Investigation of DNA damage, oxidative stress, and inflammation in synthetic cannabinoid users

2020 ◽  
Vol 39 (11) ◽  
pp. 1454-1462
Author(s):  
EM Guler ◽  
MY Bektay ◽  
AG Akyildiz ◽  
BH Sisman ◽  
FV Izzettin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Interleukin 1 ◽  
Synthetic Cannabinoids ◽  
Public Health Problem ◽  
Total Antioxidant Status ◽  
Stress Index ◽  
Important Public Health Problem ◽  
Necrosis Factor Alpha ◽  
Tnf Α

Background: The widespread use of synthetic cannabinoids (SCs) among youth has become an important public health problem. Several life-threatening side effects of SC have been reported, including cardiovascular, gastrointestinal, neurological, renal, metabolic, ophthalmologic, and pulmonary effects, besides skin toxicity and hepatotoxicity. Methods: Given that high levels of SC can lead to oxidative stress, DNA damage, and inflammation, it has been aimed in this study to investigate the effects of SC in aspects of primary DNA damage, plasma total oxidant status (TOS)/total antioxidant status (TAS), thiol–disulfide homeostasis, myeloperoxidase (MPO) level, and cytokine levels (interleukin 1 beta (IL-1β), interleukin 6 (IL-6), and tumor necrosis factor-alpha (TNF-α)) of 40 SC users (SCUs) in Turkey. Results: Mean plasma TOS levels were significantly higher in the SCUs group than in the healthy group (HG). Similarly, mononuclear leukocyte DNA damage, plasma TOS, MPO activity, disulfide, oxidative stress index levels, IL-1β, IL-6, and TNF-α levels were significantly higher in the SCU group than in the HG, whereas plasma TAS, total, and native thiol levels were significantly lower in the SCU group than in the HG. Conclusion: It is concluded that SC can cause increase in oxidative stress and in inflammatory processes in addition to its potential for DNA damage. Additional studies with larger sample sizes and longer durations should be held to understand more specific outcomes of SC use.

Oxydative stress markers and cytokine levels in rosuvastatin-medicated hypercholesterolemia patients

2018 ◽  
Vol 44 (4) ◽  
pp. 530-538
Author(s):  
Aysun Çetin ◽  
İhsan Çetin ◽  
Semih Yılmaz ◽  
Ahmet Şen ◽  
Göktuğ Savaş ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Interleukin 1 ◽  
Paraoxonase 1 ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Phenotypic Effect ◽  
Necrosis Factor Alpha ◽  
Stress Markers ◽  
Tnf Α ◽  
Before And After

Abstract Background Limited research is available concerning the relationship between oxidative stress and inflammation parameters, and simultaneously the effects of rosuvastatin on these markers in patients with hypercholesterolemia. We aimed to investigate the connection between cytokines and oxidative stress markers in patients with hypercholesterolemia before and after rosuvastatin treatment. Methods The study consisted of 30 hypercholesterolemic patients diagnosed with routine laboratory tests and 30 healthy participants. The lipid parameters, interleukin-1 beta (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), paraoxonase-1 (PON1) and malondialdehyde (MDA) levels in controls and patients with hypercholesterolemia before and after 12-week treatment with rosuvastatin (10 mg/kg/day), were analyzed by means of enzyme-linked immunosorbent assay. Results It was found that a 12-week cure with rosuvastatin resulted in substantial reductions in IL-1β, IL-6 and TNF-α and MDA levels as in rising activities of PON1 in patients with hypercholesterolemia. Before treatment, the PON1 levels were significantly negatively correlated with TNF-α and IL-6 in control group, while it was positively correlated with TNF-α in patients. Conclusion Our outcomes provide evidence of protected effect of rosuvastatin for inflammation and oxidative damage. It will be of great interest to determine whether the correlation between PON1 and cytokines has any phenotypic effect on PON1.

scholarly journals Effects of Selenium-Enriched Protein fromGanoderma lucidumon the Levels of IL-1βand TNF-α, Oxidative Stress, and NF-κB Activation in Ovalbumin-Induced Asthmatic Mice

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Guan Min-chang ◽  
Tang Wei-hong ◽  
Xu Zhen ◽  
Sun Jie
Keyword(s):  
Oxidative Stress ◽  
Interleukin 1 ◽  
Experimental Conditions ◽  
Necrosis Factor Alpha ◽  
Organic Selenium ◽  
Inorganic Selenium ◽  
Tnf Α ◽  
Liver And Kidney ◽  
Factor Alpha ◽  
Endogenous Antioxidant

The purpose of this study was to compare the effect and toxicity of organic selenium (Pro-Se) with inorganic selenium (IOSe) in preventing asthma in ovalbumin-induced asthmatic mice. After the mice were treated orally with Pro-Se and IOSe, respectively, the plasma Se levels, Se accumulation in liver and kidney, tumor necrosis factor alpha (TNF-α), interleukin 1 beta (IL-1β), oxidative stress, and NF-κB activation in lung were examined. The results showed that the serumal Se levels in the mice fed the Pro-Se were significant (P<0.01) elevations. It results in restoration of the level of endogenous antioxidant enzyme, lower levels of TNF-αand IL-1β, and activated NF-κB in the asthmatic mice. Our experiments have demonstrated profound differences between the activities of organic selenium and inorganic selenium in experimental conditions. These data provide an important proof of the concept that organic selenium might be a new potential therapy for the management of childhood asthma in humans.

scholarly journals Oxidative stress index can be a new marker related to disease severity in COVID-19

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Serdar Doğan ◽  
Tayibe Bal ◽  
Mehmet Çabalak ◽  
Nursel Dikmen ◽  
Hasibullah Yaqoobi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Disease Severity ◽  
Total Antioxidant Status ◽  
Stress Index ◽  
Oxidative Stress Index ◽  
Oxidative Balance ◽  
Tnf Α ◽  
Severe Group ◽  
Severity Of The Disease ◽  
D Dimer

Abstract Objectives The aim of this study was to evaluate the relationship between systemic oxidative balance, and the severity of the disease in patients with COVID 19. Methods Sixty-four patients were divided into three groups according to the severity of the disease: mild (n=28), moderate (n=11) and severe (n=25). Twenty-four healthy controls included to the study. Proinflammatory cytokines (IL-6 and TNF-α), D-dimer, fibrinogen, total oxidative status (TOS), total antioxidant status (TAS) were measured and oxidative stress index (OSI) was calculated. Results The mean age of severe group was significantly higher than the other groups (p=0.001). TAS levels were significantly decreased in all patient groups compared to controls, while serum TOS and OSI levels were significantly different in all three stages of the disease. Serum IL-6 and TNF- α levels were significantly elevated in severe group compared to other groups. TOS and OSI levels were also significantly correlated with IL-6, CRP, ferritin, fibrinogen, LDH and D-dimer. Conclusions TOS and OSI levels are an indicator of systemic oxidative balance in COVID-19 and related to the disease severity. They can be an important marker for evaluating the disease severity and used in the management of patients with COVID-19.

scholarly journals Vitamin C Mitigates Oxidative Stress and Tumor Necrosis Factor-Alpha in Severe Community-Acquired Pneumonia and LPS-Induced Macrophages

2014 ◽  
Vol 2014 ◽  
pp. 1-11 ◽  
Author(s):  
Yuanyuan Chen ◽  
Guangyan Luo ◽  
Jiao Yuan ◽  
Yuanyuan Wang ◽  
Xiaoqiong Yang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Tumor Necrosis Factor ◽  
Vitamin C ◽  
Tumor Necrosis ◽  
Community Acquired Pneumonia ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

Oxidative stress is an important part of host innate immune response to foreign pathogens. However, the impact of vitamin C on oxidative stress and inflammation remains unclear in community-acquired pneumonia (CAP). We aimed to determine the effect of vitamin C on oxidative stress and inflammation. CAP patients were enrolled. Reactive oxygen species (ROS), DNA damage, superoxide dismutases (SOD) activity, tumor necrosis factor-alpha (TNF-α), and IL-6 were analyzed in CAP patients and LPS-stimulated macrophages cells. MH-S cells were transfected with RFP-LC3 plasmids. Autophagy was measured in LPS-stimulated macrophages cells. Severe CAP patients showed significantly increased ROS, DNA damage, TNF-α, and IL-6. SOD was significantly decreased in severe CAP. Vitamin C significantly decreased ROS, DNA damage, TNF-α, and IL-6. Vitamin C inhibited LPS-induced ROS, DNA damage, TNF-α, IL-6, and p38 in macrophages cells. Vitamin C inhibited autophagy in LPS-induced macrophages cells. These findings indicated that severe CAP exhibited significantly increased oxidative stress, DNA damage, and proinflammatory mediator. Vitamin C mitigated oxidative stress and proinflammatory mediator suggesting a possible mechanism for vitamin C in severe CAP.

The effect of wild blueberry (Vaccinium angustifolium) consumption on oxidative stress, inflammation, and DNA damage associated with exercise

2015 ◽  
Vol 11 (3) ◽  
pp. 173-181 ◽  
Author(s):  
T. Bloedon ◽  
S. Vendrame ◽  
J. Bolton ◽  
R. Lehnhard ◽  
P. Riso ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Manganese Superoxide Dismutase ◽  
Daily Consumption ◽  
Post Intervention ◽  
Necrosis Factor Alpha ◽  
Blood Samples ◽  
Tnf Α ◽  
Wild Blueberries ◽  
Wild Blueberry

The present study examined the effect of wild blueberries on oxidative stress, the inflammatory response and DNA damage associated with exercise in untrained individuals. Ten sedentary males, aged 21-26 years, completed two single bouts of treadmill exercise at 70% of their VO2max. One bout occurred prior to, and one occurred following daily consumption of 300 g of wild blueberries for eight weeks. Blood samples were drawn during both exercise bouts and assayed for measures of oxidative stress (manganese-superoxide dismutase: Mn-SOD), inflammation (tumour necrosis factor-alpha: TNF-α and interleukin-6: IL-6) and DNA damage (comet assay). Blood samples were obtained immediately pre-exercise, and post exercise at 0, 30 and 60 min, and 3 and 6 h. A significant interaction between pre- and post-intervention over time was detected in plasma Mn-SOD concentration. Post hoc comparisons showed no significant differences between time points pre- and post-intervention, although plasma Mn-SOD concentration showed a moderate trend 30 min after exercise with wild blueberry consumption (P=0.072). A significant increase in IL-6 was observed for time (at 30 min and 1 h) following exercise, both pre- and post-intervention. No significant differences were seen in DNA damage or TNF-α either with exercise or the intervention. This study demonstrates that a single bout of exercise at 70% of VO2max is sufficient to cause a significant increase in inflammation in untrained individuals. The trend for Mn-SOD concentration to decrease after exercise post-intervention indicates a potential benefit of wild blueberries to increase antioxidant capacity and reduce oxidative stress.

scholarly journals 3-Indolepropionic Acid Prevented Chlorpyrifos-Induced Hepatorenal Toxicities in Rats By Improving Anti-Inflammatory, Antioxidant And Apoptotic Responses and Abating DNA Damage

2021 ◽  
Author(s):  
Solomon E. Owumi ◽  
Eseroghene S. Najophe ◽  
Moses T. Otunla
Keyword(s):  
Dna Damage ◽  
Caspase 3 ◽  
Corn Oil ◽  
Interleukin 1 ◽  
Enzyme Linked Immunosorbent Assay ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Liver And Kidney ◽  
Hepatorenal Function ◽  
The Individual

Abstract We examined the individual and combined effect of 3-Indolepropionic acid (IPA) and Chlorpyrifos (CPF) on rat hepatorenal function. The experimental cohorts (n=6) were treated per os for 14 consecutive days as follows: Control (Corn oil 2 mL/kg body weight), CPF alone (5 mg/kg), IPA alone (50 mg/kg) and the co-treated cohorts (CPF: 5 mg/kg + IPA: 25 or 50 mg/kg). Biomarkers of hepatorenal damage, antioxidant and myeloperoxidase (MPO) activities, the levels of nitric oxide (NO), lipid peroxidation (LPO) and reactive oxygen and nitrogen (RONS) species were spectrophotometrically evaluated. Besides, the concentration of tumour necrosis factor-alpha (TNF- α), interleukin-1 β (IL-1β) and caspase-3 activity and 8-hydroxy-2’-deoxyguanosine adducts (8-OHdG) was also assessed by Enzyme-Linked Immunosorbent Assay. Treatment with CPF alone increased biomarkers of hepatorenal toxicity was significantly (p<0.05) alleviated in rats co-exposed to CPF and IPA. Moreover, the decrease in antioxidant status as antioxidant elevation in RONS and LPO were lessened (p<0.05) in rats co-treated with CPF and IPA. CPF mediated increases in TNF-α, IL-1β, NO, MPO and caspase-3 activity were reduced (p<0.05) in the liver and kidney of rats co-exposed to CPF and IPA. In addition, 8-OHdG adducts formation were reduced in rats treated with 3-IPA dose-dependently. Light microscopic examination showed that histopathological lesions severity induced by CPF were alleviated in rats co-exposed to IPA and CPF. In conclusion, the results demonstrated that rats co-exposed to IPA and CPF exhibited reduced CPF-induced oxidative stress, inflammation, DNA damage and caspase-3 activation of the liver and kidney.

Association between calcitriol and paricalcitol with oxidative stress in patients with hemodialysis

2020 ◽  
pp. 1-8
Author(s):  
Hasan Haci Yeter ◽  
Berfu Korucu ◽  
Elif Burcu Bali ◽  
Ulver Derici
Keyword(s):  
Oxidative Stress ◽  
Vitamin D ◽  
Antioxidant Status ◽  
Total Antioxidant Status ◽  
Stress Index ◽  
Total Oxidant Status ◽  
Vitamin D Analog ◽  
Total Antioxidant ◽  
Oxidant Status ◽  
And Oxidative Stress

Abstract. Background: The pathophysiological basis of chronic kidney disease and its complications, including cardiovascular disease, are associated with chronic inflammation and oxidative stress. We investigated the effects of active vitamin D (calcitriol) and synthetic vitamin D analog (paricalcitol) on oxidative stress in hemodialysis patients. Methods: This cross-sectional study was composed of 83 patients with a minimum hemodialysis vintage of one year. Patients with a history of any infection, malignancy, and chronic inflammatory disease were excluded. Oxidative markers (total oxidant and antioxidant status) and inflammation markers (C-reactive protein and interleukin-6) were analyzed. Results: A total of 47% (39/83) patients were using active or analog vitamin D. Total antioxidant status was significantly higher in patients with using active or analog vitamin D than those who did not use (p = 0.006). Whereas, total oxidant status and oxidative stress index were significantly higher in patients with not using vitamin D when compared with the patients who were using vitamin D preparation (p = 0.005 and p = 0.004, respectively). On the other hand, total antioxidant status, total oxidant status, and oxidative stress index were similar between patients who used active vitamin D or vitamin D analog (p = 0.6; p = 0.4 and p = 0.7, respectively). Conclusion: The use of active or selective vitamin D analog in these patients decreases total oxidant status and increases total antioxidant status. Also, paricalcitol is as effective as calcitriol in decreasing total oxidant status and increasing total antioxidant status in patients with chronic kidney disease.

Role of inflammation in the development of colorectal cancer

2020 ◽  
Vol 20 ◽  
Author(s):  
Sridhar Muthusami ◽  
R. Ileng Kumaran ◽  
Kokelavani Nampalli Babu ◽  
Sneha Krishnamoorthy ◽  
Akash Guruswamy ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Chronic Inflammation ◽  
Interleukin 1 ◽  
Cell Types ◽  
Model Systems ◽  
Cytokine Gene Expression ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Proinflammatory Molecules

: Chronic inflammation can lead to the development of many diseases including cancer. Inflammatory bowel disease (IBD) that includes both ulcerative colitis (UC) and Crohn's disease (CD) are risk factors for the development of colorectal cancer (CRC). Many cytokines produced primarily by the gut immune cells either during or in response to localized inflammation in the colon and rectum are known to stimulate the complex interactions between the different cell types in the gut environment resulting in acute inflammation. Subsequently, chronic inflammation together with genetic and epigenetic changes has been shown to lead to the development and progression of CRC. Various cell types present in the colon such as enterocytes, Paneth cells, goblet cells and macrophages express receptors for inflammatory cytokines and respond to tumor necrosis factor alpha (TNF-α), interleukin-1 beta (IL-1β), IL-6 and other cytokines. Among the several cytokines produced, TNF-α and IL-1β are the key proinflammatory molecules that play critical roles in the development of CRC. The current review is intended to consolidate the published findings to focus on the role of proinflammatory cytokines, namely TNF-α and IL-1β, on inflammation (and the altered immune response) in the gut, to better understand the development of CRC in IBD, using various experimental model systems, preclinical and clinical studies. Moreover, this review also highlights the current therapeutic strategies available (monotherapy and combination therapy), to alleviate the symptoms or treat inflammationassociated CRC by using monoclonal antibodies or aptamers to block proinflammatory molecules, inhibitors of tyrosine kinases in inflammatory signaling cascade, competitive inhibitors of proinflammatory molecules, and the nucleic acid drugs like small activating RNAs (saRNAs) or microRNA (miRNA) mimics to activate tumor suppressor or repress oncogene/proinflammatory cytokine gene expression.

scholarly journals Neuroprotective effects of eugenol against aluminiuminduced toxicity in the rat brain

2017 ◽  
Vol 68 (1) ◽  
pp. 27-37 ◽  
Author(s):  
Mahmoud M. Said ◽  
Marwa M. Abd Rabo
Keyword(s):  
Total Antioxidant Status ◽  
Basal Diet ◽  
Acetylcholinesterase Activity ◽  
Aluminium Chloride ◽  
Neuroprotective Effects ◽  
Necrosis Factor Alpha ◽  
Protein Levels ◽  
Tnf Α ◽  
Total Antioxidant ◽  
Male Wistar Rats

AbstractAluminium (Al) is a neurotoxic metal that contributes to the progression of several neurodegenerative diseases. The aim of the present study was to evaluate the protective effect of dietary eugenol supplementation against aluminium (Al)- induced cerebral damage in rats. Male Wistar rats were divided into four groups: normal controls, rats fed a diet containing 6,000 μg g-1eugenol, rats intoxicated daily with aluminium chloride (84 mg kg-1body weight) p. o. and fed either a basal diet or a eugenol-containing diet. Daily oral administration of Al for four consecutive weeks to rats significantly reduced brain total antioxidant status (TAS) (11.42±0.31 μmol g-1tissue, p<0.001) with a subsequent significant enhancement of lipid peroxidation (MDA) (32.55±1.68 nmol g-1tissue, p<0.002). In addition, Al enhanced brain acetylcholinesterase activity (AChE) (46.22±4.90 U mg-1protein, p<0.001), tumour necrosis factor alpha (TNF-α) (118.72±11.32 pg mg-1protein, p<0.001), and caspase 3 (Casp-3) (8.77±1.26 ng mg-1protein, p<0.001) levels, and in contrast significantly suppressed brain-derived neurotrophic factor (BDNF) (82.74±14.53 pg mg-1protein, p<0.002) and serotonin (5-HT) (1.54±0.12 ng mg-1tissue, p<0.01) levels. Furthermore, decreased glial fibrillary acidic protein (GFAP) immunostaining was noticed in the striatum of Al-intoxicated rats, compared with untreated controls. On the other hand, co-administration of dietary eugenol with Al intoxication restored brain BDNF (108.76±2.64 pg mg-1protein) and 5-HT (2.13±0.27 ng mg-1tissue) to normal levels, enhanced brain TAS (13.43±0.24 μmol g-1tissue, p<0.05), with a concomitant significant reduction in TNF-α (69.98±4.74 pg mg-1protein) and Casp-3 (3.80±0.37 ng mg-1protein) levels (p<0.001), as well as AChE activity (24.50±3.25 U mg-1protein, p<0.001), and increased striatal GFAP immunoreactivity, compared with Al-treated rats. Histological findings of brain tissues verified biochemical data. In conclusion, eugenol holds potential as a neuroprotective agent through its hydrophobic, antioxidant, and anti-apoptotic properties, as well as its neurotrophic ability against Al-induced brain toxicity in rats.

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