Evaluation of cytogenetic and DNA damage in human lymphocytes treated with adrenaline in vitro

Djelić, Ninoslav; Radaković, Milena; Spremo-Potparević, Biljana; Živković, Lada; Bajić, Vladan; Stevanović, Jevrosima; Stanimirović, Zoran

doi:10.1016/j.tiv.2014.08.001

Cited by 11 publications

(11 citation statements)

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“…As for DNA repair, it significantly reduced damage 45 and 60 min into adrenaline exposure, which is in accordance with Djelić et al (18), where DNA damage significantly dropped after 1 h. These findings suggest that adrenaline genotoxicity decreases over time and that one hour is sufficient for cells to activate DNA repair mechanisms and compensate for the damage (33,34). This repair was significantly effective even earlier with H 2 O 2 , probably Stress increases ROS-generated damage and affects the DNA repair (39).…”

Section: Discussionsupporting

confidence: 90%

“…For negative control, cells were incubated with phosphate buffered saline (PBS, Fisher Scientific, Pittsburgh, PA). The effects of adrenaline and H 2 O 2 were investigated separately in our earlier research (14) at four concentrations (5,10,50, and 150 µmol L -1 for adrenaline and 5, 10, 25, and 50 µmol L -1 for H 2 O 2 ) that corresponded to the ones used in other studies of adrenaline-induced DNA damage (12,18). For this study we selected the concentrations of 10 µmol L -1 of adrenaline and 50 µmol L -1 of H 2 O 2 , because they produced significant DNA damage in human whole blood cells without significantly affecting cell viability.…”

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confidence: 99%

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Assessment of adrenaline-induced DNA damage in whole blood cells with the comet assay

Topalović

Dekanski²,

Spremo-Potparević

et al. 2018

Archives of Industrial Hygiene and Toxicology

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Harmful effects of elevated levels of catecholamines are mediated by various mechanisms, including gene transcription and formation of oxidation products. The aim of this study was to see whether the molecular mechanisms underlying the damaging action of adrenaline on DNA are mediated by reactive oxygen species (ROS). To do that, we exposed human whole blood cells to 10 μmol L-1adrenaline or 50 μmol L-1H2O2(used as positive control) that were separately pre-treated or post-treated with 500 μmol L-1of quercetin, a scavenger of free radicals. Quercetin significantly reduced DNA damage in both pre- and post-treatment protocols, which suggests that adrenaline mainly acts via the production of ROS. This mechanism is also supported by gradual lowering of adrenaline and H2O2-induced DNA damage 15, 30, 45, and 60 min after treatment. Our results clearly show that DNA repair mechanisms are rather effective against ROS-mediated DNA damage induced by adrenaline.

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Section: Discussionsupporting

confidence: 90%

mentioning

confidence: 99%

Assessment of adrenaline-induced DNA damage in whole blood cells with the comet assay

Topalović

Dekanski²,

Spremo-Potparević

et al. 2018

Archives of Industrial Hygiene and Toxicology

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“…Nonetheless, low-dose glucocorticoid exposure can become detrimental when repeated often enough [104, 105]. Catecholamines, released during stress by the SNS, can also affect mitochondrial function, either by increasing the metabolic state [106, 107], or by inducing ROS production leading to cytogenetic damage [108]. …”

Section: Changes In Cellular Bioenergetics Resulting From Cancer Thermentioning

confidence: 99%

Mechanisms of Neurotoxic Symptoms as a Result of Breast Cancer and Its Treatment: Considerations on the Contribution of Stress, Inflammation, and Cellular Bioenergetics

Lacourt

Heijnen²

2017

Curr Breast Cancer Rep

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Purpose of ReviewBreast cancer and its treatment are associated with a range of neurotoxic symptoms, such as fatigue, cognitive impairment, and pain. Although these symptoms generally subside after treatment completion, they become chronic in a significant subset of patients. We here summarize recent findings on neuroinflammation, stress, and mitochondrial dysfunction as mechanistic pathways leading to neurotoxic symptom experience in breast cancer patients and survivors.Recent FindingsNeuroinflammation related to stress or cancer treatment and stress resulting from diagnosis, treatment, or (cancer-related) worrying are important predictors of a neurotoxic symptom experience, both during and after treatment for breast cancer. Both inflammation and stress hormones, as well as cancer treatment, can induce mitochondrial dysfunction resulting in reduced cellular energy.SummaryWe propose reduced cellular energy (mitochondrial dysfunction) induced by inflammation, oxygen radical production, and stress as a result of cancer and/or cancer treatment as a final mechanism underlying neurotoxic symptoms.

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“…There are studies indicating toxic effects of adrenaline via signal transduction pathways [6, 7]. Also, it seems that adrenaline exerts detrimental effects via oxidative products of its metabolism [8–10]. In line with this, it was shown that autooxidation of catecholamine may generate reactive oxygen species (ROS) [11].…”

Section: Introductionmentioning

confidence: 99%

Nitroso‐Oxidative Stress, Acute Phase Response, and Cytogenetic Damage in Wistar Rats Treated with Adrenaline

Radaković

Borozan

Djelić

et al. 2018

Oxidative Medicine and Cellular Longevity

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This study is aimed at analysing biochemical and genetic endpoints of toxic effects after administration of adrenaline. For this purpose, the study was carried out on Wistar rats and three doses of adrenaline were used: 0.75 mg/kg, 1.5 mg/kg, and 3 mg/kg body weight. To achieve these aims, we investigated the effects of adrenaline on catalase (CAT), Cu, Zn-superoxide dismutase (SOD), malondialdehyde (MDA), nitrite (NO2−), carbonyl groups (PCC), and nitrotyrosine (3-NT). Total activity of lactate dehydrogenase (LDH), its relative distribution (LDH1–LDH5) activity, level of acute phase proteins (APPs), and genotoxic effect were also evaluated. The obtained results revealed that all doses of adrenaline induced a significant rise in CAT activity, MDA level, PCC, NO2−, and 3-NT and a significant decrease in SOD activity compared to control. Adrenaline exerted an increase in total activity of LDH, LDH1, and LDH2 isoenzymes. Further study showed that adrenaline significantly decreased serum albumin level and albumin-globulin ratio, while the level of APPs (α1-acid glycoprotein and haptoglobulin) is increased. The micronucleus test revealed a genotoxic effect of adrenaline at higher concentrations (1.5 mg/kg and 3 mg/kg body weight) compared to untreated rats. It can be concluded that adrenaline exerts oxidative and nitrative stress in rats, increased damage to lipids and proteins, and damage of cardiomyocytes and cytogenetic damage. Obtained results may contribute to better understanding of the toxicity of adrenaline with aims to preventing its harmful effects.

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Evaluation of cytogenetic and DNA damage in human lymphocytes treated with adrenaline in vitro

Cited by 11 publications

References 50 publications

Assessment of adrenaline-induced DNA damage in whole blood cells with the comet assay

Assessment of adrenaline-induced DNA damage in whole blood cells with the comet assay

Mechanisms of Neurotoxic Symptoms as a Result of Breast Cancer and Its Treatment: Considerations on the Contribution of Stress, Inflammation, and Cellular Bioenergetics

Nitroso‐Oxidative Stress, Acute Phase Response, and Cytogenetic Damage in Wistar Rats Treated with Adrenaline

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