vitamin E level in patients was 1488.6±692.2 nmol/l its lowest level 114.4 nmol/l and the highest level was 6235 nmol/l.Conclusions: The results of this study show that the vitamin E levels no significant difference between control and non-control diabetic patients.


2000 ◽  
Vol 279 (5) ◽  
pp. H2176-H2187 ◽  
Author(s):  
Elena E. Ustinova ◽  
Carolyn J. Barrett ◽  
Shu-Yu Sun ◽  
Harold D. Schultz

We investigated the effects of diabetes mellitus and antioxidant treatment on the sensory and reflex function of cardiac chemosensory nerves in rats. Diabetes was induced by streptozotocin (STZ; 85 mg/kg ip). Subgroups of sham- and STZ-treated rats were chronically treated with an antioxidant, vitamin E (60 mg/kg per os daily, started 2 days before STZ). Animals were studied 6–8 wk after STZ injection. We measured renal sympathetic nerve activity (RSNA), mean arterial blood pressure (MABP), and cardiac vagal and sympathetic afferent activities in response to stimulation of chemosensitive sensory nerves in the heart by epicardial application of capsaicin (Caps) and bradykinin (BK). In cardiac sympathetic-denervated rats, Caps and BK (1–10.0 μg) evoked a vagal afferent mediated reflex depression of RSNA and MABP, which was significantly blunted in STZ-treated rats ( P < 0.05). In vagal-denervated rats, Caps and BK (1–10.0 μg) evoked a sympathetic afferent-mediated reflex elevation of RSNA and MABP, which also was significantly blunted in STZ-treated rats ( P< 0.05). Chronic vitamin E treatment effectively prevented these cardiac chemoreflex defects in STZ-treated rats without altering resting blood glucose or hemodynamics. STZ-treated rats with insulin replacement did not exhibit impaired cardiac chemoreflexes. In afferent studies, Caps and BK (0.1 g-10.0 μg) increased cardiac vagal and sympathetic afferent nerve activity in a dose-dependent manner in sham-treated rats. These responses were significantly blunted in STZ-treated rats. Vitamin E prevented the impairment of afferent discharge to chemical stimulation in STZ rats. The following were concluded: STZ-induced, insulin-dependent diabetes in rats extensively impairs the sensory and reflex properties of cardiac chemosensitive nerve endings, and these disturbances can be prevented by chronic treatment with vitamin E. These results suggest that oxidative stress plays an important role in the neuropathy of this autonomic reflex in diabetes.


2017 ◽  
Vol 2017 ◽  
pp. 1-7 ◽  
Author(s):  
Ioana Corina Bocsan ◽  
Mircea Vasile Milaciu ◽  
Raluca Maria Pop ◽  
Stefan Cristian Vesa ◽  
Lorena Ciumarnean ◽  
...  

NASH consists in lipid accumulation in hepatocytes that trigger oxidative stress, secretion of proinflammatory cytokines leading to steatohepatitis (NASH). The study aimed to investigate the levels of proinflammatory (TNF-αand IL-6) along with anti-inflammatory cytokine IL-10 in patients with NASH and to correlate the cytokines’ level with their polymorphism. Sixty-six patients with NASH and 30 healthy volunteers were included in the study. The plasmatic level of IL-6, IL-10, and TNF-αwere determined by ELISA. IL-10 -1082 G/A, IL-6 -174 G/C, and TNF-α-308 G/A polymorphisms were determined using the PCR-RFLP technique. IL-6, TNF-α, and CRP levels were significantly higher in patients with NASH. There was a positive correlation between proinflammatory cytokines and a negative correlation between IL-10 and proinflammatory markers. The G allele and GG genotype of IL-6 -174 G/C polymorphism were more frequently noticed in NASH patients. Regarding IL-10 -1082 G/A polymorphism, the AA genotype was correlated with NASH and with a low plasmatic level of IL-10. The A allele in position 308 of the TNF-αgene was associated with high level of cytokine. In conclusion, there was an imbalance between pro- and anti-inflammatory cytokines in NASH patients. IL-10 -1082 G/A and TNF-α-308 G/A genotypes were correlated with the plasmatic levels of cytokines.


2021 ◽  
Author(s):  
Yanjun Gao ◽  
Shumin Duan ◽  
Lizhi Lyu ◽  
Weixing Xu ◽  
Xiaxian Ou ◽  
...  

Abstract BackgroundTitanium dioxide (TiO2) with nanofractions is increasingly applied in food products as a food additive, which makes consumers under the health risks of titanium dioxide nanoparticles (TiO2-NPs) oral exposure. The recent ban of food additive TiO2 (E171) use in France aggravated public controversy on safety of orally ingesting TiO2-NPs. This work aimed to determine biological effects of TiO2-NPs (38.3 ± 9.3) oral consumption (100 mg/kg bw, 10 days) on TNBS-induced colitis mice and healthy mice, and the additional vitamin E administration was also conducted to explore the possible mechanism of TiO2-NPs on colitis development.ResultsOral consumption of TiO2-NPs exacerbated oxidative stress status in colitis mice by decreasing the colonic glutathione (GSH) and total glutathione (T-GSH) levels, however, TiO2-NPs administration repaired the dysbacteriosis of colitis mice, and downregulated the Toll-like receptors (TLRs), nuclear factor kappa-B (NF-κB) signal pathway and inflammatory factor (IL-1β and TNF-α) transcription levels in colon tissue, which finally decreased the TNF-α expression level and participated in the mitigation of colitis symptoms. Moreover, further vitamin E intervention after TiO2-NPs consumption could relieve the oxidative stress status (mainly by scavenging reactive oxygen species, ROS) and the inflammatory factor over-transcription in colonic epithelium of colitis mice, but the effect of TiO2-NPs on dysbacteriosis repair would not be further changed by Vitamin E. At last, TiO2-NPs induced oxidative stress status and increased NF-κB signal transcription level in colonic epithelium, which increased daily disease activity index (DAI) score and caused mild mucosal inflammatory cell infiltrate in healthy mice. ConclusionOur present work showed that oral TiO2-NPs administration indeed induced oxidative stress and made an adverse effect on the development of colitis, but TiO2-NPs could also downregulate the NF-κB signal transduction level by repairing gut dysbacteriosis, which made a predominant role in alleviating colitis. On the other hand, it should also be noticed that TiO2-NPs oral ingestion caused potential colonic inflammation risks in healthy mice.


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